DIP Episode 192 - Updated USMLE Step 1 Endocrine Review Series 2 (Adrenals, complete)

Okay, welcome. My name is Divine and my residence. This is episode 192 of the Divine Intervention podcast. In this podcast, I'm just going to be finishing up the adrenal stuff from yesterday. So let's just jump right into it. So what if they give you a question about a patient, you know, they tell you over the last like six months this patient has gained a ton of weight. This patient has like new onset hypertension, has like very high blood sugars, has like I don't know like a vertebral compression fracture. And then they tell you that you see purple straya on the skin. If you see that, what are you thinking about? But I hope you're telling me that you're thinking about a Cushion syndrome, right? Cushion syndrome, again, by definition, is just anything that arises from hypercordisolism, right? And the thing is, typically, when a person has a Cushion syndrome, you know, they can have like some signs and symptoms, right? Like the ogin weight, right? They will have, because remember, cortisol is a diabetes, you know, genic hormone, right? They will also have like this weird fight redistribution, right? So their faces will be big, kind of look like the moon, like moon faces, or they can have like the buffalo hump. Remember that some of those AIDS medications, especially the pretty inhibitors, can also cause fat redistribution, right? So you know, they can have like the trunk of obesity, high blood pressures, like neon-set diabetes.

I mean, in general, I as a clinician, I try to think twice before I give steroids to diabetes, right? Because they can really, really like do a big number in their diabetes. And again, these people also have a high risk of infection, because again, by the different mechanisms, I described yesterday, cortisol kind of suppresses the immune system, right? And they do have like the purple striand, the skin and all that stuff, right? So those are the classic things you'll see on an MBM exam with regards to, with regards to Cushion syndrome, right? So the thing is, the most common cause of Cushion syndrome, like I said yesterday, is just the pressing, exogenously taking corticosteric, for maybe some autoimmune disease, for some inflammatory disorder, or something along those lines. But if you're looking in terms of endogenous causes of Cushion syndrome, I said the most common cause, about like 70% of cases, if I'm not mistaken, is Cushion's disease, right? And then another fairly common cause is a topic, ACTH production, right? From like a small cell lung cancer, for example, right? So other things, I mean, like if a person has like a general hyperplasia, or like an adrenaline, the number that's screening cortisol, right? Those can also all cause, those can also all cause hypercortisolation and Cushion syndrome. So typically, the thing you do to diagnose Cushion syndrome, right? Is you know, you can do one of two things, right?

So you can remember, where every condition in medicine, right? There's almost always some kind of screening test. And then after the screening test, yeah, all the tests you do beyond that, that's kind of like a confirmatory test, right? So the thing you do is you can do one of two things for Cushion syndrome. The first thing is you can decide to measure the 24 hour urinary free cortisol, all right? If a person has Cushion syndrome, it's going to be elevated, right? So you're like, you can do that. But actually, another screening test you can do is you can actually just go ahead and do the low dose dexamethosol suppression test, right? You give low dose dexamethosol, you'll typically expect that the person's morning cortisol, remember I said that cortisol is highest in the mornings, you'd expect that the morning cortisol should be suppressed, right? So the thing is, if you have like an elevated 24 hour urinary free cortisol or a person's morning cortisol is not suppressed with low dose dexamethosol augmentation the night before, right? Then that tells you that the person has Cushion syndrome. So that's your first step. But your second step is to ask yourself, is this an ACTH dependent cause of Cushion syndrome or an ACTH independent cause of Cushion syndrome? And the way you figure that out is literally just measure the person's ACTH, ACTH levels, right?

So you've done those first tests that I talked about the 24 hour urinary free cortisol and the low dose dexamethosol suppression test you're like, okay, these people for sure have Cushion syndrome. Well, the next thing you do is you then measure the ACTH levels. If the ACTH is low, then that tells you that the person has an ACTH independent cause of Cushion syndrome. So the problem is likely in the adrenal glands. But if the ACTH is high, then that tells you that the person has an ACTH dependent cause of Cushion syndrome. That's what you do in your second step, right? So in your second step, because if you figure out that the ACTH is low, then you know the problems that the adrenal glands, your investigation is done pretty much at that point. But if you notice that the ACTH is high, you then need to go to a third step because classically, on MDMA exams, there are two causes of ACTH dependent Cushion syndrome. It can be Cushion's disease. We have a pituitary, the nomad that's taken on Crapton of ACTH or you can have an atopic ACTH, you can have a topic ACTH production from like a tumor or something like that, right? So classically, what you then do in that third step is the high dose dexamethosone suppression test. When you do the high dose dexamethosone suppression test, if you notice that the morning cortisol suppresses, then you know that Cushion's disease, then you do an MRI of the brain to find the pituitary, the nomad.

But if you notice that the high dose dexamethosone does not suppress the ACTH production, I mean the cortisol, by like the morning cortisol, then you know that it's a topic ACTH production and then you start looking for like the small, it will almost always be a small cell long cancer on the USMEL exams. So that's how you, that's how you tease those things apart. Now some last quick things, I guess I want to go ahead and mention here is if you really think about it, right? Like if a person has Cushion syndrome, right? Let's say they have a tumor or whatever that's causing it. Obviously you want to try to reset that tumor. But one thing you may see on the USMEL step one is you may have to give those people keto-conazole. Keto-conazole is an anti-fongal, but it actually inhibits like multiple enzymes involved in the synthesis of local corticulture. So that can help, that can help with that. Actually, if you want to be a little more specific, keto-conazole actually inhibits cholesterol, desmoleys, right? Desmoleys is one of the key gateway enzymes to the synthesis of a lot of things that we find in the adrenal glands. Now the thing is if a person has an, they are just some weird things that you may not necessarily think about what I think, I want to maybe go ahead and treat here. The thing is, when a person has an ACTH dependent cause of the Cushion syndrome, you should actually, what should you expect if you look at those people's adrenal glands on imaging?

With our hope, you say that they should have like bilateral at hyperpleasure of the adrenal glands, okay? That's actually something that's very high yields to know. I'm understanding for example, right? And that should make sense because if you are systemically releasing ACTH, then that will stimulate both adrenal glands, right? Those people, those people's adrenal glands will both undergo hyperpleasure, right? So the thing is, comparing contrast with a person that has like an ACTH independent cause of Cushion syndrome. So let's say, for example, a person has, let's say a person has like an adenoma in the adrenal cortex that's decreasing a ton of cortisol, right? That will suppress those people's ACTH, right? And if a person's ACTH is suppressed, then guess what? Those people actually have like atrophy of the adrenal glands, right? Or let's assume you're exogenously taking steroids for like an autoimmune disease. That will also again suppress your ACTH and that will cause bilateral atrophy of the adrenal glands. So again, I would really hope that you understand that stuff. This stuff again, you may say you're, you know, divide your being a little too particular, blah, blah, blah, blah, blah, blah, but these things are all important to know for exams. And personally, I think that is all I want to say about, I think that's all I want to say about about Cushing syndrome.

So I think one thing that, you know, probably makes sense for me to go ahead and discuss although this should take me much time is, let's see, what are the topics that I have in mind to talk about? I guess we can talk about like, con syndrome, right? So let's, you know, let's go ahead and talk about con syndrome, right? So the thing is, con syndrome, right? I mean, sometimes you may see the name being exams referred to as like primary hyperodosteronism. This is just again, tumor, usually it's like an, it can be like an adenoma in the adrenal cortex that's making a crop tone of, of our, of our doster, right? And the thing is, if you have high levels of our doster, right? Again, remember this principle, self-business we talked about yesterday, it will increase sodium reabsorption, right? So water will follow, so you become fully expanded, so you have hypertension, right? We also talked about how you would waste potassium, also the principle, self, right? So you get a hypochemia and then we also talked about how when you have high levels of our doster and double activity, the proton pump that we find on the urinary surface of the alpha-intercalculated cells, right? So that will cause a metabolic alkalosis because you're literally like dumping protons in the urine, right? So the thing is primary hyperodosteronism, again, when you see the work primary, that means the problem is at the level of the, at the level of the adrenals, right?

So that means, so let's kind of examine, right? So what are some things that can cause primary hyperodosteronism? Because again, I just kind of said at the beginning, oh, you could have an adrenal adenoma in the cortex that's making a ton of our doster, well, that's not always the case, right? The thing is, you can actually have like just bilateral hyperpleasure of the adrenal glands and because you have bilateral hyperpleasure, you have like hyperpleasure of the zona glomerulosa in both adrenals and then you're making a crap ton of our doster with that. In fact, the most common cause, this is very high yield to know, the most common cause of primary hyperodosteronism is bilateral adrenal hyperpleasure, okay? But if you have an adenoma, right? Like in one adrenal gland that's beginning to ton of our doster, that can also cause a primary hyperodosteronism. But in that specific case, that's what's known as con syndrome, okay? Con syndrome is primary hyperodosteronism that arises from an adrenal adenoma that's making our doster, okay? But primary hyperodosteronism again, like I said, can also be caused by bilateral adrenal hyperpleasure. Now, so now that I've talked about primary hyperodosteronism, well, what can cause secondary hyperodosteronism? Because, again, hyperodosteronism can arise from many different causes that are outside of the adrenal glands, right?

The classic one you'll see is if a person has any kind of low flow state with regards to the adrenal arteries, right? Like the afrin arterial, if you want to be a little more specific. Because think about it, right? Like if you're not, let's say for example, a person has like adrenal artery stenosis, right? Or fibromuscular dysplasia, those people are not going to be profusing the afrin arterial properly. So the GG cells will freak out, so that begin a ton of rene. That rene will convert angiotensinogen to angiotensinone, and then angiotensinone will travel to the lungs, and then the endothelial cells in the pulmonary capillary will convert the angiotensinone to angiotensin II. And then that angiotensin II will go to the zona glomerulosa of the adrenal gland, most specifically the adrenal cortex, and go ahead and make you make more out of the syrup, right? So that can cause secondary hyperodosteronism. But there are other things, right? Because, again, the friends at the MVD know that pretty much everyone has memorized the spritinal arteries to know his business. So you know, there are some more things that, again, make sense if you just know them or think about them or they are brought to your attention, right? So for example, if a person has CHF, well, if you have CHF, yes, there's nothing wrong with your reneal arteries, but you're going to be hyper-perfusing them, because you don't have enough cardiac outputs to send blood forward, right?

If a person has cirrhosis, if your liver is the primary source of protein in the body, so if you're not able to make protein, then guess what happens? You will not be able to maintain adequate oncotic pressures in your bloodstream, and if you're not able to maintain oncotic pressures, then you will hyper-perfuse, because you have a lot of fluid extrovisation, so your introviscule volume will be down, and if that happens, then you will not have enough fluid in your vasculotry to produce the effinatural. If a person has like nephrodite syndrome, you're literally like PNL protein, right? So again, that kills your oncotic pressures, that kills your introviscule volumes, you hyper-perfuse the effinatural, and you kick off the reneal and retension of the certain system. Or if, for example, a person has, if a person has like a mini-trace disease, that's where you're essentially like getting rid of protein, both through your GI tract, right? That can again also kill your oncotic pressures, and that can cause a, that can cause a secondary hyper-auto-suronism, right? So again, all these things, again, the classic presentation will be a person that will have like resistant hypertension, they'll have a metabolic alkylosis, which I've talked about the mechanism behind that, and they also have hypochylenial, right? And remember, hypochylenial can cause problems on an e-key gee, right?

It can cause a prolongation of the guting interval, you can see like a flat T-wave, you can see like the U waves and stuff like that. But also remember, because these people have a metabolic alkylosis, remember, albuiumin is the primary protein in the body, and albuiumin has a lot of caboxidic acid groups, right? So if you remember from organic chemistry in college, like you know, you have like a carboneal group, like you have your carbon double bond to oxygen, and then you have carbon single bond to an oxygen, and then that oxygen is paired up with a hydrogen, right? That hydrogen is very acidic, right? So because a caboxyl group, it has like a peach of around like five, right? So the thing is that caboxyl group in the presence of a metabolic alkylosis, you strip of that hydrogen ion from the caboxyl group, you'll expose a negative charge on, so you essentially form like a caboxylid anion. So that negative charge on that oxygen that is free is very reactive, and the thing is it actually reacts very nicely with calcium, okay? So bind up that calcium, and when you bind up that calcium, that can actually cause a hypochylcemia, right? So the free calcium in a person that has a metabolic alkylosis will actually be decreased, but the total serum calcium, right, will be normal, okay?

Well the free calcium, the ionized calcium, the calcium that is metabolically active will be decreased because it's paired up basically with those free oxygen anions that we find from those caboxyl groups that have been deprotonated by the metabolic alkylosis, right? So the thing is you may say, oh divine, if a person has high proud of seronism, right? They keep absorbing sodium in the principle cell, water keeps flowing. Why do those people not keep like reabsorbing fluid, fluid, fluid, fluid, fluid, fluid, fluid, fluid, fluid, and then they explode? Well, the good thing about your body is that your body has mechanisms in place to counteract high proud of seronism, and those things are known as the aldosterone escape mechanisms. The thing is there are many mechanisms of our aldosterone escape, but probably the only one I'll say that's probably like very useful for you to know, actually not a matter of very useful, very high yield for you to know for the USMLA exams is this, right? So think about it. If you're absorbing the ton of sodium, we're absorbing the ton of fluid at the same time, that will expand you in travasculo volume, right? If your in travasculo volume is expanded, right? Then that would dilute your your heart chambers, right? And if you dilute like your ventricles, for example, you release something known as H-R-N-A-T-R-E-P-T-T. The thing is H-R-N-A-T-R-E-P-T-T-T basically makes you dump fluid.

It essentially shuts down the fluid reabsorption at the level of the nephron, right? So you dump a ton of fluid in your urine, so that helps you avoid some of the problems that happens when you have high-proudosteronism. So again, think about it's our natural nitrhytic peptide as something, like it kind of like inhibits sodium reabsorption. So because you're inhibiting sodium reabsorption, then sodium stays in the like the lumens of the nephron and water for lose, and then you have a natural recess. That's why it's called atrial nitrhyritic peptide, right? Natural retic. Remember sodium is NE, right? I mean, I think the Greek name or the Latin name for sodium is natural, right? So, natural retic peptide, right? It gets rid of sodium water for lose, right? So that's one of the outdozorinist skip mechanisms. It's a mechanism to escape from high-proudosteronism, right? And the thing is this is white typically, right? If a person has like, on syndrome, right? You may say, oh, this person has hypertension, so it's bad, bad, bad, bad, bad. So let me put them on the classic hypertensive, like anti-hypertensives, like a diuretic, for example. That's a terrible like it. If you put a person, let's say, or like a person that has high-proudosteronism, or like a lube diuretic, right? They can have a profound hypochylemia, like profound hypochylemia that can through them into a redmiens, right?

So if a person has resistant hypertension, and they have it from con syndrome, it makes more sense to go ahead and give those people, like, you want to give them something more along the lines of like sperinolectone or a pleridone, because that would directly like target the pathophysiology of their problem. Remember, sperinolectone is an outdozorin receptor antagonist, but it also has antigen receptor blocking activity, so it can cause gynecomastia. And actually, sperinolectone also inhibits five-offer inductees in the skin, so it can actually be used to treat herstautism, believe it or not, right? But a pleridone, especially in the sense that all it does is it blocks out those seren receptors. It also does not concurrently block antigen receptors, so you classically will not observe gynecomastia in a person that is taking a pleridone, but obviously a pleridone should be more expensive by virtue of that. So again, you really want to be careful, you don't want to give, you really do not want to give a loop diuretic or a thazide diuretic or anything of that sort. So a person that has resistant hypertension from like hyper-outdozorinism, right? That would not be a great idea, right? That would not be a great idea. And remember, right, the levels of reigning, right? In a person that has secondary hyper-outdozorinism, their reading levels will be high, right? But in a person that has primary hyper-outdozorinism, their reading levels will be low. That should make sense, right?

Because if you have like an agenolate normal again, making a ton of outdozorin, right? You're in javasco level, it makes your hyper-perfused your afrin material. So that would show down to gg cells so you don't make reigning, right? Versus a present that has like renal arteries stenosis, for example, given the rise to secondary hyper-outdozorinism, they are not profusing the afrin materials, right? So it's the gg cells that kick off the hyper-outdozorinism pretty much, so the reigning levels are high. So again, those are, again, it's a subtle difference, but it's one of those things people don't think much about that ends up being very high yield for purposes of the USMLA exams. So I guess to kind of wrap up today, let me just basically talk about like some malignancies that arise in like around like the adrenal glands, so let's so you know, let's talk about some like, you know, like fiochromos, like tumor and all that stuff, neuroblastoma, yeah, let's kind of mention those real quick and then we'll kind of move on and then we'll be done with this with this adrenal podcast. So basically, right? Like, I guess some key things you want to keep in mind, you can have like adenomas that like, you know, like adenomas that grow in the adrenal cortex. And the thing is actually most adenomas of the adrenal cortex, the abinine, they typically don't have like, they typically don't hypersecrete anything, but occasionally they may hypersecrete stuff, right?

Like you can have an adrenal adenoma that's making a ton of cortisol, which can give rise to like an actage independent cause of pushing syndrome, or you can have an adrenal adenoma that's making a ton of outdozorin, right? And then that will give rise to like primary hyper-outdozorinism, achy-con syndrome, right? So that's kind of like the big thing. And I mean, usually when you see these adenomas, you just go ahead and take out the entire adrenal gland on that side, okay? You go ahead and take out the adrenal gland on that side. But the thing is, in the adrenal gland, people can also have like adrenal carcinomas, right? But let me go ahead and mention this. Remember I said adenomas, right? They abinine. And I say that most of them are non-functional, right? But because most of them are non-functional, right? Like, let me put it this way. I think maybe a comparing contrast is a more appropriate way to discuss this concept. These adrenal adenomas, those abinine, these adrenal carcinomas, those are not b9. Adrenal adenomas by definition, I'll say for the most part, right, tend to be non-functional, but some of them can overproduce some adrenal gland hormone. On the flip side, adrenal carcinomas almost always tend to hypersecrete something, right? In fact, that is usually what brings those disorders to a press to like clinical attention, right? So adrenal carcinomas in general, most of them are not non-functional. Most of them actually secrete a ton of stuff, okay?

Most of them actually secrete a ton of stuff, right? So most of them can actually like hypersecrete like cortisol, most of them can hypersecrete our dosterone, some of them can hypersecrete like sex steroids, like androgens, right? So those are all things you want to keep at the back of your mind. And the thing is, one thing your friends at the MBME love to do, right? Because I mean, I've kind of talked about this in a prior podcast about like, oh, how you can use like that, like sometimes you see an MBME question, where do you draw like a bimodal graph to illustrate certain concepts like like the differences between like slow and faster sedalators or the differences between, I think like the incidents of I think like, is it like I think like Hodgkin's disease that you know shows up like very early in life, like you can show up like later in life, like there's this spike later in life. This that role that bimodal distribution principle also kind of applies to people that have like carcinomas of the adrenal cortex, right? So the thing is it can happen typically like, well, there's this big spike before the age of five, but there's also this big spike when people hit like their 50s, their late 40s and things of that nature, right? So that's one thing you want to keep at the back of your mind. And also remember again, a lot of tumors love to metastasize to the adrenal glands, right? So like like lung cancer, liver cancer, right?

Those things all love to metastasize to the adrenal glands. So that's all I think I'm going to say about like tumors that exist in the adrenal cortex. And I guess one thing I should mention is if a person has con syndrome like the screening test you will do is you measure their plasma or dostron levels, right? And you'll also measure their plasma reading levels, right? So a person that has con syndrome, aka like primary hyperodostronism, they'll have an increased PAC to PRA ratio, right? So the plasma or dostron to reading concentration will be increased, right? And then if you're like, oh, this person's plasma or dostron to reading concentration is increased. So let me then confirm my diagnosis of primary hyperodostronism. The way you confirm that diagnosis is you do something known as a salt suppression test, okay? You do something known as a salt suppression test. For the normal individual, if you give them salt, right? By the administration of salt, you actually tend to shut down the production of our dostero, right? So failure of a person's our dostero to suppress with salt augmentation is diagnostic of primary hyperodostronism, okay? And then after that, you do some kind of imaging to figure out what's going on, right? The thing is as a general principle in endocrinology, if a person has an excess of something, the confirmatory test usually involves some suppression test of some sort, right?

But if a person has a deficiency of something, the confirmatory test almost always involves some kind of stimulation of that thing, right? That's just a very nice handy dandy general principle to keep at the back of your mind for exams, right? So primary hyperodostronism, again, they have like an elevated PEC to PRA ratio. That is not the case with a person that has secondary hyperodostronism because they are reading and they are our dostero increases, like in lockstep. So typically those people may have a decreased or a normal plasma or dostero to reigning ratio. So that's one of those just weird things you want to keep at the back of your mind for exams. Now what if they give you a question about like a child, like a newborn or you know like a six month old kid and they tell you that, oh, this child, his mom feels like a mass in his abdomen when they are trying to like, give him like a shower or something, right? They will kind of set up the question that way. What do you mean see that? Oh, this child has like weird vertical and horizontal movements of the eyes, right? And then they also tell you that this child has like weird movements of the operand lower extremities. If you see that, what tumor should you think about? The thing is on the MDM is they'll be counting on you to pick WO Ms to Mer as an answer, resist that temptation, okay? The thing is WO Ms to Mer for the most part it will present with that flank mass, right?

And then the kid may have like hypertension, right? And then the kid may have hematory. That's all you will see. WO Ms tumors do not cause like the weird movements of the eyes or the weird movements of the operand lower extremities. If you see those things, you want to think more along the lines of a neuroblastoma, okay? So almost always MDM questions that test neuroblastomas, they almost always put WO Ms to Mer as an answer choice. So you won't be careful. So let me teach you some key things that can help you differentiate between a neuroblastoma and a WO Ms tumor. And then I'll actually talk about a neuroblastoma. The thing is a WO Ms tumor tends to be on one side, it does not cross the midline, right? WO Ms tumor does not cross the midline, okay? WO Ms, I'll see that again. WO Ms tumor does not cross the midline and it tends to not be calcified, okay? Contrast this with a neuroblastoma that tends to cross the midline and tends to be calcified, okay? So neuroblastomas cross the midline and they are calcified. That is classically the presentation on MDM exams, right? So the thing is what's a neuroblastoma, right? A neuroblastoma is a tumor of the Adrenal Medulla. It's not an adrenal quadricole problem. It's an adrenal medallary problem, right? And it almost always occurs in kits on MDM exams, right? And the thing is you may not just find it only in the Adrenal Medulla, you can, because it's a neurogenic tumor, you can find it anywhere, anywhere neuro tumors grow, right?

So you can find it like along the, you can find it like the sympathetic chain, right? Close to the spinal cord. Or you can find it in the mediasis, not a millimeter, not a trite. But again, remember, would you find it in the anterior mediasis, not a trite? Or in the posterior mediasis, not a trite? I would really hope you're telling me that it's found in the anterior, sorry, in the posterior mediasis, not a trite, remember? You're a genit tumors growing the posterior mediasis, not a trite. In the anterior mediasis, not a trite, you may find tumors like teratomas, thymomas, lymphomas, things of that nature, now that thing that I described about like the, like the weird movements of the eyes, right? Those things, that's what's called obso clonus, right? It's almost like the person having like a vertical and a horizontal and a stagmus, right? And then those weird movements of the upper and lower extremities that I was describing, that's what's known as myoclonus, right? In fact, the pathogenomonic feature on NBM exams of a neuroblastoma is something known as obso clonus myoclonus syndrome, okay? That's, I mean like as far as I know, I've not really seen, at least from my study, I've not really seen any good explanation of the pathophysiology behind that, right? So, just be able to recognize that as a classic finding on NBM is in neuroblastoma. And the thing is, neuroblastomas, they're not just tested on step one, they also tested on step 2ck and on the pediatric shelf.

So that's something, it's something you definitely want to make sure you understand. Now, what are some labs that classically present, you know, that you may see, in a person that has neuroblastoma, the thing is neuroblastomas can actually cause increased amounts of like metaneference in a person's urine and serum, right? So, don't just think of that as being only under the purview of fiochromosidomas, you may actually see elevated levels of like VMA, HVA and all that stuff and metaneference in a person's urine, if they have a neuroblastoma. And then, if we're looking at things from the cell biology perspective, right? People that actually have neuroblastomas, they actually tend to have like, like increase the activity of the N-MEC oncogene, right? It's like an acetyl oncogene, it actually promotes malignancy, right? So, if you see like, you know, like amplification of the N-MEC oncogene, you want to think about neuroblastoma with that. And one of the marker you may see on NBM is for neuroblastoma is something known as Bombazin. Bombazin is just something that in the body ordinarily just increases the release of gastrin from G cells, right? It's like a gastrin-releasing peptide, canadial, but the thing is if they, like they usually don't pull gastrin-releasing peptide, they usually put Bombazin because it just sounds very odd, very weird, very awkward. So, the NBM is continuing that to kind of mess with your mind on the exam, right?

So, Bombazin is a tumor marker for neuroblastomas. And the thing is neuroblastomas, right? Like, when you, these people, because you may actually see these kids present with like fevers and stuff, right? Typically, neuroblastomas, you may see it actually present with like, elevated erythrocyte sedimentation rates on NB Ms, right? And then on the marker, you may also see that's increasing the serum is just in known as a neuron-specific inolates, right? So, again, let me, let me back track on some more ice here. A person that has a neuroblastoma, they will have an elevated ESR, Bombazin is like a tumor marker, right? They can also have elevated levels of NSE, right? Like neuron-specific inolates, right? And it's associated with an amplification in the N-make oncogene, right? And on histology, you may also see like those homerite pseudo-resets that we classically find in neuroblastomas. Remember, neuroblastomas have a homerite pseudo-resets, where you can also find those in a neuroblastoma. Again, remember, a neuroblastoma is a neuro-based tumor, a neuroblastoma is also a neuro-based tumor, okay? So, that's again, just one of those weird things you want to keep at the back of your mind, for example. And then, if you want to diagnose a neuroblastoma, right? Like, you can do like abdominal imaging, you can do like an MIBG scan, it's like a new climatic in study that we occasionally do in radiology, and that helps you kind of see what's going on.

Or though on X-ray, again, let me tell you that, oh on X-ray, you see a mask that's crossing the mid-line and it's calcified. If you see that, again, you want to think about a neuroblastoma on that those are circumstances. And actually, most neuroblastomas, they're just like spontaneously like resolve over time, but if you don't resolve, again, you can, you know, you can do like surgical resection, or you can do like chemotherapy, and all that stuff, but that's not what they're going to go after on Mbim exams. Now, the last thing I think I'm actually going to go ahead and talk about is a fiorromositoma, right? A fiorromositoma, again, it's an adrenomitillary tumor, right? Although, again, remember, you don't just only find the adrenomidola, you can find it again in the busiomy, the stynum, you can find it along the sympathetic chain, juxtaposed to the spinal cord, and remember that fiorromositomas, right? Like they have these, kind of like the way-makers that have particular, has like those two percent rules, it also has like those 10 percent rules, right? So like a person that has fiorromositoma, like 10 percent of them, 10 percent of like 90 percent of fiosabeline, but 10 percent of them can be malignant, right? 90 percent of fios, you typically find them in the adrenomitola, right? But 10 percent of them, you may find them outside the adrenom glands, right? 10 percent of them can be bilateral, 10 percent of them can calcify, right?

And like 10 percent of them, like most people that have fiorromositomas, the classic presentation is they'll have like episodic headache and hypertension, right? But they are 10 percent of people that, like if you take off, if you take off the pool that present with it, then ultimately that ignores with fios, 10 percent of them will not present with hypertension, right? So they may just present with like headache, right? Like they be present, like you know, like pressure styles in terms of they may have like headache, they may have like palpitations from like tacky cardio because again, they have secretion and corruption of karekulo means, they may have like paler, right? They may be because remember that visual constriction will cause a lot of supply to like key regions of the body, right? Or they may have like these episodes where they just have like headache and sweating, right? So those are the big things you want to keep at the back of your mind with fios. And the thing is, it's actually very high to remember that there are certain genetic conditions that have an association with fiochromosidoma, right? Like MEN2, A and 2 B, right? Those have associations with fios, NF1, neurofibromatosis type 1, right? Also has an association of fiochromosidomas and also VHL, right? Von Hippolyn down, remember VHL has a lot of high-old associations that you want to know for the USMED Is, right?

Like it has an association like Himandru, Blastomas, has an association with like pancreatic cysts, has an association like bilateral, renossal, charsinomas and things of that nature, right? So VHL, remember it's a chromosome 3 problem, or a zomodominant inheritance, also has an association with a fiochromosidoma. And one thing you may also want to keep in mind with fiochromosidomas is that if you want to, you don't think these people will search you or whatever, or you just want to treat them, right? You want to remember that you give alpha blockers first before you give a beta blockers, right? You give an alpha blocker first because if you give a beta blocker, right? You can have an opposed alpha stimulation and then those people can have a hypertensive crisis and that, right? That's not an ideal outcome, right? So you want to, you know, give an alpha blocker first like phenoxybenzamin of entulamine and then after that you give a beta blocker, right? And then you can then take them to surgery, right? You don't want to like be messing with the tumor and then say, oh, you know, we'll be careful with the tumor during surgery. Now, if you're, if you have that massive systemic release of calycholamine during the cause of the surgery, the patient will very likely die on the operating table, right? So again, usually this is done like two weeks ahead of time, you do like very good pre-op planning, you block our first receptors first.

So go with your AB4 UB and then you block a beta receptors. So I think that's all I'm going to say about the fields, but again, fields. If you see an adrenomabular tumor in an adult, not in a kid in an adult, think about a field. If you see an adrenomabular tumor in a kid, think about neuroblastone, okay? Think about neuroblastone. So I think that's all I'm going to say from the adrenal perspective and really I feel like I don't think there's any major thing that I'm missing from my mind. I feel like if you listen to a piece of one 91 and one 92, you'll be coming an adrenal master, right? So in the next podcast, again, I'll talk about more endocrine concepts and then we'll go from there. So as I do at the end of every podcast, I go for one or one two-year-in for many exams. Step one, step two, seek is step three, step two, CS. If you're a medicine resident, I offer tutoring for like the medicine, training exam, the ABIA and board exam. I also tutor for like pre-clinical medical exams, third year shelf exams. And then if you're like if you have like a college buddy that needs tutoring for like Gen. Chem, O Chem, Physics, Biochem, Histology, Physiology, I tutor for all those things. And then I also do like coaching for like if you're like a medicine or a plant to residency so like an ERAS application or like a college student applying to medical school so like an AMCA application. I have a lot of experience working with people.

Many people have worked with a much of their first choices and I have admissions committee experience at a top two med school. So like you know coaching with like you know like mocking interviews, personal statement writing, editing applications, things of that nature. Again I've worked with tons of people on those. And again for all these different exams that I'm mentioning right be it small group tutoring, be it large group tutoring. Again just reach out to me that through the website or you send me an email at divine intervention podcasts with an SADN at gmail.com. And then I also offer like this thing I call like a USMLE booster course. It's like 10 hours for step two CK or step three or 20 hours for step one where if you are at the end of your day get it period or you know you kind of want to put everything together for you really quickly in a Q&A format where you essentially review like many of the most news for the exam. Feel free to reach out to me. It's kind of special pricing on that but we can always talk about that over email. So have a wonderful rest of your day. I'll see you in the next podcast. God bless you. Thank you.

Central obesity, hypertension, and purple striae (or moon face/buffalo hump).

Bilateral adrenal gland hyperplasia.

Measuring the Plasma Aldosterone to Plasma Renin Activity Ratio (ARR). High ARR suggests primary; normal/low ARR suggests secondary.

A calcified mass crossing the midline.

An alpha-blocker (e.g., phenoxybenzamine).

Adenomas are often non-functional, while carcinomas almost always hypersecrete hormones.

Excess cortisol (hypercortisolism).

Low-dose dexamethasone suppression test (LDDST).

Adrenal glands (ACTH-independent cause).

Renal artery stenosis or fibromuscular dysplasia.

High (elevated ARR).

Bombazin.

Neuroblastomas tend to cross the midline and calcify; Pheos usually do not exhibit these traits.

Excess cortisol (hypercortisolism).

Low-dose dexamethasone suppression test (LDDST).

Adrenal glands (ACTH-independent cause).

Renal artery stenosis or fibromuscular dysplasia.

High (elevated ARR).

Bombazin.

Neuroblastomas tend to cross the midline and calcify; Pheos usually do not exhibit these traits.