DIP Episode 194 - Updated USMLE Step 1 Endocrine Review Series 3

Okay, welcome. My name is Divine, I'm a resident. This is episode 194. I believe of the Divine Intervention Podcast. And then this podcast, I'll be continuing the updated US Family Step One review series for endocrinology. This will be series number four. I mean series number three. So let's just jump right into it. So what if you get a question about the five-year week guy, um, presents with a new murmur. Let's say the new murmur is like a, you hear like a holostolic murmur at the left-low external border that increases with inspiration. And then they also tell you that he's been having like this new onset asthma like symptoms and he's been having like chronic diarrhea for the last three months. If you see that, what should you think about? So this presents chronic diarrhea, neon serasma and a murmur that if you go by what I just described right, so left-low external border that's the tricospid area. It's a holostolic murmur, increase with inspiration, right? That tells you a likely dealing with tricospid insufficiency, right? That's something known as Carvalos sign. Basically on an in-bim exam, you tell you that a person has a murmur and it increases with inspiration is very likely a right-sided heart murmur. That's what's known as Carvalos sign. That's a very high yield to know for the USMLA exams. So this person essentially has carcinoid syndrome, right? This person has carcinoid syndrome, right?

So carcinoid syndrome, there's a classic presentation that you'll likely see on an in-bim exam. For the most part, the pneumonia uses BFDR, right? So like BFDR. So the B is for bronchospasib, right? The F is for like flushing of the skin. The D is for diarrhea, right? And then the R is for a right-sided heart lesion. So although there are other things you'll see as I will describe as you go along, right? So you're like, okay, divine. Well, one in the world is carcinoid syndrome. Well, the thing is carcinoid syndrome is basically a syndrome where you have a tumor. It's usually in the small intestine, usually around like the Iliol appendiceal area that secrets a ton of serotonin, right? It's usually a ton of serotonin. And it's actually very high yield to know that the cells that secret all the serotonin, they tend to be neuroendocrine cells, okay? They tend to have this neuroendocrine origin for the most part. And the thing is for the really carcinoid doesn't cause any problems if it's in the small intestine because remember, most of the parts of your GI tract, they drain into the portal vein, right? The thing is your liver. If you remember, I think I may have said this in one of my podcasts where I talk about first pass metabolism, the liver is capable of first pass metabolism. So the thing is that first pass metabolism converts the serotonin to 5 HIA on the the atron of monominoxidase.

So the thing is if you get to the liver, the serotonin gets delivered, gets metabolized appropriately, it will become 5 HIA, 5 HIA is largely useless, doesn't do anything to the body. So usually people may have a carcinoid tumor, but they may not necessarily have symptoms. They only begin to get symptoms when the tumor metastasizes to something that can deliver blood to the systemic circulation that essentially bypasses the first pass metabolism in the liver. So basically like circulation that is not part of the portal vein of system, right? So that's how people get into trouble. So basically for the most part, if you have like met to like the, met to like the lungs or let's say for whatever reason, the tumor is making so much serotonin that the liver's monominoxidase cannot deal with it, right? Then those people begin to have, those people begin to have a systemic symptoms. So again, like I said, carcinoid syndrome, tumor making a ton of serotonin. I remember that that tumor making a ton of serotonin can also cause a niasin deficiency, right? So I can already see your friends at your friends at the DMB me, me in the US, I'm going to step one question where a person has carcinoid syndrome, but in that carcinoid syndrome, they also happen to have pelagra, right? Remember pelagra with the diarrhea dermatitis, dementia and death, right?

In fact, that may actually be one of the causes of the diarrhea that you observe in people that have carcinoid syndrome because remember, another name for serotonin is 5-HT, right? 5-hydroxychriptofet. So the thing is, triptofet is a precursor for the production of niasin and serotonin. So if you take up all your triptofet and it's been made into serotonin, then if you're looking at a low-shuttley principle, it's just less available to make niasin and the person can get a vitamin B3 deficiency with that, a niasin deficiency and get a pelagra. So the big thing is, so like I said, the classic presentation of carcinoid syndrome, right? Obviously the person will have skin flushing, you'll have diarrhea, you'll have right-sided heart problems. You may say, okay, divine, why do they not have left-sided heart problems? Well, that's an easy explanation. Pretty much the thing that happens is that the lungs also have monomino oxidies. So the lungs can metabolize the carcinoid, can metabolize the serotonin to 5-HTI on the monomino oxidies. So the person will not necessarily get into problems, or not necessarily getting into problems with that. So that's actually one key high-eal thing to keep at the back of your mind. So they won't have left-sided heart lesions because the serotonin is metabolized before it gets there, right? And then like I said, they will also have, they can also have like triacospital regurg or they can have like pomonic stenosis, right?

So those are the classic right-sided heart lesions you find with those people. There's an amonic there, tips that can help you remember those findings, like triacospital insufficiency, pomonic stenosis. And again, these things can cause like, you know, like they can cause endocraditis, they can cause all these problems with the right-sided heart valves. And really, how do you meet the diagnosis of carcinoid, you know, just check the urine, check the serum, you'll find the increased levels of metabolites of serotonin, 5-HTI, right? 5-HTI drugs in the domestic acid. And then typically for these people, you know, you go ahead and treat them like octurotide. I mean, you know, also if there's an actual tumor that you spot, you know, you can try to do like, you know, resect it surgically, use chemotherapy, but the chemotherapy is beyond the scope of the USMLA exams. So I'm gonna skip that. But for the most part, you know, octurotide. And then those people will also typically need via vitamin B3 supplementation, right? That's a unique question that I miss hearing your exams. So I will say for the most part, those are the big things you want to see. Think about with carcinoid syndrome. Now, what if they give you a question about a patient and they tell you that, oh, this patient has been having like chronic abdominal pain, this patient comes in, this patient's like volume depleted, blood pressure is real low, they've been pain a ton.

And then they also tell you that this person had an uncle that died of like some neck mass. If you see that, what are you thinking about? I really hope you're thinking about maybe like any and two A, right? Like whenever they tell you like another family member having like a problem in an MBA, me question, testic and strategy dictates that you already begin to imagine that being a genetic problem, right? So neck mass, so maybe I don't know, maybe like medallary thyroid cancer. And then this person having like this stones, bones, groans, psyche, overtones kind of business, maybe guide you towards like hypercalcemia from like a primary hyper thyroid is it? So when you see that, I hope you're thinking about a me and two A, if you want to be a little more specific. So let's I guess maybe talk about all the amy and syndrome. So the amy and syndrome is there's three of them. There's amy and one. There's amy and two A, there's amy and two B. The big thing to keep in mind with these disorders is all of them inherited in an autosomal dominant fashion. And amy and one, right? It's the easy way to remember the findings just remember parapanpit, right? So they have parathyroid problems, they have pancreatic problems, and they have pituitary problems, right? The thing is the parathyroid problems, again, it will be primary hyperparathyroidism because again, look at the name of the disorder, multiple endocrine new pleasia, right? So you have a new pleasia of endocrine glands, right?

Your parathyroid gland is an endocrine gland, right? So these people, you know, they'll have parathyroid problems, and usually the parathyroid problem is usually actually like a parathyroid adenoma. So if you read the literature, they kind of seem to go back and forth on this, but actually I kind of resolved it from like a deep search. People that have amy and syndrome, they tend to have parathyroid adenomas. Multiple parathyroid adenomas, not necessarily parathyroid hyperpleasia, mean the cause of their primary hyperparathyroidism. So again, they'll have primary hyperparathyroidism, that's the parathyroid problem. So they can have like signs and symptoms of hypercalcemia. So like a short QT interval on EKG, they'll have the storms, like the nephrodisiases, they'll have the bones, they'll have the bone pain, right? Typically you see like the superior still resoption, right? Along the phalanches of the fingers, they'll have like volume depletion because remember hypercalcemia can cause nephrodisiac diabetes and simpitis. I'll talk about that in a bit. So you know, they can get all those parathyroid problems and all those signs and symptoms you'll find with people that have hypercalcemia, right? And then they can also have pancreatic neuroendocrine tumors, right? So again, like things like gastronomas, so like the Zon genocene syndrome, so the pressure has like genital ulcers or ulcers that don't seem to respond very well to ppi therapy, right?

Just some usual ulcers in like unusual places like very distal small bowel ulcers, those are kind of weird, right? If you see that, think about gastronomers, also insulinomas, right? Or weepos triad, right? So like, you know, the hypoglycemia, signs of hypoglycemia, relief of symptoms with the administration of glucose, right? Think about those with insulinomas. There are some rare pancreatic neuroendocrine tumors these folks can have, right? So they can have things like they can have like a glucanoma, remember that's what like a new onset of diabetes, in an older person that has like a skin rash, so like the classically described that necrolitic migratory or thema, or they can have like a vaipoma, right? They'll present with a WDHC syndrome, right? Where they have like watery diarrhea, they have low potassium, so hypokillemia, and then they have a echeloritri, right? Those are all things you can find as the pancreatic neuroendocrine tumors in MEN1, right? And then the pituitary problem, so the most part, think about prolectenomas, that's the most common pituitary, neoplasm that you find in people with MEN1 syndrome. So they can have prolectenomas, those prolectenomas, that's one thing, but probably like the second more common one is like a growth hormone secreting tumor, right? So like acromegaly, for example, and the thing with MEN1, right? Like I said, again, otosomodominant inheritance, it's a mutation in chromosome 11, okay?

That's very high utinol, it's a mutation in chromosome 11, and it's like in a tumor suppressor gene, it's like the men 1 tumor suppressor gene, it makes like a protein thing known as a menin, MEN, IN, right? So like menin, men 1 tumor suppressor gene, oh, chromosome 11, those are big things to keep in mind for exams. The thing is step one, unfortunately, is one of those exams, we're just need to know your details, right? So it's a detailed, heavy, detailed heavy test. Although again, when you're reading questions, go more big picture, you'll likely get the answer correct if you follow like big picture thinking. Now, MEN2 A, right? So MEN2 A, it's a triad, right? For the most part, these people have like parathyroid problems, right? And they will have fiochromosytomas as well. Remember fiochromosytomas as they're filled with MEN2 A, MEN2 B, Von Hippolyndal, Neurofibromatosis type 1. Those are four high-yield disorders that are filled with fiochromosytomas, right? So MEN2 A, they'll have the parathyroid problems, so they'll have primary hyperparathyroidism, they'll have fiochromosytomas, and they also have medallary thyroid cancer. And that just as a general rule, people that have the MEN2 syndrome, they require like a prophylactic thyroidectomy, because the is not a matter of if they will develop medallary thyroid cancer, it's not of when they will develop medallary thyroid cancer. They're going to get MTC, they're going to die from it, right? So you don't want that.

So all these folks get a pervillactic thyroidectomy. So again, they'll have parathyroid problems, they'll have fiochromosytomas, and they'll have medallary thyroid cancer, right? And the fiochromosytomas, or remember, typically is like the episodic headache hypertension, does the classic presentation, I kind of talked about that in the adrenal, the adrenal podcast, and these patients that have MEN, the MEN2s, right? When they have like the fiochromosytomas, it actually tends to be bilateral. If you remember from the adrenal podcast, I say that there's this rule of 10s, right? For the fiochromosytomas, right? I said, oh, feels, you know, 10% of them are bilateral, that's not the case with the MEN2 folks. They have fiochromosytomas tend to be more often than not bilateral, right? So that's actually very, very high yield to no for purposes of the USML exams. And again, they could have these signs and symptoms of primary hyperparthyroidism. And again, like I said, there's a more dominant inheritance, but one thing you do not want to forget is that the mutation is in chromosome 10, right? Chromosom 10 is like a proto-oncogene, right? Remember I said that the many gene product for MEN1 was a tumor suppressor gene, not so for MEN2 A or 2 B. MEN2 A, it's a mutation in a proto-oncogene, right? So something that actually drives my lignessy chromosome 10 and it's a ret proto-oncogene, okay? Ret proto-oncogene, ret proto-oncogene.

Again, that's very, very, very high yield to no for MEN2 exams. And then MEN2 B for the most part, it's pretty similar, although there are some key differences. So people that have MEN2 B, they don't have any parathyroid problems, right? They just have like the, they have the fucromosythoma, they have that, they have like a medallary thyroid cancer, right? Again, so those people also need prophylactic thyroidectomy. They can also get like mecosone aromas, so they're gonna get like these, these nerve tissue groups, like on their lips, on their skin, on mecososophysis that line the respiratory or GI tract, they can get those problems. And they can also have a morphineoid habit. So remember if you see a person that's super tall on MEN exams, I want to think about like Marfan syndrome. Remember that's like a chromosome 15 problem in the fibroling gene, right? Homosis, stenoria, right? Where those people have like the, like lens dislocation, they get like recurring M Is, they have intellectual disability. I don't forget, there's don't, down those syndrome, right? Those who that can get like ericane resums, they can get like a rupture of the uterus when they're trying to deliver their kid, so they can get like bor rupture. And then also don't forget, um, was the name of this disorder, client-felture syndrome.

That's also a sort of a morphineoid habitus on MEN exams, but also in MEN 2 B, I think I'm pretty sure I've talked about this in a prior podcast, like this differential that you should think about when you see a morphineoid habitus. So again, so again, phyocromosythomas, right? Mydlerotheric cancer, mecosone aromas, right? morphineoid habitus, those out, thanks for for MEN 2 B, right? And MEN 2 B again, chromosome 10, rect, predominculation, mutation. I remember this regime, you see like why is an important thing? It's a tyrosine-kines gene, right? So obviously it's mutated that can cause like cell proliferation and then patients can get can get into trouble. So again, all big things to keep in mind, MEN syndrome is just one of those is almost like the, the apogren by refringions on congrats steaming with with amyloid. This stuff is going to show up on every exam you take step one, step two, ck, step three, right? So just burn it into your brain forever, you'll always see it on exams. It just, just doesn't go away pretty much, right? Now, next thing I guess I'll talk about, I mean, I've been talking about like these prolactinomas and all that stuff. Let me just go ahead and talk about these particular, the normas real quick. And then because I want to keep this podcast short, I don't actually don't have, don't have all the time in the world. So for the most part, right? Petrotary are the normas, right? There are tumors that grow in the pitrotary gland, right?

They can be silenced, they may not make anything or they can make something, right? Those are the ones that, you know, kind of have that cling to fame. And for the most part, the ones that mix stuff we think mostly, or at least on envy mix, and so you think mostly of prolactinomas, right? Which are the most common and the pitrotary are the normas that make a growth hormone, which can cause like gigantism or acromegaly, depending on your age range, right? And the classic presentations, right? Like those people, patients can have like symptoms of overproduction of any of these hormones, right? But another thing they can also have, they can have by-temperohemia nopsia, right? So they can show you like those visual field cuts, cut diagrams on envy mix exams, where personas lost like the right visual field and the right eye and the left visual field and left eye. You see that? You know, like a by-temperohemia nopsia, because you have compression of the optic chiasm by the pituitary tumor, right? They can have like signs and symptoms of increasing trochanial pressures, you know, like chronic recurring headaches, especially when the week up in the mornings, right? Or those cells can grow so big, they can overshadow the other cells in the pituitary, so they have like signs and symptoms of high pool pituitary isn't, right? So prolactinoma, again, like I said, is the most common one, perisocraftin or prolactin, right? And you know, it's like the lactotrophs, the lactotrophs, right?

They sells that are that are trophic, right? For your lactating organ, basically your breasts, right? And for the most part, like if you see like a premenopausal female, because the thinnest, right? Like signs of infertility don't matter to someone's postmenopausal. So premenopausal person will be like, yeah, you know, not necessarily my period, mean fertile, yada, yada, yada, right? So premenopausal females, we usually because the thinnest, a premenopausal female will be the ideal each bracket, right? That they'll throw on an envy mix exam. So that's where you should kind of look out for a test. So, you know, they'll have like emenoria, because if you think about it, right, prolactin is an inhibitor of genareach, right? So if you shut down the HVG axis, you're not going to be having men's ease, you're going to be infertile, right? You're going to have decreased libido, right? Because you're not producing testosterone, remember testosterone controls libido. For whatever reason, it's a factor that's not in many resources, but it's very, very high yield to know for many USML exams. They can also have osteoporosis, because again, if you're not making estrogen, right? Remember, estrogen increases the synthesis of osteoportagrin, right? Which points to rank ligand and inactivates it, right? So if you're making less osteoportagrin, then rank ligand begins to interact with rank, the rank receptor, and you have osteoclasts doing the abidin, and you have osteoporosis, right?

And then this people can also have galactoria, right? So they can have like weird milk production, even if they're not pregnant or recently of that sort, right? Because prolactin, like milk let down. I mean like milk production, it's prolactitional, right? And I mean in guys, the symptoms are practically identical, but guys, you know, they'll be important to low libido, they'll be infertile, they'll have like no growth of their breasts, right? So like they'll have like an acomastia, they'll have galactoria, but galactoria usually is a classic presentation in females, premenoposal females with with a prolactinoma on MBM exams. And the thing is, you may say, okay, so define how do we treat this, right? For the most part, I'll say like maybe like 99.99% of the time on MBM exams, usually prolactinomas, no matter how large the R doesn't matter on MB Ms, with carburegolino bromo cryptin, you give a dopamine agony strike, because remember, another thing for dopamine is prolactin inhibiting factor, right? So if you give a drug that is pro-dopaminurgic, like bromo cryptin or carburegolin, right? And I'll say carburegolin is actually preferred over bromo cryptin, has fewer side effects. You give any of those drugs, that was the first prolactin release, it controls pro-dopaminomas in almost every case, right?

So see in general, surgery should not be the first thing you pick on an MBM exam for a pro-dopaminoma, you see that that's kind of different for the tumors that make a tone of a growth hormone, so definitely, definitely keep that at the back of your mind, right? So if for example they tell you that, oh, this patient, you've tried medical therapy, they're not getting better, the tumor is getting bigger and bigger, blah, blah, blah, blah, blah, blah, right? Or let's say they're about to regate, because they have like a bad lesion, then you can do like a resection through the spinoid sinus, right? That's what's not as a transphenoidal resection, but again, I promise you pharmacotherapy, even if the person is having like symptoms of like compression of a structure, you give the dopamine agony, they get better within like days, right? So that's something you want to keep at the back of your mind, for example. And then the second big one, right? So like tumor that makes a tone of a tone of growth hormone, right? Basically, if you're less than the age of 18, or you know, you're like in your your epithetial pleat has not closed, you did gigantic them, for the most part, people that have gigantic, you have like super, super long limbs, right? So be like super tall versus agromically, right? That's where your epithelial pleats have closed. Those people, they'll have like, it's almost like an overgrowth syndrome, right?

So, you know, they'll have like frontal bosseine, so like they'll forehead will be big, they'll have like prognothia, so like they're lower jaw will be huge as well. They'll have like big tongs, they'll see that their friends don't recognize them from like years ago, their rings don't fit, right? They'll have like coarse facial features. If you see all that stuff, you know, think about it acromagaly. And for the most part, these people, they can also have like a deep voice. So don't think of a deep voice as just being like something to happen with puberty. I can also happen when a person has agromagaly, especially when a person like in the 40s, 50s kind of develops a deep voice in the 40s, 50s. That's kind of weird, right? When you see that, you really, really want to think about people having like some kind of agromagaly going on, right? So, growth hormone problems, or they may also have like a tumor that's making a crap ton of testosterone, like crap ton of of androgates. So people that have over-secretion of growth hormone, right? So what are the big things you want to watch out for in exams? I've talked about kind of like the things you miss on a physical exam, but on labs, right? These people can have like diabetes. Remember that growth hormone is a diabetes genic hormone, right? I mean, think about it. When you make a ton of growth hormone, what's the next thing that comes after that that's made in the liver? It's insulin like growth factor, right?

So it's something like, you know, like a growth factor that's like insulin. So it's kind of related in some way, shape or form to glucose metabolism, right? So if you see in your own say diabetes, again, you can find that in pushing syndrome. We can also find that in in a chromegaly. And then these people, right? Because again, they have like overgrowth of their visceral organs. They actually have a pretty high risk of like colon cancer. And that treat, they can also have like overgrowth of the heart, right? So they can actually get like a cardiomyopathy. In fact, that treat heart failure, believe it or not, is this very high yield to know for exams? Is the most common cause of death very high yield? Heart failure is the most common cause of death in patients with with a chromegaly, right? And how do you make the diagnosis, right? Remember, I give you this general principle. I said that whenever a person has a deficiency syndrome in in endocrinology, you typically do some kind of stimulation test to meet the diagnosis when a person has an overproduction syndrome in endocrinology, you really do some kind of suppression test to confirm the diagnosis. So the first thing you do is because growth hormone is created in a post-tile fashion, doesn't really make sense to try to measure people's levels of growth hormone, right? So the thing you do is you check the levels of IGF1, right? So like insulin like growth factor, remember that comes from the liver, it'll be elevated, right?

So you're like, hmm, okay, this person seems to pass the screener for acromegaly. And the next thing you do is you confirm the test, right? You confirm the results by doing a suppression test because in acromegaly, you're making a crap ton of growth hormone, right? So the thing is you give glucose, or you give like a 75 gram glucose load, right? Typically when you give a person glucose, right? That suppresses the production of growth hormone. So if a person has like failure of their growth hormone to suppress, so you measure their growth hormone levels before you do the test and growth hormone levels after you do the test, right? So failure for a person's growth hormone, just a press after you give like oral glucose augmentation, that's confirmatory of acromegaly. And then you know, you just get an MRI of the brain. Generally, if you want to image a brain tumor, don't pick a CT scan on the exams. That's usually not a stellar idea, right? Go ahead and pick an MRI. You see things a lot better. And the thing is remember for a prolettonomize, I actually didn't talk about the diagnostic testing there. Typically for that, you just check proletton levels. That's all you need to do. It'd be super elevated. That's it. But basically, unlike a prolettonoma, where like first line is pharmacology, for a person that has a growth hormone's equating tumor, the first line is actually a surgery, right? So you do like a, again, you're a sect through the sphenoidsynas, right?

So you do a transfer noidore section. If for example, the transfer noidore section doesn't work out so well, or the patient is like an awful surgical candidate, you can consider drugs like octo-type, right? Octo-type, remember, it's a somatosetarin analogue, right? It can suppress the production of growth hormone alternatively. You can give those drugs known as big viso-mount. I've talked about that in the endocrine form podcast. It's PEG, the ISO MENT, big viso-mount. It's a growth hormone receptor antagonist. I can already see that your friends at the MDM are writing a question and asking like, where's the side of action of this drug, right? Make sure you pick that it's in the liver, okay? That's like the big thing you want to keep in mind because remember, growth hormone is secreted, it goes into the periphery, acts in the liver, liver makes IGF1, and then IGF1 medits many of the effects of growth hormone, right? So that has just an easy question that you can ask on exams that many people will get around, right? But hopefully you won't get it wrong because you listen to this podcast. And then the last thing I'll talk about with this is, I mean, think about it, right? Let's assume a person has like really bad cushions disease, right? Remember, cushions disease I talked about it in the Adrenal Podcast. It's where a person has hypercortisolism because they have a pituitous endomani that's making a crap ton of ACTH.

So the thing is, you know, typically for those folks, one thing you can consider doing is you reseg both Adrenal glands, right? Because that's the systemic ACTH. It's causing like big, big, big Adrenals, right? For both, right? And those, both of those Adrenals are making a crap ton of cortisol, right? But the thing is when you reseg those two Adrenal glands, well, one bad thing can happen is essentially that negative feedback on ECTH production is gone, right? So because the negative feedback is gone, those people will begin to have like that pituitous endomani that was originally making ECTH just gets bigger and bigger. Because there's nothing to suppress it. There's no cortisol to suppress it anymore, right? So typically these people have like, you'll be like a person that's gotten like a bilateral adrenal ectomy and then you have like skin hyperpigmentation. Remember that POMC business? I talked about in my Adrenal podcast, right? They can have like a bite, temporary, an upsea, they can have like headaches, right? If you see that, you know, think about something called an elsense syndrome. I just want those weird things that the NBA needs beginning to care about. So it's something I want to keep in mind. So just basically a pituitous endomani that makes ACTH that starts growing after you've got in a bilateral adrenalectomy for really bad questions disease. And for the most part, you treat an elsense syndrome.

You just, you know, resect the tumor or you read the pituitary, or the way you read it, the pituitary, you can kind of create like a diabetes and sepidos as a problem because you're damaged. You may not be super specific for the tumor. You can damage other cells in the pituitary, but we'll talk about that later. So I guess to round up because again, this podcast, if you notice, I'm covering a very limited number of topics in this podcast because they are all high topics for the all kind of detail. And I don't want to zoom through things here. So what if they give you a question about a patient, you know, that's thirsty all the time, has like hypernatrimeolapse. Let's say like their sodium is like 151. And the earring is like super, super, super dilute. If you see that what I'm thinking about, well, I hope you're thinking about diabetes and sepidos, right? The diabetes and sepidos. Don't confuse the diabetes and sepidos. On the example, we diabetes, meledis, right? So diabetes, meledis, or those people have sweet earring, diabetes, and sepidos, if something is insepid, means it doesn't taste very good, right? So people that have diabetes and sepidos, you know, when you taste the earring, the earring doesn't, doesn't have any taste to it. Only people with diabetes, meledis, where the earring has that sweet taste to it because it has glucose.

You probably don't do that, but I think I remember here in a story that back in the day, that's actually one of the ways they, like a person with polyurethane, they're like, oh, you either have diabetes, meledis, or insipidus. So the physician, I think, back then, again, I don't know how true this is, will taste the person's earring. If the earring tastes good, diabetes, meledis. Your intake is awful. The diabetes and sepidos. So, so the diabetes and sepidos, right? For the most part, it's just a problem with EDH. And now, let me just go ahead and tell you a rule. In general, hypernatrimeolapse. On an MV me exam, so I'll see it again, hypernatrimeolapse on an MV me exam, is diabetes and sepidos until proven otherwise. In general, if your EDH mechanism is intact, you will never develop hypernatrimeolapse. That's just a shrewsamp in medicine that you need to go ahead and commit to memory. Very rare, they are very rare situations without roaders and work, right? So let's talk about the diabetes and sepidus, right? So basically, the diabetes and sepidos, again, the classic presentation, presently like dilute urine, they will have hypernatrimeolapse, again, look out for the hypernatrimeolapse on an MV me exam. So they'll be super thirsty, right? Because they're just losing all the volume in the urine, right? And the thing is, there are two types of diabetes and sepidos, right? There's central DI, right? And then there's nephrogenic DI, right?

So there's central and there's nephrogenic DI. Central DI, you know, making EDH. The phrogenic DI, you're making EDH, but the key is that they're responding to it, right? So, obviously you can already tell one point of delineation on MV me exams, people that have central DI, the EDH levels will be low, right? People that have nephrogenic DI, the EDH levels will be normal or high. Usually it'll be high on MV me exams for the most part, right? So how do you tease those two things apart? Well, for the most part, all you just need to do is you do a water restriction test, right? The thing is, for the most part, you start by, you know, restricting those people's intake of water, you know, for like three hours, right? The thing is, when people do not drink water for three hours, the body will be like, hmm, okay, I'm kind of volume down. So you release a crap ton of EDH, right? So you retain a ton of volume from your Euro, right? That's the normal situation, right? So if you're a healthy person, typically, if you deprive the water for like three hours, your Uranus molarity will be at least, at least double your serenus molarity. And hopefully, I would hope that you know to calculate serenus molarity, right? It's like your two times your sodium plus your glucose divided by 18 plus your B in divided by 2.8, right? That's a higher formula to come into memory. I don't know, I feel like I got pimped a lot in my intraneture and this stuff as well.

So just, you know, something you kind of keep in mind. So if you're a healthy person, they do the water deprivation test, your Uranus molarity usually becomes, you know, at least twice your serenus molarity at least, it could be more, but at least twice your serenus molarity, right? But the thing is, if a person has like diabetes and syphilis of any sort, right? Actually, you check the Uranus molarity after you deprive them of water and it'll be less than 300, right? The less than 300 million, millions of them per kilogram, okay? So, the reason you're Uranus molarity is like super low, despite water deprivation, right? Or it's like less than two-fold the serenus molarity that tells you this person has diabetes and syphilis, right? So you're like, okay, well, to treat, you need to know what type you're dealing with, right? So, to know what type you're dealing with, you're the second part of the test where you give the smoke pressing, okay? Give DDP. Remember, DDP is an analog of 80, right? So, you know, you give DDP. The thing is, if you had a deficiency that was causing your symptoms by giving water to your missing, right? Like in Chinese, or the smoke pressing, presence problems will go away, right? So like the serenus molarity or the molarity maladies will correct. But if they don't correct, then that means your kidneys will not respond. So it was not like the deficiency that was causing your symptoms in the first place, not by the Virginii, okay?

So if a person's urine or a similarity rises by more than 50%, okay? After giving this more person, that tells the person has central DI. If the urine or similarity doesn't change significantly or it changes by less than 50%, the person has a nephrogenic DI. And the thing is, especially on step 2, CK, if your friends at the end of them, you want to be a little more complicated with you, they can give you some surrogates for preserving, so they may not give you like a urine or similarity. They may just give you a person that, you know, has hyperinitremia and then they will give you urine specific gravity and you'll be super low, it'll be like 1.002, something like that. Basically, if your urine specific gravity is less than 1.006, that means your urine is super dilute, okay? Super dilute, right? That will tell you that again, this person has diabetes and symptoms of some sort. And you may say, okay, divine. What can cause central diabetes and symptoms? Well, the thing is central diabetes and symptoms for the most part, you can treat it with, it can be caused by, you know, like a mass lesion in the brain or like a brain tumor or if a person has like radiation, right from one of these like pituitary adenomins that I cannot talk about a few minutes ago, those things can all cause a, if you get like radiation or surgery again, you can inadvertently hurt those cells that, you know, can help with your EDHS secretion.

Because remember, EDH is originally made in the super optic nucleus of the hypothalamus, right? So anything that messes of the brain can cause, can cause central diabetes and symptoms. And the thing is, if you damage the one thing I guess you should maybe keep in mind, this is just semantics, but the semantics that your friends at the endemic kind of care about, the thing is if a person has like a pituitary problem, yeah, they can have like transient diabetes and symptoms like transient central DI, it will likely not be permanent, right? Because the thing is remember again, like I said, this is just a backhand we have them testing this concept. EDH is not meeting your pituitary. EDH is made in the hypothalamus and then is secreted into that hypophysiope, like is secreted into like there's this protein known as a neurofising from non-staking that kind of transports it down the axon all the way to the posterior pituitary, okay? So again, EDH may be secreted from the posterior pituitary, but it's actually made in the hypothalamus. I think of the posterior pituitary as like a distribution center for EDH and also the same rule applies for oxytocin. So that's something to, something to keep in mind, right? So, well if you have a hypothelomic problem that can cause a permanent central diabetes and subiters, I really for the most part of these people because they lose a ton of volume, how do you treat them?

You know, hydrate them a ton and then just give them what they're missing, give them EDH and they'll be fine, right? Now, the Virginia DI again, classically that arises when the kidneys don't respond, they don't respond to EDH, right? So what are things that cause the Virginia DI, right? Many people just think of lithium and the mechalocyclic on exams. So they may give you a present that has a histral bipolar disorder that's not all that can cause an infogynyc DI. Many of the things, especially electrolyte abnormalities, that's something the Amymi has been caring about quite a bit this year, right? So like hypercalcine, so they give you a present that has like a short cutine interval or primary hyperparthyroidism and they have like the ask for the mechanism behind the volume depletion. It's from an infogyny diabetes in this. Also, if a person has hypokillin, remember, they'll have like the flat T waves, U waves, prolonged cutine interval, right? Unlike hypercalcine, that's the short cutine interval. And if you see that, you know, that can also cause an infogynyc DI and also people that have sickle cell, right? People that have sickle cell, they also tend to get like a really bad infogyny diabetes in C-B-D-S as well, right? And really, how do you treat this infogyny DI? It kind of depends on the cause. For the most part, most causes of infogynyc DI are fiddle hydro-HCTZ, right? And you say, hmm, divide, you see TZ, that doesn't make much sense. How does that work there?

Well, the thing is, if you, I think of it this way, right? So let's say, um, you know, you're a truck kid and there are big kids on your way home, right? And those big kids are always bully, right? When we bully you, they ask you, what are you having your pocket? Give me your 10, you get to them, you're like, oh crap, the sucks, the sucks, the sucks. There's nothing you can do. Well, think about it. If, for example, you're like, okay, I'm not going to see these big kids on my way home from school, they're going to bully me. Just put 50 cents in your pocket. Well, if they bully you and take whatever is left with you, because you're just carrying less with you, right? And there's less for them to steal. There's just not enough on you for me. Like, feel it, you know, they can pick your pockets, check everything. 50 cents, they take it and move on the emergency ring, right? So that's kind of the thing that happens when you take HCTZ. When take HCTZ, um, that will cause like a volume depletion, right? And that volume depletion will force earlier parts of your nephron to become more efficient at reabsorbing water and sodium, right? So it's like if before, like, maybe you did 10% of your water absorption in the, at the level of the principles, some of the collecting doctrine, the action of the visual present V2 receptors, you're probably start doing like maybe like a like 2%. Right? So that's how HCTZ can help.

So initially, you're simply not getting better, but you will get better with time. As you're in and you're tensed now, those as your kidneys just adapt and start reabsorbing things much early in the nephron, at least more proximal to the principles. So nothing you can also give you, you can give in the methancene, again, in the methancene, right? It's an insect, right? So you can inhibit cocks. So you will hype up or refuse the afrin material, right? So again, that will cause less fluid to be flowing to the kidneys. So the kidneys will just get more efficient at reclaiming. And let me know you's reclaiming reclaiming is a term that's if again, if you're an effronologist, a term, if you see reclaiming with water absorption, they probably get pissed, so you probably don't want to do that. So reclaiming something is usually by carb, but you know, they'll be better at reabsorbing water, again, watch earlier in the nephron. But if a person has an effrogenic GI from a lithium, right? The thing is lithium causes these problems because it enters that in a channel that we find that the level of the principle cell of the collecting duct. So the thing that happens is if you can show them that because remember, lithium is in group one in the periodic table, kind of like sodium. So they use very similar transporters. I mean, lithium is like a lemon three. So it means like a lemon to 11, right?

So they have in all similar charge similar chemical very fairly similar actually, they have very similar chemical properties, right? So if you could block that in action, I would have drawn like a milleride or triameterine, remember those potassium sparing diuretics that work by being in echelon blockers, right? Those can help tremendously intrudine and treat in effrogenic diabetes and sepidos cause by lithium use. And remember, anything that makes you anything that increases the activity because they love this thing on ambient exams as well. And it's kind of hard for people to remember all the different scenarios. Let me just tell you this, if you have anything that increases the activity of the reigning and your tens and our dose-dron system, that would exacerbate lithium toxicity. That's just one rule you want to again, burn into your brain forever. So if you take an NSAID, right? That will cause hyper proficient of the afferent material that will rev up the reigning and your tens and our dose-dron system. So more dose-dron, more sodium being reabsorbed through that in a channel, but that means more lithium will be reabsorbed through that in a channel as well. So just whatever scenario they give you on an exam, just put it in terms of did it increase the activity of the reigning and your tens and our dose-dron system? If it does, then that person can potentially worsen lithium toxicity.

And then I guess what we're talking about, EDH, SIDH, I guess I'll just go ahead and talk about it real quick. So basically SIDH is just syndrome of in a perpetrator EDH secretion. These people have like low sermosmalarity because the area has been a ton of water, right? Because EDH is on board and you have very high hearing concentration. Usually these people on MBA exams, they will have like a UVO limit style hyponitrymia. So you know, they won't have peripheral edema, they'll just be thirsty. No, sir, they won't have peripheral edema, right? But they will be like relatively symptomatic, but you have like a certain of like 120. And this is actually also how this presents clinically, believe it or not, right? So if you see that, think about, think about SIDH. And you know, what can cause SIDH? Any brain problem, any pulmonary problem, I'll just give it that to you as a big categorization. Any brain problem, any pulmonary problem, those can all cause SIDH. So if a person has like meningitis or a person has like a pituitary tumor or a recent Hectroma, or they have like a psychiatric illness, right? Like psychogenic polydipsia, that can, I mean psychogenic polydipsia causes SIDH style symptoms, but the labs are different. And I'll talk about that at the end. So hold that thought for now. It doesn't cause SIDH, but it causes SIDH style symptoms, like hyponitrymia basically. I'll talk about that in a second. So think about your drugs, like your SSR Is, cyclophosphamide, right?

That alkalithen agent, carbamazepine that we used to treat the tigblur, right? Like trigeminal neuralgia, clopropomide, right? Remember that's one of those are very like old style, like first generation, sulfonyluria, those things can all cause SIDH. And then also we're presenting a small cell lung cancer. That's probably what you see like 98% of the time when in-beaming exams, cause an SIDH, small cell lung cancer, if you're presenting like an infection in the lungs, those can again, those can all cause a SIDH, right? And the way you treat SIDH for the most part, you know, just for free water restriction, they will try to trick you on your exam, into giving into giving a hypotonic ceiling. In general, hypotonic ceiling is the wrong answer on exams. On MDM As, you only give hypotonic ceiling when a person has hyponitramine, they have seizures. That's the only indication on MDMA exams for that. So that's something to keep in mind. And remember, if you fix a person's hyponitramine too quickly, right? You can essentially kill your ponds, right? And then you have locked in syndrome. Remember, there's no one like, right? That from low to high, the ponds will die and from high to low, the brain will blow. Right? So, if you fix hyponitramine too quickly, that can cause an osmotic germination syndrome. Previously, I think known as like central point in my analysis, right? And as we have locked in syndrome, basically like their corticospinal tract will be completely gone.

So they will lose control of all their limbs, all their crinonins will not work with the exception of like the crinonins that control like eye movements, this is terrible situation. So you don't want to, again, basically for a person, this is just a real-of-learning medicine. For a person who has like an electrolyte thin, you generally don't fix it very quickly. It's usually not a good idea, right? If you fix hyper, it trims me a too quickly, right? So from high to low, the brain will blow, that'll cause cerebral edema. Also kind of the same thing if a person has like DK or HHNS, if you fix their hyper, glycemia too quickly, that can also cause cerebral edema death. So you don't want to do that, right? So just something to keep in mind. So like I said, for SIDH, you can treat it with like, you know, water restriction. That's probably the most common correct answer on exams. But other things you can do, you can give them a close cycling. Remember, the microcycling is a tetracycline that causes nevargenic diabetes in symptoms. So you're basically using the side effect to treat SIDH, right? Because it's kind of like the reverse situation. Alternatively, you can also use an ED receptor antagonist, right? So like honeyvaptan, toevaptan, those will block those ED receptors, like the visopressin V2 receptors, right? And that can relieve the signs and symptoms of SIDH. Those drugs are super expensive. So to kind of round up here today, let me talk about three scenarios, right?

So like, if you see a scenario where a person has a high-serum of similarity, but a low urinous similarity, what should you think about? I hope you're telling me that it is inseparably, right? Because again, you're not having an EDH effect, so you always have ton of water in the urine. So your serum, osmolarity will be high, urinous molarity will be low, right? Now, what if a person has a low-serum of similarity, but a higher-inous molarity? What should you think about? I hope you're thinking about SIDH, right? Again, you have too much EDH effects. So you're observing a ton of water in the nephron, right? At the level of the principle, some of the collecting duct, right? So your serum of similarity will be low, but your urinous molarity will be super high, right? Now, what if a person has a low-serum of similarity, and a low urinous molarity? What are you thinking about? Well, I would really hope you're thinking about psychogenic polypipsia under those circumstances, because again, usually it will be a person like psychiatric illness, the drink or a graptone of fluid, the diluted serum that will suppress EDH naturally. Those people are completely normal, just see for the fact that they drink a ton of water, right? So because EDH is suppressed, they will lose a ton of water in the urine, right? So low-serum of similarity, low urinous molarity, that's psychogenic polypipsia. So I think I'm going to go ahead and pause here for today.

As I do at the end of every podcast, I do offer both large rupturing and one on one turene for many exams. You have a semelapse step one, step two CK, step two C S, step three preclinical medical exams, 30-ish-off exams. If you're a medicine resident, you need turene for like the intranine exam and the board, EBI and board exam, or your college student, an insturin for like Gen CAM, OEM physics, biochemistology, physiology, etude for all those tens. And then also for some courses, I call them like booster courses. It's like 10 hours for step two CK, step three, 20 hours for step one, where if you're at the end of your dedicated period, or you know, you'll feel like you have a good knowledge base, or you want to put everything together, like knowing the most notes for the exam, and a very quick rapid fire high format reach out to me, either reach out to me through the website or send me an email at Divine intervention, podcasts, with an S at the end at gmail.com and I'll be more than happy to point you in the right direction. And then if you're a college student or planning to med school, so like an AMAQAS app or a med student or planning to residency, so like an ERAS app, I'd refer like one on one coaching, you know, like personal statement, editing, mocking reviews, editing applications, rec letters, you can have a lot of people, most of the people have worked with have much of their first choices.

And I actually do have admissions committee experience, I've been on the admissions committee of a top two med school for like a year, right? So if you need help with any of those things, I feel free to reach out to me, I have a wonderful rest of your day. If I don't make another podcast before Christmas, I'll try not to, I'll try to make that not be the case, I'll really try hard to make a podcast before Christmas, but if I don't make a podcast before Christmas, have a Merry Christmas and a wonderful new year in advance, and I'll see you in the next podcast. That'll be episode 195. So have a great rest of your day, and I hope the leakers win today. Thank you, God bless you.

MEN2 A, MEN2 B, VHL (Von Hippel-Lindau), and Neurofibromatosis type 1.

BFDR: Bronchospasm, Flushing, Diarrhea, Right-sided heart lesion.

Monoamine oxidase (MAO).

MEN2 A typically involves primary hyperparathyroidism due to multiple parathyroid adenomas, while MEN2 B usually does not have parathyroid issues.

A suppression test (e.g., 75g glucose load). Measuring IGF-1 (Insulin-like Growth Factor) is better because it reflects chronic GH activity and comes from the liver.

CDI patients will show an inadequate rise in urine osmolality; NDI patients will have normal or high ADH levels despite dehydration.

Small intestine (ileoappendiceal area); Serotonin (5-HT).

Tryptophan is a precursor for both serotonin and Niacin. High serotonin production depletes the pool of tryptophan, leading to secondary Niacin deficiency.

Dopamine agonist (e.g., Cabergoline), as they suppress prolactin release.

MEN2 A.

Acromegaly (GH excess) requires surgery first; Prolactinoma requires dopamine agonists first.

Diabetes Insipidus (DI).

Low serum osmolality AND high urine osmolality.

Small intestine (ileoappendiceal area); Serotonin (5-HT).

Tryptophan is a precursor for both serotonin and Niacin. High serotonin production depletes the pool of tryptophan, leading to secondary Niacin deficiency.

Dopamine agonist (e.g., Cabergoline), as they suppress prolactin release.

MEN2 A.

Acromegaly (GH excess) requires surgery first; Prolactinoma requires dopamine agonists first.

Diabetes Insipidus (DI).

Low serum osmolality AND high urine osmolality.