DIP Episode 343 - Paraneoplastic Syndromes and The USMLEs (Step 1-3)

Okay, welcome. My name is Divine. This is episode 343 of the Divine Intervention Podcast. In this podcast I'm going to be addressing a pretty significant topic for all the USML exams. Step one, step two, you can step three. Now topic today is going to be a Parano-plastic Syndrome. Parano-plastic Syndrome. I'm going to walk through most of the common ones that are tested on the USM Ls. Basically, if you know what I'm discussing in this podcast, you should be pretty set for the USML exams from a Parano-plastic Syndrome perspective. And before I go in, if you're taking the USML step two, see your step three exams on a complex level two or three exams any time soon. I do have a review course that's starting next week. On Monday we'll be having the famous MBME Testic and Strategy course from 2 to 430 PM Pacific Standard Time. And then we'll be having a review course for these different exams starting on Tuesday from the 5th to the 8th of October. And it's going to be from 10 a.m. to 4 p.m. Pacific Standard Time each of those days. Again, I've had many people attend these courses that have ended up doing really well on the exams, recorded some pretty huge-score improvement. So if you're interested in any of those things, just reach out to me and I will give you some more information on payments and the registration. So let's jump right into it.

So what if they give you a question about a patient and they tell you that, oh, this patient is a 62-year-old male and they tell you that over the last, you know, five, six days, he's having an ultra-demental status and they tell you that he has also had one seizure, right? And they give you all these electrolytes. And you notice that this person has a sodium of 121. And they tell you that, oh, he's Uranus, he's Uranus-specific gravity is 1.022. So that tells you he's Uranus very concentrated because remember, Uranus-specific gravity, the magic number for step, the USM at least is 1.012. So Uranus-specific gravity is really high, right? And then they tell you that he has been a long-term smoker. Well, what should you be thinking about? Well, I'm really hoping those circumstances, you're thinking about SIDH, right? Remember SIDH, the classic association on in-beaming exam is with small cell lung cancer, right? It's a small cell lung cancer, right? So remember, in small cell lung cancer, there's actually a bunch of primary or plastic phenomena that you can be exposed to an exam, right? The first one is SIDH, right? So that person, they will be producing a ton of ADH. So that ADH will cause their serums' malarity to go down because the area absorbing a lot of free water from the urine. Both the urine and malarity will go up, right?

But again, the in-beaming is not going to see your patient presence with long-term history of smoking, with low-serum malarity and a higher-in-nosmolarity. That's too easy, right? They're not going to do that. So what they're going to do is they're going to give you hyponitremia, and then the person is going to have a higher-in-specific gravity. Remember, specific gravity is a density measure, it's a concentration measure. It's basically like more if you really think about it, should have learned this in college, about this whole concept of relative density. Specific gravity is a relative density measure. So basically, the higher the number is above 1.012, the more concentrated your urine is, right? So this person has SIDH. And remember, it's mostly a long-cancer, though, can also cause a topic ACT production, right? Remember, that's the one that does not suppress with high-dose dexamethas or treatment. So the producer's ton of a topic ACT, so many times you'll have skin hyperpigmentation, right? But those people will have double fallon, and they'll have weak gain. In general, if you see a person that has a long cancer that is gaining weight, one of the first things you need to think, because most times when people have cancer, they're supposed to lose weight, not gaining weight. So you're a person that has cancer, and they're gaining weight, especially the long cancer, one thing of a topic ACT.

If you see a person that has a woman that is gaining weight and is not long cancer, and she has a side-east, right? Like she gets full early. That's a pretty classic finding of variant cancer, one in being exempts, right? And then you give your question about a person that has most of a long cancer, and then the person is just having trouble climbing stairs, right? Coming in your hair, things like that. That's going to be pretty classic for a lumbar etymisthenic syndrome, right? Remember, in a lumbar etymisthenic syndrome, you're pretty much making order antibodies against the presynaptic voltage-gated calcium channels. So that's why the person ends up getting this muscle weakness that improves with improves with use, right? Because basically the more you use the muscle, the more you recruit more calcium, how compete those bad auto antimities on the presynaptic voltage-gated calcium channel. And again, this whole concept of, oh, it gets worse, it gets better with use. Again, that's almost something you should not expect from your exams, right? The way you're going to describe that to you is, they're going to tell you that a person has muscle weakness that improves with, like the person has an incremental response, right? Notice incremental, right? So that means better, right? Incremental response to repetitive nerve stimulation. That's how they're going to channel that on a test.

Okay, so what if they give you a question about a patient and they tell you that this patient for the last four days, they've been having an ultra-demental status, they tell you that the patient has also been having a lot of polyureum, polydipsia. This is very high, you know, right? Polyureum, polydipia, it's been drinking a ton, peen, a ton, and they tell you that the person has like 67, I mean, 68, packaged, working history, right? What should you be thinking about? Well, I'll really be thinking about my hypercalcine, right? Remember, hypercalcine can be caused by PTHRP, right? When you make a thoroughchrome related peptide, that's something that can certainly literally works like PTHRP, right? So that's going to raise your blood calcium levels, and that can cause hypercalcine. So some of you may notice that, hmm, what is the vine harping that you know for hypercalcine that used to the stones, bones, bones, and psychic overtones? The one thing I want to tell you about people that have symptomatic hypercalcine, especially from a leg density on the immune exams, is that many times they'll give those people polyureum, polydipsia. The reason behind that is that when your calcium is really high, it inhibits the activity of EDH in the nephron, especially with the principal cell of the collecting duct. So essentially, you think that's going to happen to you is that you're going to have a nephrogenic diabetes in Cypidus, basically, right?

So when you have that nephrogenic diabetes in Cypidus, you don't respond to EDH. So you're just going to be dumping a ton of free water in your urine, right? So essentially, your urine or similarity will be low. You'll have a very low urine specific gravity. It'll be much less than 1.012, right? It'll be 1.006 or something like that. And then the person will be hypercalcemic. And many times, they'll also be hyperni-trimic, because again, they're just losing so much free water, right? So again, remember, SIDH is to small cell lung cancer. As PTHRP production causing hypercalcemia is to square-mocell lung cancer. Remember, another cancer that can cause hypercalcemia is going to be multiple myeloma, right? Although that in that situation, they're going to be giving these pathologic fractures, they're going to be giving urinal failure, right? You see the kidneys feeling, you see the presence, hemoglobin hematocrate going down, right? It's going to be multiple myeloma, the mechanism there is different, right? Remember, the plasma cells that constitute multiple myeloma, the medium-micentral looking 1, another name for interleukin 1, as you well know, is osteoclast-activating factor, right? So that thing's going to activate osteoclast, going to true up your bone, going to cause hypercalcemia, right? So in that case, these people's endogenous PTH will be low, just in response to that hypercalcemia.

Remember, people that have squamous cell lung cancer, the endogenous PTH will also be low, right? Because PTHRP, it works like PTH, but it's not the same thing as PTH, that's very high urinal, right? And then what if they give you a question about a patient? And they tell you that this patient for the past two weeks, he has been having like crazy weird headaches, and the detail that is also had like some etaxic problems, and they give the detail that, oh, they obtain imaging of the brain, and they find the posterior fosomast with punctate calcifications, and then the detail that is that died of renonocelocrosinoma. If you see this, I really want you to think of, unless it may be the give it like the, the hematocritis like 75%, which is astronomical obviously, right? If you see this, you know, I want you to think of a ipoproduction, right? This person has amalignancy. The brain malignancy I'm referring to in this case is a hemangioblastoma, right? Remember, hemangioblastoma is the classically shown, people in kids are adults, but in being exams, they will be in the posterior fosom, not anywhere else, they're going to be in the posterior fosom. So around the cerebellular area, you know, medulla area, they're going to be in the posterior fosom, and they're going to contain calcifications. That's very high you to know, they're going to contain calcifications, and they're going to make evil in a panioplastic fashion, right? Area through poeting.

So those people tend to have polycyphemia. Remember, renonocelocrosinoma is also a sociopolisiphemia. Now, let me ask you this, what genetic syndrome does this child have? Well, I hope you're saying, hmm, divine, this sounds an awful lot like one hippo lendao, Vichel, remember that's an autosomodominant, the sort of from chromosome three, right? This is something we classically find in these people tend to have like hemangioblastomas, they tend to have a bilateral renonocelocrosinomas, and they also tend to get pancreatic cancers, especially like pan... they can even get pancreatic cysts. That's actually a very high-yod association to keep out the back of your mind for for exams, right? And then, what if they give you a question about a patient, and they tell you that, oh, this patient, for the past like four weeks, actually, okay, let me set it up this way. For the past four weeks, this patient has been having like swelling of their face, swelling of their neck muscle, like of their neck veins, right? And then, they be having pain in the upper extremities, right? And then they tell you that, the, also being having like deplopia and the sapher, right? They have trouble swallowing, and then the patient has trouble keeping our eyes open during the physical exam. If you see something like this, right? It will be a thing about like a thymoma, right? Remember thymomas haven't been shown by a steamy of gravies, right? So that's why this patient has this deplopia and the sapher.

Right? So remember, the sapher is a modal speech impediment, right? So the muscles that make you produce speech would appear to be working very well, right? So don't forget, this thymomas, because the thing is our friends at the NV Me, they realize that, you know, everyone that has the job description of med students is like, ooh, SVC sing from, SVC sing from long cancer, long cancer, long cancer, long cancer, long cancer, that's true. But don't forget that SVC syndrome can also be caused by thymomas these days. It's very high up to not, right? SVC syndrome, so if you're having a cave of syndrome, it can be absolutely caused by thymomas these days on NV Me exams, right? So that's why this patient had SVC syndrome and had these myesthenics symptoms, right? So that's something they really want to keep, keep at the back of your mind. So many times in those circumstances, when a person is actually initially diagnosed with my steamy one of the things you're doing the work-op is you're going to go ahead and get a chest CT just to make sure they don't have thymomas because for some people removing that thymoma actually helps with essentially fixing their myestheniography symptoms. Remember thymomas, right? They're going to be in the anterior medias thymoma, right? So they can absolutely cause a severe vein to keep a syndrome, right? So remember thymomas are not going to be post-traumatic asthythomaases. I mean, make that clear. They're going to be anterior medias thymomasis.

I remember you're anterior medias thymomasis, they have thymomas, your tera tomas, and your lymphomas. And also if you just have lymphatic synopathy, your pulmonary area, that's going to be more of an anterior medias thymomas. Post-traumid asthythomaases tend to be more neurogenic tumors like neuroblastomas, phyocromosythomas, where if you see like a phyllo in the medias thymoma, it's not going to be anterior medias thymomas, it's going to be post-traumid asthythoma. I know this podcast kind of sounds a little weird, but the stuff I'm discussing is extremely high yield, right? It's something that just cuts people down on exams, right? So just, I want to encourage you to pay attention. You may see me begin to integrate other things as we go along. All these other things I'm trying to integrate, they're extremely important. Now what if they give you a question about a guy, you know, they tell you that he's a, you know, like a 65 year old guy, and they tell you that, oh, for the past three weeks, he's been having just severe pain in his elbows, in his knees, in his hips, right? And then they tell you that he has also developed digital clubbing. And then they ask you for your next best step in management, if you see a situation like that, you should be getting some kind of chest imaging, chest x-ray chest CT, whatever, right? This guy likely has something called hypertrophic pulmonary osteoarthropathy. I'll say that again, hypertrophic pulmonary osteoarthropathy or HPA, right?

That's a pain your plastic syndrome associated with lung cancer, right? So the classic setup on MBM exams is you're going to see this person that seems to develop this very rapidly progressive arthritis, arthropathy and digital clubbing, right? Digital clubbing is something that develops over a long time in a person, not like over like these two weeks, whenever you see stuff like that, that's going to be a relatively specific finding for lung cancer. It tends to be associated with adenocarcinomas, but it can also be associated with many other kinds of of lung cancer. Now what if they give you a question about a patient, they tell you that this patient has a, has a history of like newly diagnosed diabetes and then they tell you that he also complains of these red lesions on his, on his lower extremities. They tell you that, you know, that he tells you that oh, he was on his legs, I don't know, like at the beginning, but the lesions on the legs resolved. Now it seems to have come towards his thighs, they're now spreading towards his perineum. If you see something like this, I really want you to think of a glucagonoma, right? So these things I'm describing, right? I mean, obviously we know that glucagon's job is to raise your glucagon's levels so that diabetes part is not a big mystery there. But these red lesions on the skin that seem to disappear and reappear, disappear and reappear. And the thing is the, many times, disappear and reappear in a centrifugal fashion, right?

So the com closer and closer to the center of the body, that's the necrolitic migratoryory theme, right? So necrolitic migratoryory theme, those are patholomonic findings and people that have a glucagonomas, right? So that's very important to keep in mind for, for example. Now what if they give you a question about a patient, and they tell you that, oh, this patient, you know, over the last two, three, four weeks, that they've developed these thickened lesions, these hyperpigmented lesions on their, on their axilla or on their neck. If you see this where we all know what this is, this is a cantosis migratory. And they can't, those these migratory cancels associated with gastric admocarcinoma. And then what if they give you a question about a patient, and they tell you that, wow, over the last three weeks, this patient has been having a lot of e-taxia, you know, it kind of swim from side to side, cancestate, and they tell you that a physical examiner, you notice that this patient has my stagmus and the patient is just not able to participate in the interview because he's struggling to kind of produce the words. Whenever you, and that, you know, it's got to be worse over this, this time period. Whenever you see something like this, and they let's say, you know, they tell you the person may have had like a history of breast cancer that was treated with like radiation in the past, or the person has a history of like lung cancer or variant cancer.

If you see something like this, I don't do you think of something called parnioplastic cerebellar degeneration. I'll say that again, parnioplastic cerebellar degeneration. These people tend to present because I'm going to try to differentiate this from something else that's actually coming up right after this, right? So, these people tend to present more with neurologic problems, right? And many times the NBM is not giving you that, oh, they have a cancer right now. No. In fact, you should almost not expect that cancer in the question because actually when people have this problem, it shows up many times sometimes months, sometimes years before the atromalignancy begins, right? But basically, these people have a lot of cerebellar like symptoms, ataxia, lystagmas, dysaphria, right? So, they're having trouble, again, that motor component, those muscles that help you produce speech become weak, right? If you see something like this, I really, really want you to think of parnioplastic cerebellar degeneration. Basically, these people, they have some malignancy. Remember, your body is almost like first line of defense against malignancy. That is your T cells, right? Your T cells, your immune system, they try to help you destroy those cancer cells. Well, the problem is, sometimes as your immune system is fighting of the cancer, they then start fighting of your perkingy cells.

If you fight of your perkingy cells, that will not be good because perkingy cells, they are one of the predominant cells that we find in the cerebellar, right? So, these people can get parnioplastic cerebellar degeneration, again, it tends to be rapidly progressive over a few weeks, and it's very high you to know that this has an association of something called an anti-yo antibody, it's very high you to know, anti-yo, like y-o, right? So, y as in yellow, right? So, anti-yo antibody, that's very important to keep in mind, for example. Now, compare all these neurologic deficits I say, lystagmas, itaxia, and stuff with. It can give you a question about like a young woman, right? And they tell you that, oh, for the past two weeks, you know, she's been having like these fevers, she's been having a lot of headaches, having a lot of fatigue, right? And she's developing all these memory deficits, and they tell you that she's been hearing voices, and it kind of looks like she asks it's a freinia. But you notice that, oh, on physical exam, she seems to have like a pop-upal adnexal mass, right? Or they tell you that a transvaginal ultrasound or transabdominal ultrasound, sure, some kind of adnexal mass. If you see this, I really want you to think of something called limbic esophilitis, right? Very high you to know. limbic esophilitis. Sometimes, they describe it on imbim exams as a perinoplastic encephaloma inelitis. I'll say that again, perinoplastic encephaloma inelitis, right?

So encephaloma inelitis is spelled as ENCEPHELO, in cephaloma inelitis, MYELITIS, okay? So a perinoplastic encephaloma inelitis, right? So you may say, okay, they find how do I differentiate this from perinoplastic cerebral edegeneration? The thing is, in general, perinoplastic cerebral edegeneration, they have, again, neurologic symptoms. People that have a limbic encephalitis, they have more neuropsychiatric symptoms, right? It'll be like a reading a schizophrenia question, but many times these people have like fever, they'll have headaches, right? Those are kind of unusual things in a person that is schizophrenic or they're going through psychosis. So they'll have like psychotic symptoms, they'll have headaches, they'll have fever, they'll have fatigue, right? Whenever you see something like that, they really want you to think about limbic encephalitis, right? Now limbic encephalitis tends to be as such, there are certain malignancies, right? So the first one is, the first one is a small cell lung cancer. That one tends to have the anti-hue antibodies, right? So anti-hue, heat you, the anti-hue antibodies. Another one is if you see it in a guy, especially a guy that has like a germ cell tumor of the testis, I want you to think of the anti-machu, right? So ME2 antibodies. And then if you notice that, again, this is a woman because this woman that has this like, next cell mass, right?

You know, if there being kinds to you on the exam, the media describe that, you know, you seek outifications within the mass, blah, blah, blah, blah, right? Which tells you that, oh, that's basically a tear of tumour of some sort, right? Remember, these tear of tumour sometimes on exams, they're called dermoid cysts, right? So D-E-R, M-O-I-D, right? Dermoid cysts, right? So these tear of tumour slash dermoid cysts, one thing that, you know, that they can be associated with, is this limbic encephalitis, right? So if you know that a dexomast has fatigue, fever, headaches, all these problems, right? Now, these people, again, they tend to have more neuropsychiatric symptoms. So the thing is, how do we treat this on limbic exams? Well, we're going to treat this in general, is we can use like IVAG, we can do plasma ferrisis, like, you can do it, talk to them up, they're not going to make you choose one over the other. You can pretty much use any of these modalities. Treating a limbic encephalitis is quite the challenge. I think that's kind of like one big thing I want to emphasize. Now, what if they give you a question about a patient, and you tell you that, oh, this patient has lost like 10 pounds over the last like month, and this patient also over the last two days, they've noticed like, this sodium breakout of like hyperpigmented lesions over their back and their upper abdomen.

If you see something like that, right, I want you to think of this person potentially having some kind of GI tractable carcinoma, right? Remember, this is the Lesa Trellat sign, right? Lesa L-E-S-E-R, then Trellat is T-R-E-L-E-T, right? The Lesa Trellat sign sometimes they call it the sign of Lesa Trellat, right? Remember, classical disease, there's no gastric adenocarcinomas, but it can also be associated with any kind of GI tract adenocarcinoma. Even some people with pancreatic cancers will have the sign of Lesa Trellat, right? So, again, remember, it can dosis-nigricants, the Lesa Trellat sign, those tend to be associated again with gastric adenocarcinomas, most commonly on MBME exams. And then what if they give you a question about a patient, and they tell you that, oh, the patient, you know, has a profound bone marrow suppression, you know, in fact, maybe let me introduce it this way. So, let's see this patient, they tell you that, oh, the patient has the history of DIC, and that we're going to right now, they own all transferred, noic acid for tributal of some malignancy.

And they tell you that, oh, for the past like two weeks or so, they've been having like really high fevers, they've been having the, and they tell you that, oh, you see, they're labs, they have a very high white count, and then they have these like red lesions, like on their back, and the lesions are very tender, and then they say, oh, biopsy of one of these lesions are reveals multi-nucleotid leukocytes, right? Which tells you that they're neutrophils, right? Again, it'll be nice if they see neutrophils, but hey, what's one guru of making exams tough, just be descriptive, right? So like, oh, more tiny-nucleotid at leukocytes, that's going to be a neutral failure, right? You see a neutral feeling in these lesions, if you see this, I really want you to think about something called good syndrome, right? I want you to think about something called good syndrome. So good syndrome, again, classically, these people, oh, sorry, sweet syndrome, what am I saying? Sweet syndrome, good and sweet, they almost kind of similar words, but no, good syndrome is very different from sweet syndrome, right? So these people, right, there will be people that have some kind of history of like a hematologic malignancy. Classically, an embankment exams, that hematologic malignancy is going to be AML, right? That's why those people have a history of DIC.

Remember in AML, the classic one they love to test on exams is that could promote lositic leukemia, and I could promote lositic leukemia for whatever bizarre reason, you know, has these those are our words can trigger the coagulation, can scale and cause DIC, right? So many times, it'll be a person that has a history of hematologic malignancy and they'll have fevers, they'll have very high fevers, very high white count, and then you see red lesions that are very tender, they are not non tender, they are tender, right? And if you buy up to one of those lesions, you notice that they have a lot of neutral feels. If you see this, think of sweet syndrome. Many times these people also have like arthritis, they have like conjunctivitis, so they have like red eye. If you see this, again, think about sweet syndrome for the most part, just give these people like these steroids, I know, completely remit. But again, remember, association hematologic malignancies. Now, if you want to be really mean on an exam, which are friends that the MDME have been known to be every now and then, one way they can absolutely test this is they can test this in the context of a person having like neutropenia and getting like GCSF or GMCSF therapy, right? Remember GCSF means granulocyte, colonist, stimulating factor, GMCSF is granulocyte, macrophage, colonist, stimulating factor. Sometimes you may see these as drugs on MDME exams refer to as a sagramostim and feel grasty, right?

So feel grasty, man, sagramostim. Those drugs, they actually have an association with a person developing sweet syndrome. Now, if they give you a question just to, you know, to wrap up here or quick, they give you a question about a person that just keeps having like low blood sugars, right? Think about these solenoments, remember whipples, try it, you know, they'll have hypoglycemia, signs of hypoglycemia and the symptoms get better when give them a glucose supplementation, right? And then don't forget carstinoid syndrome, right? Again, these are people that will be healthy, you know, they'll have a lot of like, you'll have these bronchospastic symptoms, you know, with their, their airways begin to close, right? You can have like right side of your heart problems, especially like try, try to cause a bit of regurg, or pomemonic stenosis, right? And you'll have like these diarrhea, right? When you see that cluster, right? Like, you know, like diarrhea, flushing, right? Side of your heart problems, bronchospastic problems of the airway, you know, think about carstinoid syndrome, remember, carstinoid syndrome, these people, they make a ton of serotonin, right? And that serotonin can cause problems. They don't have left side of heart problems because the, the pulmonary capillaries have very powerful body regulatory function. They have all these enzymes that can activate serotonin, the avianzimes that can convert and you're tensing, one to one to tenzin, two, right?

So those are all key things to kind of keep out the back of your mind with, with carstinoid syndrome, remember, in carstinoid syndrome, you can also develop pelagra, right? You can develop pelagra, because you're essentially taking all your triptophan and using it to make serotonin. Remember, triptophan, and literally serotonin is 5 HT, right? What do you think 5 HT stands for? Right? This is going to be 5 hydroxy triptophan. So they can develop pelagra because they have a deficiency, because that triptophan that's used to make serotonin, you can use it to make niacin. Remember, niacin is vitamin B3. Again, just these, the thing about the USML is, that's why, especially for step 2, CK step 3, all this holy show of, you see people like memorizing, memorizing, memorizing, don't get me wrong, you need to memorize stuff, but you need to be able to integrate stuff. That's the way you're going to do it on, on, on, on the USML exams, even step 1, just in general. Okay, now what if they give you a question about like a three-year-old boy, and they tell you that his mom, for the last five days, she noticed that a child has been completely in abdominal pain, right? And then they tell you that, you know, on physical exam, you can pop it on midline abdominal mass. And then you also notice that this child has like a lot of like rapid eye movements, right? And you know, some of these rapid eye movements will be interrupted by the child just rolling his eyes.

And then they tell you that, ooh, this child has like a taxia, you know, has been swimming from side to side, like they tell you that, you know, his mom says he's seen, he used to walk pretty well in the past, but he's walking as just regressed significantly, and he has these unquadinated twitches of his upper and lower extremity muscles. If you see this, don't you think of a child having neuroblastoma, right? Neuroblastoma, remember neuroblastoma, again, is associated with something called the obso clonus myoclonus syndrome, right? Obso clonus myoclonus syndrome, it's actually a panneoplastic phenomenon, associated with neuroblastomas. And again, remember neuroblastomas, because they're neurogenic tumors, if they don't show up in the abdomen, they're going to be in the posterior medius thine, it's very high, you know, they're going to show up in the posterior medius thine. And remember, when they're shopping the abdomen on Indian exams, they're going to cross the midline, that's very important to know. They're going to be calcified and they're going to cross the midline. That is a very nice way of differentiating a neuroblastoma from a womb stumer, which is not calcified and which will not cross the midline. I'll say that again, womb stimmers are not calcified, they do not cross the midline, but neuroblastomas are calcified and they do cross the midline. That's very important to keep in mind on exams. And then the final panneoplastic syndrome, I'll talk about, right?

Like if you see a person with like fevers and they have like this new murmur and they have a histr off cancer, right? That's going to be something called marantic endocraditis, right? Sometimes they call it MBTE, right? On MBM exams, right? Like non-bacterial thrombotic endocraditis, it's just basically like like flex of the tumor or the tumor secreting substance is like new sin, that then goes sets up shop at the presence like, you know, valve leaflets and then the developer endocraditis, right? Because it begins to cause a valvella dysfunction. Again, many times these things we have sort of like mini cancers, like lung cancer, breast cancer, things like that. So I think I'm going to go ahead and pause here. As I do at the end of every podcast, I do offer one or one tutoring for all the USML exams, step one through step three, pre-clean cometsk exams, 30-year clerkship shop exams. And I have these podcasts on Apple Google and Apple podcasts, Google podcasts on Spotify. So if you subscribe, you have access to the most recent 150. If you want all the podcasts from episode one or even the Power Points associated with Power Point slash PD Fs, as you know, some of my podcasts, you need to go on the actual website and download them from there. And then I have a You Tube channel, I call it Divine Intervention, USML podcast and videos. That's where I post the videos I make.

And then I also made a life lessons website because many people, they are like, ooh, Divine, I love your life lessons. So many of you listen to this podcast on a Christian. So I decided to start a new website. I called it Divine Intervention Lifelessens.com. In fact, there is actually a podcast on Apple Podcast on that. It's called Divine Intervention Life Lessons. Essentially, I try to add like two or so messages a week for most of them right around 10 minutes. And again, just very insightful teaching on just a life lesson that applies to many people. So if you're interested, just go to Divine Intervention Lifelessens.com or find the podcast, Divine Intervention Life Lessons on the Apple Podcast app. And then, again, I offer these review courses for the USML is the juicy key step three exams. We're going to be having some step one offerings coming out coming out again pretty, pretty soon. So thank you for listening to me. I wish all the best with the ERAS cycle. I know today's the ERAS application. You know, programs can start downloading your application, you know, about 55 minutes ago. So thank you for listening to me. I'll see you next time. I hope you found this podcast to be helpful. God bless you and all the best for your exams. Thank you.

SIADH (Syndrome of Inappropriate ADH secretion).

SIADH, Lambert-Eaton Myasthenic Syndrome (LEMS), and Limbic Encephalitis.

Necrolytic Migratory Erythema (NME).

Squamous Cell Lung Cancer.

The anterior mediastinum (remembering that SVC syndrome can also be caused by thymomas).

Neuroblastomas are typically calcified and tend to cross the midline, whereas lymph nodes are usually not calcified and do not cross the midline.

Lambert-Eaton Myasthenic Syndrome (LEMS).

Anti-Hu antibodies.

Sweet Syndrome.

Serotonin excess due to neuroendocrine tumor secretion.

Low (much less than 1.012), indicating nephrogenic diabetes insipidus.

Von Hippel-Lindau Syndrome.

Lambert-Eaton Myasthenic Syndrome (LEMS).

Anti-Hu antibodies.

Sweet Syndrome.

Serotonin excess due to neuroendocrine tumor secretion.

Low (much less than 1.012), indicating nephrogenic diabetes insipidus.

Von Hippel-Lindau Syndrome.