DIP Episode 145 - USMLE Step 2CK Rapid Review Series 14 (Surgery)

Welcome. My name is Divine, I am a resident. This is episode 145 of the Divine Intervention Podcast. In this podcast, I'll be continuing our Rapid Review series for the USMLSTEP2 CK exam. This will be series 14 and in this podcast I'll be talking about general surgery. So let's go ahead and jump right into it. So what do they give you a question about a that you know has like, let's say it's like an 18 month old kid has like mild regular quadrant pain and they tell you that he stools a guillac positive. What's your diagnosis? I hope you're thinking about like a mechal's diverticular, right? And remember, your friends at the MBA me kind of expect you to know the Bosworth pathophysiology behind mechals diverticular right? It kind of arises from a failure of obliteration of the Vittalinduct, V-I-T-E-D-L-I-N-E duct, right? Occasionally, you see it referred to as all field obliteration of the omphalum is enteric duct. It's one and the same thing. And generally, for the most part, people tend to find mechals diverticular in the right lower quadrant. Now, one high you think you want to keep at the back of your mind for MBA mechals to know that you can make the diagnosis right by doing what kind of scan. It's called a mechal scan, right? The thing is, they're highly very likely not to put mechal scan as an answer because that basically gives the way the answer, right?

Basically, what they're likely to do on the exam is they'll write something along the lines of protectnated scan, okay? It's a nuclear medicine study with something called a technician 99 M protectnated, okay? And the reason that those people get the bleeding, right? The wire positive stool says, essentially, those people get what is it called? The mechals diverticular, right? They contain a topic gastric mechals, okay? And with those a topic gastric mechals, right? Those secret assets, so that can cause, like, you know, like erosion of like, of the mechals, of the GI tract and that can cause bleeding. And the thing is, one weird unusual thing that they could ask instead of to seek is to ask. Well, I guess I'll just tell you the fact. The thing is, most mechals diverticular, believe it or not, do not contain gastric mechals, I'll repeat that again. Most mechals diverticular do not contain gastric mechals, however, if a patient presents in clinic, right? Like the two-year-old boy, bloody, bloody, blood, firstborn, blah, blah, blah, and it's like, and it's, they have like wire positive stores in Discover Mechals diverticular, it's very likely to contain gastric mechals, okay? But if you take all the population of people that have mechals diverticular, it usually does not contain gastric mechals, and then what if they give you a question? And I mean, obviously the way you treat it is with, is with resection.

Now, what if they give you a question about a patient that, you know, has a history of like Crohn's disease and then they tell you that this person over the last two days has been vomiting, has been having a lot of like nausea and they've not had any bowel movements. It could even be a person that has a history of all straight-of-collitis, but this is likely going to be a Crohn's disease question on the exam. What are you thinking about? I mean, this person obviously has signs of a small bowel obstruction, right? And Crohn's disease, small bowel obstruction, what is likely causing the small bowel obstruction in the setting of Crohn's disease? Those will be structures, right? Remember, structures occur quite commonly in patients with Crohn's, and that can present with signs and symptoms of a small bowel obstruction. Remember that, structures, if a person also has like a history of like long-term good, they can also have dysphysia from that because the good with all the acid and reparative fibrosis, they can get structures with that, and that can cause signs and symptoms of like an esophagella obstruction. Now, what if they give you a question about a patient that has a history of all straight-of-collitis?

And this patient has like severe abdominal pain and the abdomen is like, you know, severely distended, they have rebound on garden or they may try to mess with your head on the test and tell you that the patient doesn't have rebound or garden, they just have severe abdominal pain, history of all straight-of-collitis, and they tell you something along the lines of the fact that, oh, they may be sure you're an X-ray or they tell you that, oh, they got some imaging and the obtained measurements of the diameter of the transverse colon, and I think the colon of is like six centimeters or something. If you see that, what are you thinking about? I would really hope you're thinking about toxic-mega colon on that circumstances. Once you see toxic-mega colon, what is your next best step in management? I would really, really hope that you're saying to go ahead and perform an exploratory laparadomy. Okay, remember, toxic-mega colon is super life-threatening, okay, and it's actually kind of high to know the other things that can cause toxic-mega colon on NVME exams, right, so you can have things like, come on, divine think, C-Death, right, so, can a stadium difficile? Can cause toxic-mega colon, and then remember that South American bug, right, tripe on a soma cruzii, okay, it can also cause a toxic-mega colon. So again, those people need the exploratory laparadomy, and those are kind of like big things you want to keep in mind.

And then remember, right, if a person has a history of Australia, let's assume the diagnosis is made right now, like in 2019, those people need screening colonoscopies eight years after the initial diagnosis is made, right, so, like, so let's say starting in year 2027, those people need screening colonoscopies. But there's a small twist with that, that your friends at the NVME are beginning to think more about on exams, okay, if a person has a history of Australia, and PSC is diagnosed at the same time, so like, primary sclerosis in colonitis, remember, that's usually a PN-castle shielded. You actually begin to screen those people for colon cancer, starting at the time of Osreative colitis diagnosis, believe it or not, that's actually something very high yield to know. Now, what if they give you a question about a patient, and they tell you that this patient, you know, over the last three months, this patient has been having, you know, like, feeling fatigued, tired, low mood, they give you like vitals on the exam, and the patient has like a respiratory, I mean, sorry, a heart rate of 46, so they're pretty cardiac, and let's say maybe these people have like a couple of tunnel syndrome-like presentation. What are you thinking about? I would really hope you're thinking about Hashimoto's thyroiditis, right? Hashimoto's thyroid is, remember Hashimoto's, right? These people, it's the most common cause of hypothyroidism in the US, right?

One thing you don't want to mix that up with is a newborn, the most common cause of hypothyroidism in a newborn, right? So like congenital hypothyroidism is actually thyroid dysgenesis. That's a high yield thing you want to keep at the back of your mind for tests. And remember Hashimoto's, right? So she's got like auto-antibodies against like thyroid peroxides. Sometimes you may also see auto-antibodies against thyroid globulin, but for the most part it's anti-TPO antibodies, right? And if for example you were to perform a raius scan, right? A raius scan in a patient that has a history of Hashimoto's, what would you expect with really active iodine optic? I would hope you're telling me that you would observe no optic, right? Very minimal optic on a raius scan, okay? That's pathonomonic for, that's pathonomonic for Hashimoto's thyroiditis, right? And obviously you know you go ahead and give those patients a thyroid hormone replacement and they should be fine, right? So because they are hypothyroid, right? Their T3, T4 will be no, and their TSH will be elevated, right? But remember that there are many other things that can cause hypothyroidism, right? Like the quervings thyroiditis can also cause hypothyroiditis, actually I take that back. Yeah, actually I'm not taking that back. The quervings thyroiditis can certainly cause hypothyroidism, right?

And you can actually have very similar values like you have like low levels of T3, T4 elevated TSH, but the thing that will help you differentiate and also like on a raius scan you have like decreased optic on a raius scan. But the thing that will help you differentiate the quervings thyroiditis as the cause of hypothyroidism from Hashimoto's thyroiditis as the cause of hypothyroidism at a physical exam findings they will give you in the test, right? People that have the quervings thyroiditis will have like a painful tender thyroid gland and they may or may not give you like, so they may or may not. They don't always give this, but they may or may not give you a history of exposure like a history of like a recent viral or respiratory infection. Although don't take this to mean that the quervings cannot cause hyperthyroidism. The in fact in the early phase of the quervings thyroiditis those people tend to have hyperthyroidism, but as the thyroid gland kind of burns out from all the inflammation they tend to get hypothyroidism, okay? So in the early phase of the quervings, right? They will have hyperthyroidism, so their T3 because all that inflammation, right, can cause release of preformed thyroid hormone, right? So those people will have hyperthyroid symptoms, their T3, T4 will be high, so their TSE should be low under those circumstances, but again, they will still have the exquisitely tender painful thyroid gland, okay?

And you also want to make sure you remember that again, even if a person that has the quervings can be hyperthyroid, they will have decreased radioactive iodine optic on a rye of skin, okay? And if a person, let's assume they tell you to try the differentiate between a person that is going through the thyroid toxic phase of the quervings thyroiditis versus a patient that has, that is, you know, fictitiously injecting thyroid hormone. How do you differentiate between those two? Would you want to use the T3, T4 levels? No, right? Because the thyroid hormone levels will be elevated in those people in both patient populations, and the TSE should be low in both, okay? Now, would you want to use like a rye of skin to differentiate those two? No, you can't, right? Because a rye of skin will have decreased optic in both situations. If you are fictitiously injecting thyroid hormone, your TSE should be low, so because the thyroid gland is not being stimulated, you have decreased optic on a rye of skin. And if a person has the quervings thyroiditis, the thyroid gland is inflamed, so you will have no ability to optic thyroid hormone, and into optic iodine, so they will also be decreased optic on a rye of skin. And I mean, the thing is your friends at the MBMD will very likely not give you the physical example finding of all the also painful tender thyroid gland, because they know that will make it easy for everyone to get the answer correctly.

And then, if they don't give you that, right? What's the key thing that will help you differentiate between the thyroid toxic phase of the quervings thyroiditis and fictitiously injecting thyroid hormone? I hope you're telling me thyroid levels of thyroid gland, or I remember thyroid gland is the CPET type of thyroid gland, right? So if a person has, is in the thyroid toxic, thyroid toxic phase of the quervings thyroiditis, the thyroid gland levels will be elevated, because that elevated thyroid hormone is coming from the thyroid gland, versus a person that is, you know, trying to maybe lose with whatever by injecting thyroid hormone. It won't work out so well for them, because the thyroid hormone you can buy at a store, or like as an nutritional supplement or whatever, or I'm fairly certain that is not so, as an nutritional supplement can be associated with, it doesn't contain thyroid gland, right? So the thyroid gland levels will be normal on that those are circumstances or decreased. And then, remember, a person has grieves disease, right? Obviously, those people, you know, they will be thyroid toxic, right? So they will have a levity, 3 T for their TSH will be low, but if you get a rye of scan, remember, these people have auto antibodies against the TSH receptor, right? They are called thyroid stimulating immunoglobulins, right? So, because the TSH receptors are being stimulated, there's actually a diffusely increased optic on a radioactive iodine optic scan.

And then, remember that if a person has like a an ovarian mass like stromal ovarian, believe it or not, your friends at the end of the end, we can give you some pretty nasty questions on that. Those people will have a levity thyroid hormone levels, right? So T34 will be elevated, TSH will be low, right? TSH will be low, but they'll also be again decreased optic on a rye of scan, because that TSH being low means that the thyroid gland is not being stimulated. And then, remember that if you're thinking about, like, you know, toxic adenoma versus a toxic multilogoydor, right? You present the same way, thyroid toxic symptoms, elevated T34, low TSH, right? But the rye of scan results are different. They'll be increased optic on a rye of scan, but the results are different. For a toxic adenoma, you have only one hot spot on a rye of scan. For a toxic multilogoydor, you have multiple hot spots interspersed with cold spots on a rye of scan. I'll repeat it again. For a toxic adenoma, you have one hot spot, and then the rest of the thyroid gland is cold. For a toxic multilogoydor, you have multiple hot spots interspersed with cold spots on a rye of scan. So I know, again, I probably took more time than I expected to talk about these rye of scan results, but I promise you that thyroid stuff is like fluoridly high-yield in general for surgery questions on the USM Ls, and also for like your surgery shelf. And vaguely, maybe you go see some more things with thyroid, right?

So what is the biggest risk factor for thyroid cancer? I hope you're telling me like prior exposure to like head on neck radiation, right? Like radiation therapy to the head and neck. And what's the most popular kind of thyroid cancer? I would hope you're saying papillary thyroid cancer. Remember, a papillary thyroid cancer is popular, okay? That's a very high of thing to know. And then what's the kind of thyroid cancer that loves to spread hematogenously? That'll be follicular thyroid cancer, okay? In general, an MBM is follicular thyroid cancer, does not spread through lymph nodes, is spread through the bloodstream, okay? And remember that papillary thyroid cancer, right? What's a unique histologic feature? What are actually two unique histologic features of papillary thyroid cancer? So those are the Samoma bodies, right? Samoma bodies. And then another thing, those are often any eye nuclei, whatever thing is, okay? So just sort of keep that at the back of your mind. And again, remember, papillary thyroid cancer is the most common type of thyroid cancer. What if they give you a question about like an 80-year-old guy, a high-profile weight loss in large-end thyroid? What kind of thyroid cancer are you thinking about there? This is the big bad one, right? That's an aplastic thyroid cancer.

And then what if they give you a question about a patient that has had multiple kidney stones, and this patient has chronic recurring abdominal pain, and they tell you that this person has, you know, like an enlarged thyroid gland. What kind of thyroid cancer are you thinking about there? I would hope you're telling me medallary thyroid cancer, right? And if you wanted to be more specific, what kind of MEN syndrome does this patient have? Does it mean 2 B? Or MEN2 A? Or MEN1? Again, I would hope you're telling me MEN2 A. Remember, MEN2 B does not include hypercalcemic problems, right? They don't have the papillary tissues. The papillary tissues, you find those in MEN1 and MEN2 A. So this person specifically has MEN2 A because medallary thyroid cancer is not a finding in MEN1, right? So this person has, you know, medallary thyroid cancer. Remember, the tumor marker is calcytonin, right? And if you do like staining of the thyroid gland, the people that have medallary thyroid cancer, they'll have like the apple-green birefringens on congurate, whatever thingy, because that calcytonin can sort of form all these polymers that can essentially become amelone, okay? So if you ever see a person that has thyroid cancer and they have like a prolonged acute interval on EKG, really think about a, really think about a medallary thyroid cancer, because that calcytonin, remember, my numonic calcytonin calcytones down block calcium levels, okay?

So those are high yield things you sort of kind of want to keep at the back of your mind for tests. Now, what did they give you a question about a patient that has a rock heart thyroid gland on an ambient exam? I would really hope you're thinking about our right delves thyroiditis on the other circumstances. So right del is spelled R-I-E-D-E-L, right dels thyroiditis, right dels thyroiditis. Remember that in right dels thyroiditis, right? You have like this fibrosis and badness that happens with the thyroid gland. You certainly want to make sure you remember that right dels thyroiditis has an association with IGG4 related diseases, okay? These IGG4 related diseases, believe it or not, they are florally high yield for the US semilist exams, right? So the IGG4 related disease, they are things like autoimmune pancreatitis where you have like a sausage shaped pancreas on imaging. They can also have like autoimmune cold blooded disease, they can have like retroperitoneal fibrosis. So that can cause like a bilateral hydron and fibrosis, right? Because we essentially fibrosin, the ureters, right? So it's kind of making it hard for the kidneys to drain. And then I know that I talked about, I know that I talked about Sanmomo buddies. I think it's you know kind of imperative for exams to know the other things that are so though Sanmomo buddies, right?

So you want to remember things like, so I mean there's this component you probably find in first aid, it spells out Sanmomo, I'm the piece for like papillary thyroid cancer, right? That has the Sanmomo buddies. The S is like a kind of ovarian malignancy, come on divine thing. Yes, there'll be a serous cystadlock arcinoma, right? Of the ovaries, right? And then remember many engeomans, right? Many engeomans remember those things tend to be parasaginal, right? The tend to have like this drool tail, right? Those also have the Sanmomo buddies. And then remember that misothelomas, right? I remember again, asbestos exposure, phyrrogenous buddies with asbestosis and all that crap, misothelomas certainly also has some Sanmomo buddies. Okay, so I think that's me, I think the Sola should maybe say about like thyroid, I think you know kind of hit that pretty hard already. So hopefully you get that, I mean I, I don't know, I just always feel about when people get endocrine questions wrong on exams, because usually pretty straight, they're not usually pretty, they're pretty straightforward if you know what you're doing, but most people just try to like memorize an endocrine blind and then they end up hurting themselves on exams.

Okay, now what if you get a question about a patient that has, a patient that has a, let's see, a patient you know, they've been having like moisture vomitting, they tell you that the colon is distended and let's say they show you like a coffee bean sign on imaging and the head of the coffee bean is pointing towards the right upper quadrant. What's your diagnosis there? That will be what? That will be a sigmoid voluulus, okay? Well the thing is your friends are the, are the MDM, you're kind of realize that everyone has a med school or even maybe the Lee public, they've all memorized the word sigmoid voluulus sigmoid voluulus sigmoid voluulus right? So these days they are beginning to test a sigmoid voluulus pretty commonly. The thing is, it's actually very easy to differentiate sigmoid voluulus from sigmoid voluulus right? The thing is both of those disorders have the coffee bean sign, but in sigmoid voluulus the head of the coffee bean points towards the right upper quadrant, in sigmoid voluulus the head of the coffee bean actually points towards the left upper quadrant, okay? Believe it or not, those are things that are floridly high you to know for MDM exams. Now what if they give you a question about a patient that has you know smoked two packs a day 50 years, I mean you probably kind of know what I'm going towards here.

So like two packs a day 50 years three months weight loss, don't ask to per caution on or quotation on the chat like with a long exam, decrease break sounds at the right long base, bloody bloody blah, and then they tell you on imaging you know you see a large plural of fusion, you see a coin shaped lesion, right? This person clearly has lung cancer, right? So if a person has lung cancer, right? What's your, if you see a person that has lung cancer and they have a plural of fusion, what is always your next best step in management? It's actually to get a thoracin thesis, right? You get a thoracin thesis and you send that for cytology because here's the thing. For prison has lung cancer and you find malignant cells in the thoracin thesis, your workup is done, the patient has stage 4 cancer, there's nothing you can do for that patient anymore. I mean you can maybe try to prevent the you know the the plural whatever the plural fluid from building up by you know doing like putting like talc or doing like a plural thesis or whatever but yeah once you see malignant cells in the plural of fusion that stage 4 lung cancer end of story, right? Again, obviously bad prognosis, on that those are circumstances and remember that if a person has lung cancer and remember that the like the most common if they give you like a non-descript question no parneoplastic phenomena, nothing especially like a female and then they tell you that this person has lung cancer and you have to pick the type.

I really hope you're picking like an admo carcinoma, on that those are circumstances, I remember radio scrimal cell carcinoma, right? That's the one that they can give you like histology results and they describe something like a keratin pearls, on that those circumstances, I remember those scrimal cell lung carcinomas, right? They tend to produce a pth RP, right? So like paraffired humona, related peptide. So by producing pth RP those things can cause hypercalsemia. So those are key things you want to keep at the back of your mind. Remember that a small cell lung cancer, right? It's the type where it has like three big time high-yoda parneoplastic phenomena, right? So one can be like the Lambert ET-MI Sthenics Syndrome, right? Where you make auto antibodies against the presynaptic voltage, get it at calcium channel, right? So those people get like proximal muscle weakness, right? That improves with use. Remember, so it's actually kind of important to be, I guess be able to distinguish Lambert ET-MI Sthenics Syndrome from myestinia gravis on mbim exams. The thing is myestinia gravis tends to cause more like bobar symptoms, right? So they'll have you know like trouble swallowing, droopy eyes, you know like almost like head and neck symptoms, but Lambert ET tends to cause more proximal muscle symptoms, difficulty rising from a chair, difficulty coming here, so the deal, okay? And then remember that in small cell lung cancer those people can also have SIDH, right?

So those people obviously, right? If you have SIDH, they'll have like hypo-osmolar serum because they are absorbing a crap ton of water in the nephron and they'll have hyper-osmolar urine, right? Because again, the urine is super-concentrated. And then remember that this is, small cell lung cancer can also produce acetyl, right? That's the one that does not suppress with the high dose of the xamethasone. And then remember that some of these cancers, right? It can also cause it can also cause like a superior venocative syndrome, okay? Right? So they're a describe person, you know, that has like swelling of the face, prominent vessels, you can see them in the face, the neck vessels are kind of like the standard. Think about it as V Cs syndrome. If the ask for your next best step in management, go for addition therapy first. They will try to master your head by giving you an answer that it wants to give like IV steroids. Don't pick that. Pick radiation therapy first and then ask questions later, okay? To treat as V Cs syndrome. And then remember that lung cancer can also cause a pancus tumor, right? So those people have like a honor syndrome. So they'll have like the classic, like, droopy eyelids to the toses. They'll have the popular construction. So they'll have meiosis. They'll have anhydrosis, right? And then remember that if they describe a person that, you know, is a long-term smoker.

And then for whatever reason, over the like a month, the person gets like this, sodding onset of thropathy. You don't go from having like no arthritis to like arthritis within like a month. And then the person has like this rapidly progressive finger clumping. And if you see that, you want to think about this paranel plastic phenomenon known as hypertrophic, pulmonary osteoarthropathy. That's pathonomonic for lung cancer. Your next step in management is to pick some kind of answer choice that released to get in chest imaging. Okay. Let's see. Is there anything I want to say about lung cancer? No, that's all that really does come to mind. I mean, remember, right? Small cell, squamous cell, those are both essential. I remember that small cell is actually of neuroendocrine origin. So neuroendocrine origin. That's kind of like something high you know. And small cell once you meet the diagnosis, it's already metastatic. And I know that I said that Pancus tumors right now. So she did with, so Pancus tumors associated with what is it called? Like honours syndrome. What if a person has like a partial honours syndrome? What's the MBME disorder that's associated with a partial honours syndrome? Well, I would really hope you're saying you're telling me a cluster headache, right? People that have cluster headaches, they tend to get like toses and myosis, but they actually do not get an hydrocyse.

Again, that's one of those like weird high yield things you want to keep at the back of your mind for MBME exams. And then to round up today, let's talk about some classic findings in certain diseases, especially maybe more you know like classic CSF findings. So Zancthochromia is a classic CSF finding in what? That's a sub-rocknoyed hemorrhage, right? So like again, worst headache of a patient's life, you know, worst headache of a patient's life, what should always be your first step in diagnosis? It would be a non-conheads CT, right? You get a non-conheads CT, if that's negative, you get the lumber puncture, you see Zancthochromia. And the thing is, again, your friends at the MBME, right? They know that again, every human being has memorized. In fact, maybe you've probably seen on Rez Anatomy, oh, worst headache of a patient's life, blah, blah, blah. So they don't really do that crap anymore, right? The thing they do these days is they give you a question that kind of looks like meningitis, but it's a sub-rocknoyed hemorrhage question, right? Because and here's how you differentiate those things. You don't get meningitis in 12 hours, right? So if you see a person that has like fever, nuclear rigidity and sort of like started like from like the patient was normal and he just started like sodding these, almost like they just boom, like dropped meningitis on that person like 30 minutes ago. Think about sub-rocknoyed hemorrhage, don't get tricked by that on MBM Es.

And I remember, if a person has a sub-rocknoyed hemorrhage, they have blood pressure, super high, you know, try to control the blood pressure. And then you want to give them my mymodepine, right? To present, prevent a superimposed ischemic stroke on top of the hemorrhagic stroke, be just happy. So Zancelchromia, classic CSF finding in sub-rocknoyed hemorrhage. Remember, if a person has what is it called? If a person has herpes, right? And cephalitis, right? Or heaps, herpes, meningitis, you'll have like hyper intense signaling on like like on like MR of the brain, like in the temporal lobes, they can actually give you that MRI, I guess it's supposed to kind of like be able to pick that up. I remember those people tend to have like red blood cells in the CSF, right? And you cover that with IV acyclover. Remember, if a person is not admitted for herpes-related syndrome to the hospital, they have no business getting IV acyclover. They get oral acyclover. That's a high-yield concept, you know? If you're not admitted in a patient in general, giving IV medications on MD in the exams, you know, it's probably not the smartest idea in the world. And then what's the classic CSF finding in, I don't know, let's say like a person that's like an archaeologist and this person, you know, over like six over like a six-week period, Luzi Sol is memory, has myoclonas, bloody, bloody, blah. What are you thinking about there? I hope you're thinking about CJD, right?

So, Kartsfeld, Ayakova disease. I remember in CJD, right? Those people tend to have, you know, myoclonas, it's a bad disease. It's really no cure. A person has essentially screwed. And remember that those people have elevated levels of the protein 1433 in their CSF. You may see, hey, you find that sounds low yield 1433. Who cares? I promise you you should care, especially if you have had an injury, you certainly should care, especially if you're a person taking an NV Me-based exam. And then what's the classic CSF finding in people that have, what is it called? Narcolepsy. So those people actually have low levels of orexin, right? Remember orexin, they also be called a hypochritin on NV Me exams. And you make the diagnosis of narcolepsy, obviously, with a sleep study, right? They may not put sleep study. The 5 for sleep studies, like a polysumnography, right? Okay. And remember that narcolepsy, right? You can treat, you know, with like, you know, scheduled maps during the day, you can give them stimulants like more daffinial or armodaphenial. And you can actually treat the cut up like C, right? So like the person would like narcolepsy, the laugh, and then boo, the kill over and forth. That's what's called cut up like C, you can treat cut up like C with a drug known as a sodium oxybit on NV Me exams. So sodium oxybit, oxybit is spelled Oxy, B-A-T-E. So I guess those are, let me go ahead and stop here. This is going on for more than 30 minutes.

As I do at the end of every podcast, right? I do for one or one tutoring for ton of exams, right? So step one, two CK, step two CS, step three. And if you're medicine resident, I actually tutor to the ABI M board exams and the internal medicine training exam. And then if you're, you know, med student, I tutor for the pre-clean, all the pre-cleanable exams, and also the 30-ish off exams, I tutor for those. And then I also do this thing I call longitudinal tutoring. I've kind of talked about it at NOSM. But basically, it's one of those tutoring setups that essentially like if you're like a newly minted med student, like you're starting first year, it's actually a pretty, like the people have done this with they've been like super successful on the USMLA exams, essentially tutor them for their class exams and for step one throughout their first years of med school. And then when, as I'm doing that, I'm like infusing step one knowledge along the way. And then they end up crushing the USMLA step one exams. Same thing, if you're newly minted 30, you're a contributor for all your shelf exams. And then I also tutor for step two CK again. People that have done, they're just some very competitive advantages to having the longitudinal tutoring, like essentially everyone have done it with. Most of those people have gotten like super high scores on the like super high scores, like way, way, way, way above the national average on the USMLA exams.

So if you're interested in any of that, reach out to me. And then if you know college students, you need to do it for most of like the MCAT disciplines, like Gen CAM, O-CAM, Physics, Biochemistry, Histology, Physiology, offer tutoring for all those things. And then if you need like you know, consultant, right, or advice for the ERAS applications, right? So like writing personal statements, writing recommendation letters, because sometimes some people that write reclaters, they say, okay, you know what, write the rec letter. And you know, I'll edit it and all that blah, blah, blah. I've worked with students on all those things. So like writing rec letters, assisting with personal statements, mocking interviews, all that. I do offer all those things, editing your ERAS application. Same thing with the AMCA's applications, right? So if you're like a college student applying to med school. So I hope you've gotten something from this podcast. I really cannot wait for the MBA season to begin. I don't know, just literally don't watch TV anymore. There's really not much that's going on these days. And I'm really hoping that this is the championship year for the leakers. So I will see you in the next podcast. Have a wonderful rest of your day. God bless you. Thank you.

Low or absent radioiodine uptake (low/minimal uptake).

Exploratory laparotomy due to high risk of perforation.

Toxic adenoma shows only one "hot spot," while a toxic multinodular goiter shows multiple hot spots interspersed with cold areas.

Xanthochromia (yellow discoloration of the CSF).

Squamous cell carcinoma.

Sigmoid volvulus presents with the "coffee bean sign" pointing toward the right upper quadrant (RUQ).

Papillary thyroid carcinoma; Samoydes bodies and Orphan Annie eye nuclei.

Technetium-99m pertechnetate scintigraphy (Meckel scan).

LEMS causes more proximal muscle weakness (difficulty rising from a chair); MG causes cranial/bulbar symptoms (droopy eyes, difficulty swallowing).

MEN2 A.

Low levels of Orexin (Hypocretin); Sodium oxybate.

IgG4-related diseases (e.g., autoimmune pancreatitis, retroperitoneal fibrosis).

Papillary thyroid carcinoma; Samoydes bodies and Orphan Annie eye nuclei.

Technetium-99m pertechnetate scintigraphy (Meckel scan).

LEMS causes more proximal muscle weakness (difficulty rising from a chair); MG causes cranial/bulbar symptoms (droopy eyes, difficulty swallowing).

MEN2 A.

Low levels of Orexin (Hypocretin); Sodium oxybate.

IgG4-related diseases (e.g., autoimmune pancreatitis, retroperitoneal fibrosis).