DIP Episode 564 - 2024 USMLE Step 3 Free 137 Discussion Part 11a (Q101-104, super helpful for Step 2!) + Thoughts on Episodes before 400 and Critical Reasoning

Welcome to episode 564 of the Divine Intervention Podcasts. Into this podcast, I'm gonna be continuing the series on the USM Lys Step 3, free 137. This is gonna be Party 11. Now, there's one thing I wanna say here. There's, again, it's kinda common sense, but I guess I kinda figure I should speak to it. So, there's this prevailing thought out there that, oh, the episodes before episode 400 on the website are not worth your while. I mean, if that's the case, I guess it's your decision. But, I'll just kinda leave you with a few thoughts. So, say, for example, immunodeficiency diseases. Have immunodeficiency diseases magically changed over the last like four years? Or does hyper-out-dostrownism like magically not cause hypokillemia anymore? Again, it's just common sense. Don't get me wrong, do medical guidelines change? Yeah, they do. And typically, from time to time, you'll notice that I will say, oh, in the past I used to say XYZ, but now this is what is done. In fact, I think there is an episode 446, where I have something, I think the podcast is titled Divine Patch, where I just kinda talk about some things that have been updated over the last couple of years, and stuff like that. So, I think I'll just say this. You'd be doing yourself a pretty huge disservice, saying, hmm, all this stuff before episode 400, yeah, it's completely outdated. I would argue that, again, at least I'm the one that actually made this podcast.

I'll argue that about 97 to 98% of those things are still pretty accurate for the exams. I'm like, for example, you know, I read a comment yesterday on PAD, it's like, ooh, PAD, PAD, you know, whatever, aspirants, they lost the zone, da da da da da da da da da da da da. Well, if you think about it, people that have PAD still need to get to the lost the zone, that's actually the first life of an aquotherapy after you've tried like a walking program, and everybody that has PAD has to be an aspirant. All right, so just something to keep in mind. Medical knowledge does not just magically change, significantly in like three or four years to where, oh, wow, the stuff from three years ago is like just 100% irrelevant. That's actually pretty naive, if I may. So I'll just encourage you to just use common sense. All right, don't get me wrong. Have things like colon cancer guidelines changed. Yeah, they have, but colon cancer guidelines do not represent 98% of all of thought in the past. So just something to be kind of wise about, right? Again, I think it's just kind of wise, it's not everything you read online that you just kind of jump on. At the fact that somebody says something online, I guess even the fact that I see something, doesn't necessarily mean that it makes sense. You have to learn to think for yourself and evaluate the evidence, which sadly a lot of people don't seem to do these days. All right, so let's jump to question 101.

So it says 49 year old woman is brought to the ED by her husband, because of one of her history of generalized weakness, disinness and palpitations. The patient says she has felt like she is going to faint. She also reports a three day history of a URI for which she has taken over the counter-cord remedies. Medical history is remarkable for hyperthyroidism that agnostic one month ago, for which she was given prescriptions for several medications, none of which she has failed. She is five full three inches tall and weighs 119 pounds, a BMI is 21. She appears anxious. Temperature is 102 degrees Fahrenheit, pulses 168 and irregular, respirations are 26 per minute, and blood pressure is 124 for 56, while supine. O2 side is 97% on room air. Physical examination shows mild muscle wasting, mild pharyngeal air is femur without exudate and water-innesal discharge. Examination of the neck discloses goiter, an audible brewery and no GVD. Longs are clear to us quotation with good breath sounds. Cardiac examination shows an irregularly irregular rhythm and a grey three out of six is stoic ejection murmur, heard best along the left streono water. The abdomen is soft with no tenderness, a tremor of the upper extremities is noted. There is no clubbing, sannosis or a dimo of the extremities. Neurologic examination shows no abnormalities. ECG shows a fib with a rapid ventricular response. The patient is placed on a cardiac monitor and is given a liter of a liter of bolus of isotonic saline.

Which of the following is the most appropriate next step? So what do you think this is? Let's frame this, right? So this is a person that is hyperthyroid and you prescribe some medications for them, they've not filled any of them, but we see this person has very high body temperature, very high heart rate, has an irregular rhythm. And this is an acute presentation, the person is pretty unstable. I don't know about you, but this sounds an awful lot like thyroid storm to me. This sounds an awful lot like thyroid storm. Thyroid storm is a life threatening condition. I think the mortality is about 40 or 50% if you don't treat it. And whenever a person has thyroid storm, again, some of these symptoms make sense, right? Like for example, why is the present-archic heartic? Well, we know that thyroid hormone, one of the things it does is that it leads you to insert more beta-1 receptors on the surfaces of your cardiac myocytes, right? So you're gonna increase the chronotropy of the heart. You're gonna have an increased heart rate. And remember, a feb, this person has an irregular rhythm, is the most common rhythm you have found in people that have, in people that have hyperthyroidism, right? And you may wonder why those this person have fever. Well, remember, thyroid hormone raises your metabolic rate. It causes you to insert more sodium potassium pumps in the membranes of your cells.

So if your metabolic rate increases, that's gonna cause you to have just a generalizing increase in your body temperature. So again, many of these findings make a lot of sense. So if you wanna treat a person's thyroid storm, what's the thing you do? The first thing you're gonna do is you're gonna give a beta-blocker, right? Something like propronolol. And why do you do that? And by the way, this part 11, maybe an 11, 11, 11, be, there's a lot of kind of weird basic science that I need to discuss here. And in addition to that, there's a lot of pathophysiology. I need to discuss here. And then not just that there's a lot of test-eaking principles I need to discuss here. You know, this free 137, there's just a bunch of things, a bunch of sections here is like, man, this will, this kind of thing, it's a useful, more elaborate discussion. So when a person has thyroid storm, what do you wanna do? Well, you wanna give them something that will prevent t3 formation. That's why the first thing you give is an IV beta-blocker. Don't give oral medications to start in thyroid storm. That's not very wise at all. So you wanna give an IV beta-blocker like IV propronolol because that inhibits an enzyme known as the 5-prime diodeanase. When you inhibit that enzyme, it's gonna be a lot of things. When you inhibit that enzyme, it's gonna prevent the conversion of t4 to t3 peripherally.

And that's gonna be very helpful because t3 is the very reactive form, very metabolically active form of thyroid hormone. And then after that, you can also give PTO. PTO is an anti thyroid medication, right? It's a thyroid peroxidase inhibitor, it inhibits thyroid peroxidase. That's the recimiting enzyme of thyroid hormone synthesis. But in addition to that, it also shuts down that peripheral 5-prime diodeanase. That converts t4 to t3. And then after that, you can do other things. You can give me thymazole if you want. You can give super-shash-riches solution of potassium iodide because that's gonna basically make it harder for a thyroid hormone to be made. It kind of completes with certain transporters. And also, you're gonna be taking advantage of certain phenomena that are pretty in the thyroid gland with regards to you making less thyroid gland. It's almost like when you give your, you know, remember how amyote-roan can cause either the iod-based alphenominoid or the wolf-chicoph effect. I did actually talk about this in earlier podcasts. You know, how amyote-roan is able to cause both hypothyroidism. Well, the thing is, in this case, by giving that super-saturated solution of potassium iodide, you're actually trying to induce like a transient hypothyroidism if you may. And then sometimes these people also get steroids because there is actually an association between thyroid storm in some cases and adrenaline and sufficiency. So those people may get steroid.

But to be honest with you, what is the thing you really want to know for your exams? The thing you really want to know for your exams, start with an IV-bit of blocker like propanolol. And then after that transition to IV-like PTEU. And then after that, you can do any other thing you want. Usually they kind of stick with the first two wrongs on the ladder. So I'm gonna say for this one option D makes the most sense. You don't want to give the ulti-as-n. The ulti-as-n is a non-dihydroperidine calcium channel blocker. It does not do anything to that peripheral 5-primedia iodine. Dexamethosone is something you can give. But again, it's something you give down the line. It's not the first thing you give. And cardioversion, again, if you're a person that just focuses on the IV-bit and ignores every other thing they see in the question, then, yeah, I guess option A works for you, but that's wrong, right? This question is clearly a thyroid storm question. It's kind of helpful to frame questions first. Before you jump two feet into answering them. And again, Oropotasium iodide is not the right first thing to do. All right, for reasons I've explained. Okay, now, question 102. So we have a 20-year-old male who's coming to the Student Health Center. So the patient presents because of a 3-day history of burning on your initial and penal discharge. He says he has had, he says he had unprotected sexual intercourse a week ago with a woman he met at a nightclub.

He describes his usual state of health as excellent. Medical history is unremarkable. He takes no medications except for vitamin supplements and protein powder that he buys at the local health food store. He drinks two to three bears on weekends and not bears, but beers. On weekends and smokes cannabis approximately once monthly. He's 6'1", tall and weighs 180 pounds. BMI is 24. The patient appears embarrassed and uncomfortable. His temperature is 99.2, pulse is 80 per minute. And our respirations are 14 per minute. And blood pressure is 120 over 70. So physical examination discloses a circumcised penis with a white T-shellow discharge at the urythral orifice. There are no penal lesions or restorations. Rapid HIV antibody test is negative. A swab of the urythral discharge is obtained and sent for culture. Antibiotic therapy is initiated for empiric treatment of chlamydia and gonorrhea. And the patient is notified that he'll be contacted with the final results. Assuming that the patient symptoms improve with the prescribed pharmacotherapy, which of the following is the most appropriate follow-up plan? Right? Okay, so let's frame this question right. So this guy, you know, I don't protect it sexually intercourse. So now he's having burning, having a discharge. So he probably has like urythritis, some kind of STI. Well, we know that he were kind of worried about gonorrhea and chlamydia. Right? So rightfully, he empirically studied in one pharmacotherapy.

So I would hope that you're thinking that, ooh, divine, this person probably got tetriaxone and doxycycline. Remember these days we prefer doxycycline over easy thromising for chlamydia. Because doxycycline is associated with fewer treatment failures compared with easy thromising. So septriaxone and doxycycline. Septriaxone and doxycycline. Until you get your results back, and then you can either deescalotherapy, you know, appropriately. So the thing is though, this is like a general principle on imbim exams. When a person is diagnosed with an STI, it's usually prudent to screen them for other ST Is. So we're going to find the answer that it was screening for other ST Is. So like for example, option A says consult with the patient's parents before determining appropriate follow-up. This guy is a 20-year-old, he's no longer a minor. Nothing we have to do with the parents. Option B says schedule follow-up examination in one week. Hmm, I don't know about that. Well, I mean, this guy you're giving him the right therapy. He's probably going to get cured. There is a pretty reliable high rate of cure with getting septriaxone and doxy. I don't see why he want to follow up in a week. Option C says schedule HIV serology testing in three months. HIV serology testing in three months. Let's keep that because he had a test at the present for HIV. But of course, it's probably negative. It may not have seroconverteid yet, right?

It kind of takes a while for HIV to kind of make its way through an individual. The option D says no specific follow-up is necessary. I don't know about option D. I like option C more because what if he actually does have HIV and has not seroconverteid? And then you don't do the follow-up and then this person actually does end up having HIV. And then they go and slip with other people and spread it to other people. That will not be a very good thing to happen, right? That's not good medicine. So I think I like option C a lot for question one or two. I like option C a lot. All right. Now, question 103 says, a 36 year old woman comes to the emergency department. Because of abdominal pain, nausea and vomiting that began suddenly, 12 hours ago, and I was worsened since that time. The patient reads the pain as a 10 on a 10 point scale and describes it as stabbing and rededing to her back. She's not had him a themesis. Her last bound movement was yesterday. She's never had a similar episode in the past. Oh, this is her first time. Now, medical history is on remarkable and she takes no medications. She drinks one to two alcoholic beverages weekly, usually on weekends. Temperature is 99.3, pulse is 116 per minute. Respirations are 20 per minute and blood pressure is 118 over 88. The patient appears uncomfortable, the conjunctivy, anecteric. Abdomin is mildly distended with guardian and tenderness to parpecia. Notalingic tissues are noted. Results of serenal lab studies are shown.

So the presence, our force, let's look at the labs. The our force is elevated. Okay, so there's some obstructive liver thing going on or biliricin going on. Tulabili rubin is elevated as well. Triglycerides are, again, I don't know what normals are, but that number looks pretty high to me. A lipase is pretty high, right? So we know this person probably has acupuncturitis. Calcium is not that bad. Criatin is elevated, I guess. But the other labs, they're not that bad. So in addition to beginning IV fluids, which are the following is the most appropriate next step in management. So let's frame this question. This is a classic slam dunk case of acupuncturitis, right? A big gastric pain going to the back. Your lipase is elevated. This is probably three times your perimeter of normal. Right? And we see the out force is elevated. What's about it? What are the two most common causes of acupuncturitis? Number one, you know, number one, you know, in no particular order, there is alcoholism and then there is ghost stones. This person does not drink enough to get pancreatitis from drinking. Only one to two average alcoholic beverages weekly. No, that doesn't make any sense. This out force elevation is kind of worrisome that, hmm, they may be some obstructive liver thing that's causing this issue, probably a ghost stone. You know, so I think for this, we should kind of interrogate those ghost stones. I wish you kind of interrogate those ghost stones actually.

So let's see what answer choices make sense, right? So I wish I can use a CT scan of the abdomen with contrast. No, you don't need that. You know, you, this person has the classic description of acupuncturitis. A big gastric pain, it is into the back. The lipase is elevated. It's three-fourth of your upper limit of normal. You only do those CT scans when you're not really sure of what's going on, right? We're pretty sure of what's going on, so I'm not going to do that, right? Don't do that. Option B says phenofibrate therapy. This is actually one that people could jump on saying, oh, divine. This person sounds like they have hyper-trageless rightemia. Because remember, fibres are very good for lowering the presence of triglyceride levels. But again, this is why context matters so much on the USMLE exams. When you ignore context, you're going to get in a lot of hot water, right? That's why just memorizing some algorithm is not particularly useful on the exams. The thing is, don't get me wrong. Does hyper-trageless rightemia cause acupuncturitis? It does. But triglycerides of 275, really? No, come on. Usually before you get acupuncturitis from high triglycerides, triglycerides have to be really, really elevated. Almost a thousand, like a really high number, 275. There's many people that are walking around with triglycerides of 275. So I'm not going to do phenofibrate. I just won't do that. Remember, your fibres are those people are alpha agonists. People are alpha.

Don't confuse them with the people are gamma agonists that are the thiosolidin dions that use for diabetes. I don't know for whatever reason, the fibrate mechanism of action is something they love to test on the USML Es. And then option C says, in the penemcila statin therapy, that's a little much, right? We should not do that, right? This person doesn't have like some kind of a life threatening infection. Option D says insulin therapy. So the thing is actually, you actually do give insulin when people have acupuncturitis, that's caused by hyper triglyceridegibia. But the thing is again, as I've explained, this person probably does not have acupuncturitis because of high triglycerides. So we're going to get rid of that. So option E is the only thing, honestly, that I guess we be mixed sense here. Or trust the logarithmic of the right upper quadrant. Yeah, yeah, because this person probably has gold stones, right? This person doesn't seem like a person that is an alcoholic drink, only like one or two alcoholic beverages a week. So you know, so we can spot the gold stone and then we may be able to intervene, maybe I don't know, do an ERC, or something to fix the person's problem. And then, you know, they probably need some kind of interval, alcoholicis, that to me. Although, you know, while this person has this problem, you know, you're giving them IV fluids, make sure you give them pink control, right? Give them opioids. The pen of acupuncturitis really hurts.

And you know, you keep them in peel. These people should not, they should really not be eating anything. So, you know, the bulk and cannot show for a bit. All right. I'm going to go to question 104. All right. So, four month old male infant is brought to the office by his parents. Because of a 1 D history of lethargy and constipation, the parents say that the infant has not been breastfeeding well during the past two weeks. And it's not had a bowel movement in two days. He has not had fever and has not been exposed to anyone known to be ill. He was born a term to a 26 year old woman, gravity 2.1, violent, complicated, spontaneous, vaginal delivery. Birth weight was 3000 grams, so that's 6 pounds 10 ounces, that's 25%. Medical history is on a remarkable and it receives no medications. Vaccinations are up to date. Family history is on a remarkable. The patient is 23 inches, so it's less than the third percentile long, for length, and weighs 12 pounds, so less than 3%. A head circumference is 16.1 inches, that's 25%. His temperature is 99.1, pulse is 116 per minute, respirations are 16 per minute, and blood pressure is 88 over 54 millimeters of mercury. The patient is less or less upon examination, or that's not good. Physical examination discloses weakness of the upper and lower extremities bilaterally against active resistance. Abdominal and rectal examinations disclose abnormalities. Results of fasting lab studies are shown. So we look at his fasting lab studies.

His calcium, look at his labs. Sodium is kind of low, his potassium is really low, 2.7. His bicarb is really low, so this kid has some kind of metabolic acidosis. His glucose is fine, his phosphorus is pretty low. Species gravity is fine, I guess. Urine pH is normal, glucose, 2-plus glucose in the urine. So I wonder if this child is having some diabetic issue. But then his glucose is 84. I'm not going to be going to diabetic issue then, that doesn't make any sense. So we should fully be most likely to develop in this patient. These are good examples of, again, let's be realistic. These are good examples of a question where a lot of people are probably going to be scratching their heads. Like what is this question talking about? What's this question talking about? And again, when you see questions like this, this is where process of elimination comes in very, very handy. We see that this child, if we're framing the question, he's lethargic, he's constipated. And it kind of seems like this child is having a failure to thrive, in a sense. His weight is pretty low, his length is pretty low. Though that could be normally many kids. I feel like in this country we kind of skew the father that a kid is small. It doesn't mean they're unhealthy. Because there's a lot of unhealthy people here, right? And we see the diet of this nation. It doesn't really, so just kind of be careful about that. The father of the person is like 30% out, doesn't mean they're unhealthy. Just FYI. All right.

And you know, the child seems to be a little bit unstable, right? It appears less, right? Like, up-tunded and stuff. And then you see like just muscle weakness, just profound muscle weakness. Which makes sense, given the level of hypochylemia. Many people think that it's only like calcium problems that can cause muscle weakness. I'm telling you one thing the USML is classically doing a lot of the time is, you see people, they have like muscle weakness because of potassium problems. And then we see the labs, right? And we see just this kind of weird cluster. You see a lot of glucose in the urine. You see the person is hypochylemic. You see the person has a metabolic acidosis. And you see the person has hypophosphatemia. Right? This is kind of hinting at some kind of disease. But it says which of the following is most likely to develop in this patient, right? So option A says congestive heart failure. Honestly, I would not go with that. Again, let's do process of elimination. What are the genetic things or you know, pediatric things that are a congestive heart failure? Well, if the child has like the George syndrome, right? Those tend to be as little things like truncose arteriosus, tetralogy of the low. But this child does not have the antecedents of the George, right? They've no had recurring infections. They don't have hypochalcemia because of LOPTH. They don't have abnormal facial features. So that's wrong, right? Cushing syndrome. Again, pushing syndrome is something.

And I guess CHF, also if we think of other things like Down syndrome, right? You can have those endocardial Cushing defects. We don't really see that here. Or another one to I guess consider is like the shane muscular dystrophy. But the thing is people that have kids that have muscular dystrophy, they're not going to start up manifesting symptoms at four months. And again, many of these other labs just don't really make sense for muscular dystrophy. So option B says Cushing. Again, Cushing is something you'd suspect when a patient has like hypochalemia, which his person has. But instead of having metabolic acid, those are the metabolic alkalosis. Right? Because remember, when you have Cushing's, you have a lot of cortisol. Cortisol has a lot of out-dosterone-like properties. A lot of out-dosterone-like properties. A lot of out-dosterone-like properties. Right? Something to kind of keep in mind. So because he has out-dosterone-like properties, he can cause hypochalemia. But he also causes you to lose a lot of acid in your urine. That'll cause you to have a metabolic alkalosis. Right? And many times they'll have like hypochalemia, or at least the assurion will be normal. And you know, they'll be obese. They'll have a, you know, a proper strile, those things. We don't see any of those things here, right? So I don't think I'm going to pick option B. Yeah, this question is kind of weird. And honestly, option D, I'm not going to pick option D either.

Because most times, type 1 diabetes is something that pops up in your teenage years, or later. And I mean, if we're thinking DK or in this child or HHS, it doesn't make any sense because the child's blood glucose is completely fine. Right? But again, this child has a lot of glucose in the urine. That's actually a very nice clue here. You probably know the genetic disease or the disease I'm kind of hinting at with this. We see somebody that has normal blood glucose levels. But they have like a lot of glucose urea. And then you notice that they have hypophosphatemia, and they have metabolic acidosis. And they have hyponitremia, and they have like hypochylemia. But the urine pH is like completely normal. What does this look like? This is actually fancone syndrome. Please, fancone syndrome. Please don't misconstruf fancone syndrome with fancone anemia. Fancone anemia is like a bone marrow failure, fancone syndrome. And people that have fancone anemia, they tend to have like, you know, finger problems. There's no one's been talked about here. This is fancone syndrome. So let's talk about the pathophase. The pathophase behind fancone syndrome, because we wonder why is it that they have us to Malaysia? The pathophysiology there is that it's like a proximal renal tubular reabsorption defect, like a global defect in the proximal tubules. Now, this can be a genetic disease, but it can also be associated with things like, you know, like multiple myeloma or amyloidosis.

You can also find it in people that have, that have taken certain drugs, actually certain drugs that can cause this, this problem. Right? So if you have a global proximal renal tubular reabsorption defect, you can already begin to see that, ooh, the person may have like a type 2 RTA. Remember, a type 2 RTA is like a proximal RTA. Remember the type 1 is the more distal RTA. Be careful, right? That's something people mess up on the exams, right? The fact that it's a proximal tubular problem doesn't make it type 1, it's type 2. Right? So because remember, the proximal tubular, that's where you reclaim a lot of bicarb into the body. But if you have a global transporter issue there, then you won't be able to reabsorb that bicarb, and the bicarb will be dumped into your urine. So you're losing so much bicarb, so you're going to develop a metabolic acidosis. You're going to develop an RTA, type 2 RTA, actually. Right? So that explains why this prescience metabolic acidosis. But also we reabsorb a lot of phosphate in the proximal tubular. But if, again, you have a global proximal tubular reabsorption defect, oh, that phosphate is going to get dumped in your urine. So you're going to have hypophosphatemia, but you have hypophosphaturia. You have a lot of phosphate in your urine, actually. So that's part of why this book can develop osteomalasia. And the people who think that, oh, it's only if you have low calcium, you have osteomalasia, that's not true.

In fact, this prescience probably has normal calcium reabsorption in the kidneys, because a lot of calcium is reabsorbed like a little bit later in the kidneys, not really in the proximal tubular. So this prescience calcium in makes sense that it's fine. But again, to mineralize bone, remember, you need the solubility product of like calcium and phosphate. So you have calcium or you ain't got phosphate because you're wasting a lot of it in your urine. So that's going to cause you to have osteomalasia. So option C is definitely the right answer. And again, remember, many people keep forgetting this, but there are SGLT2 transporters in the kidneys. Remember, those are the targets of drugs like your flosin, right? Can I get flosin, the baggly flosin, and baggly flosin? Those drugs, they target the proximal, convoluted tubular, the SGLT2 transporter, so that you can prevent glucose reabsorption at the proximal tubular, right? So obviously that's going to cause like UT Is, kind of diocese, phonies, can create a lot of problems. And again, these people have this global transporter reabsorption defect. So there are SGLT2 transporters do not work. I kid you not have friends that the NV Mes can slot in a question here. Where they say, oh, which of the following molecular targets, you know, maybe ineffective in this patient or may not work in this patient? It's going to be the SGLT2 transporter. Again, I know you may say there's no video lever test that on step three.

Until you end up seeing it on step three. Again, remember, step three, they do love these are basic sciences, right? So just something you want to keep in mind. These people's SGLT2 transporters in the proximal tubular do not work. So they'll have normal blood glucose numbers, but they're actually going to have quite a bit of glucose in their urine because they're literally wasting it because SGLT2 is not working. Right? So that kind of explains a lot of the symptoms that they have here. And I know some of you may be like divine type RT As cause a normal anion gap in a Baleca. So let's calculate the anion gap here. If you do sodium minus chloroplos bicarb, right? So the chloride here is a 105. The bicarb is 11. So that's, you add those of that's 116. So try that from 133. That actually gives you an anion gap of 17. So this patient actually does not have a normal anion gap. This patient has a high anion gap. Right? So I know some people may be like, ooh, divine. So because it's that, hmm, hmm, hmm, hmm. It cannot be a proximal tube problem. Well, no, that'll be pretty unwise. Again, you cannot just completely conclude that something is wrong because one tiny part doesn't fit with your schema and your brain. No, right? It's not every time that you have an RTA that you have a normal anion gap in a Baleca. The key thing to just know is that an RTA will pretty much always cause metabolic acidosis.

But in some rare cases, it may not be normal anion gap in me, be completely high anion gap as we see here. All right. So just something you want to keep at the back of your mind. Right? And again, remember when you have acute illness, that can kind of fuzz off some of your serum lab values. Just something to keep in mind as well. So this child could have osteomalysia. So how do you treat a fancuni syndrome? You're going to treat it by obviously supplementing phosphate. For these kids, vitamin D supplementation. So they don't be developed by osteomalysia. And they want to be taken like sodium bicarp pretty regularly because of the chronic metabolic acidosis that they have. And then sometimes unfortunately these kids may actually need a transplant. They may need a kidney transplant. Now there's one other thing I want to highlight here for these folks. One other thing to highlight here for these folks. I want to highlight this one. I want to highlight this one. I want to highlight this one. I want to highlight here for these folks. One other thing to highlight here for these folks is that people that have a fancuni syndrome, they may actually have it concurrently with cystinosis. Remember cystinosis is actually a disease where there's this colat transporter that does not work in your kidneys, especially in your proximal tubule. So these people will be dumping a lot of cystine. So the coli COLA. It's probably a lot of cystine in your urine.

So they can actually have kidney stones. In fact, they can give you a question about a person with a fancuni syndrome that has flank pain and hematuria. And then they will say, you know, which of the phylobe found on your urine? You know, urine microscopy or whatever. And you want to pick like hexagon-shaped crystals, right? Because remember these cystine stones, they are shaped like benzene rings. They are like six-membered rings. And then this 104, there's like way too many questions they can write on this stuff. And this is like a very good classic example of the whole thing behind like multi-systems, processes, and disorders, and things like that on the USMLE. So I would not ignore a question 104. I would not ignore this series actually if I were you. That would kind of be a mistake. All right. So I think this has been going on for about 32 minutes now. So I'm going to pause here, but I want to say a few things actually. That will actually help you examine wise. Because I think it just kind of goes off of what I kind of said at the beginning. The thing is just be careful of the fact that something is commonly pedaled around or let's say like your med school administration pedals it around. Or a lot of people online say it doesn't necessarily mean it makes sense for your situation. Let me give you a few examples that I've seen in my years as a teacher and a tutor, right? So a common one is just do questions, right?

So you see a person, they're like struggling, mighting, they're dedicated periods. You know, they're not passing any practice exams. And then they go to their dean's office or they go to their academic success counselor. And said academic success counselor says, hey, just do more questions. You know, and of course they read online. Oh, I did 7,000 questions and I got a 260. Again, the fact that a person did 7,000 questions, I got a 260. It doesn't mean that that's precisely what's going to work for you. That's one of these things that many, many people don't, don't understand, right? There are some people that actually believe it or not getting the 260's, 270's on their exams. And they only do like a thousand questions, right? So the thing is you need to find what works for you. They're actually sometimes, and I've seen these numerous times over the years. It's actually a certain subset of people were doing like an extreme number of questions. It's not the winning strategy for them. Those people, the way their brain works, they just need to spend more time like actually like studying. And then like doing very critical analysis of a very limited number of questions. And they're going to be more than fine on their exams. To be honest with you, I'm probably one of those kinds of people. Again, I did a ton of questions in med school, but doesn't necessarily mean that it actually offered me a ton of benefit.

It's just one of these things you want to keep at the back of your mind, right? That classic advice you may see for people is, um, um, they may say that, uh, Oh, your personal state should only be like one page long. No, no. Yeah, it may be you want to keep it to a page, but that hard and fast road that people just pedal, pedal, pedal online. It doesn't make any sense. It literally makes no sense. What if you have special circumstances that require you to maybe go a page and a half? Was that mean that you'll get like zero interviews because you wrote a one and a half page personal statement? No, my personal statement I promised you was not one page, right? So again, just, I will just encourage you. I just feel like we kind of live in a, in a, in a phase of this world where people just kind of follow the crowd. You need to kind of learn to think for yourself. I guess you kind of consider this to be a, to be a life lesson, right? Consider this to be a life lesson. I know this may seem like a rant, but consider this to be a life lesson. Whenever you hear something from somebody, it doesn't matter how authoritative the person is, you should sit down and think. So say for example, I tell you something on this podcast. You shouldn't just believe everything I say on this podcast, whole client and sinker, but go down and sit down and think like, wait, this thing that the vine is talking about. Does it even make any sense?

Just logically, let me actually like use my brain for a change. Does this thing the vine is talking about a mix sense? Right? It's just a smart thing to do. You'll notice that you will not be deceived if your person that applies just basic critical reasoning. Right? Like for example, on the USML, you see a lot of people get a lot of questions wrong. Because again, they just don't apply basic critical reasoning. So again, I really encourage you. Consider this to be a life lesson on critical reasoning. But you need to evaluate things. Like you see a lot of like crazy stuff in the media. But if you don't go and actually dig in and actually like reason through, they because people put like a sensational headline behind something just to drum up clicks. Right? Have you seen this on You Tube? Where a person will say something sensational, but then you watch the video and you're like, man, this thing is like a pile of hoobers. Right? So just I will encourage you to think, you know, you have a brain. Use it. Don't don't be dumb. The thing is if you don't reason, you'll be deceived in the world we live in today. There's so much missing information out there. Like for example, people say, oh, vaccines are a cause autism. Okay, you've heard that. I'm not saying just disregard everything a person says. But go and like review like, wait, this thing is person saying, why are you saying it? Does it even make any sense? And then it will lead you to see that, wow, that's actually pretty dumb.

That vaccines don't cause autism. Right? So just evaluate things, right? I don't know why I'm kind of seeing this, but again, I just see this so many times. You know, you see young people, they are just completely blindsided by some authority figure. No, like actually like think, man, this thing I'm seeing does it make any sense? Or this thing I'm doing does it make any sense for my particular specific situation? So I'm going to go ahead and stop here. Again, if you're interested in any of my classes for those thinking step two, step three, I have a last minute review this evening. And I have a 20 hour class, a pretty comprehensive class that starts next week Monday, goes from Monday to Thursday, is over Zoom. And then I have a 50 hour step, just a three class taking place in the month of May. Actually, I have a tail end of May. I'm going to make a podcast where I talk about that shortly. And then I also offer, you know, other classes, I have some classes in the month of February. I also want to want you to info the USMELY and complex exams. And then I have these podcasts on Apple, Google and Spotify. And I have a You Tube channel you can check out as well. And I also have with mock interviews, errors, applications, rec letters, personal statements, and things of that nature. And then finally, I have another website called divineinterventionlifelessens.com. Divineinterventionlifelessens.com.

Basically, every week I post like one or two podcasts where from a biblical perspective, I address a life lesson. And I will also say that there's actually an Apple podcast for that, the divine interventionlifelessens podcast. Again, we have like 300 episodes on there. Many people have listened to those and they found it to be really, really helpful. So until the next episode, have a wonderful day. God bless you and bye for now. And again, use your brain. Thank you.

1) Beta-blockers (IV Propranolol) for rate/temp control; 2) Anti-thyroid drugs (PTU or Methimazole); 3) Iodine solution (SSKI).

To rapidly decrease peripheral sympathetic tone, controlling the dangerously high heart rate and preventing cardiac complications.

It inhibits both Thyroid Peroxidase (TPO) and 5'-deiodinase, which prevents the conversion of T4 to the highly active T3 form.

Comprehensive screening for other ST Is (e.g., HIV, syphilis), even if symptoms improve quickly.

Glucoseuria and/or phosphaturia with normal blood glucose levels, coupled with metabolic acidosis.

Cystine stones (due to concurrent cystinuria).

Fanconi Syndrome.

Hypophosphatemia and Metabolic Acidosis.

To control severe tachycardia and fever, which are immediate life threats.

Hexagon-shaped crystals (like benzene rings).

Phosphate wasting (Hypophosphatemia/Hypophosphaturia) leads to poor mineralization.

Ceftriaxone plus Doxycycline (Doxycycline is preferred over Azithromycin due to better efficacy).

Fanconi Syndrome.

Hypophosphatemia and Metabolic Acidosis.

To control severe tachycardia and fever, which are immediate life threats.

Hexagon-shaped crystals (like benzene rings).

Phosphate wasting (Hypophosphatemia/Hypophosphaturia) leads to poor mineralization.

Ceftriaxone plus Doxycycline (Doxycycline is preferred over Azithromycin due to better efficacy).