DIP Episode 182 - Comprehensive NBME Emergency Medicine Shelf Review Series 2

Okay, welcome. My name is Devine, I'm a resident. This is episode 182 of the Devine Intervention Podcast. And in this podcast I'll be continuing the comprehensive review series that is ongoing for the emergency medicine shelf exam. And in today's episode I'll be talking primarily about endocrine emergencies, right? All the ones that occur in diabetics and the ones that do not occur in diabetics, like essentially like other like non-diabetic emergencies. So the thing is, what if they give you a question about a patient? You know, patient comes in and they tell you that for the last two to three days, this patient has been having a lot of, you know, nausea and vomiting, has not been able to eat, has been doing, you know, pretty poorly from a clinical perspective. And then they give you some relapse. You notice that the person's glucose is like 300. And the person's bicarb is like five, right? And the person has like a sodium of like 130. What's your diagnosis? Well, I hope you're seeing that this person's got a decay. So this person has got a decay, right? So obviously you want to know how to manage decay. And you want to know how to manage a HGCNS. And the good thing about these disorders is that for the most part of the management is the same. So I'll probably focus the most on the management of decay. But basically the first thing is how do you establish the diagnosis of decay, right?

So the thing is, many people make this mistake commonly on exams and the MBM may kind of counsel you to make that mistake. Like you see like in some medical institutions they teach, oh, you know what? If your glucose is more than 600, it's HGCNS. If it's less than blah, blah, blah, it's decay. I would not use those rules on MBM exams. If I were you at focus more using the bicarb. If a person has a profoundly depleted bicarb, they have decay end of story. If a person's bicarb is normal or just like low normal, thinking about HGCNS, regardless of the glucose number, right? And you may say, okay, so why do people that have decay develop an acidosis? Well, the reason they develop the acidosis is because they have an usually people that have decay, they have like an absolute insulin deficiency. Essentially like a type 1 diabetic, right? And if you have an absolute insulin deficiency, then you will not be able to inhibit glucose gone because if you remember from maybe studying for step 1 or something, you remember that the beta cells in the pancreatic islets they are centrally located or the alpha cells that produce glucose gone are eccentricly located and once the beta cells secret in insulin, that insulin on its way out from the center of the pancreatic islets, it actually goes ahead and inhibits the production of glucose gone from the alpha cells.

So the thing is people that have type 1 diabetes, they have an absolute insulin deficiency, they have no ability to inhibit glucose gone and glucose gone is one of the, is essentially the primary hormone that stimulates the production of ketone body. So that's why people that have decay, you know, because they can, they have this absolutely insulin deficiency, they tend to be profoundly acidonic. Now, people that have hegeic shenanes, right? Again, typically it's a type 2 diabetic, a type 2 diabetic has for the most part insulin resistance, not insulin deficiency, right? So the thing is they do have enough, typically they typically have enough insulin around to inhibit the release of glucose gone, right? So if they inhibit in the production of glucose gone and those other nasty counter-agulatory hormones, then these people generally tend to not have, these people generally tend to not have anacidosis, right? Because again, they've inhibited glucose gone enough to work ketone body synthesis, it's not stimulated. And remember in a person that has like these, they have like especially decay, right? The big thing one remembers those ketone bodies, right? It can be like acidosetit, to like beta hydroxybutyrate. And then people that have, you know, these hyperglycemic emergencies they generally tend to have, you know, pretty elevated, pretty elevated glucose, right?

So it can cost like almost like a pseudo hyponitremia where essentially if you actually do like the correction, you'll notice that all this person's sodium is actually quite normal, right? So for example, the correction factor, let me give you an example here, right? So let's say a person that's in hegeic shenanes or something, let's say their glucose is 125, right? I mean, sorry, let's say their glucose is 1000. And let's say their sodium is 128. Let me use 120 as an example, right? That 128 number for the sodium, you really cannot believe it, right? Because again, they have like a hyper or smaller hyponitremia, pretty much right? So how do you do the correction? The correction is basically, at least the way I do it is, you take the number of 100s above 100, right? And multiply that, multiply that by 1.6 and then add to the sodium number, you're giving it the question stem. So let's assume, again, let me make up some numbers here. So let's assume the person's sodium is 128, right? That you measure when they get their diabetic crisis. And then their glucose is like 1000, right? So the way you calculate what their normal sodium should eat, like the actual sodium is, is you take 1.6. So there's, there is 9 100s above 100, if a person's glucose is 1000, right? So you take 1.6 times 9. If I'm doing my math correct, so 1.6 times 4 is 6.4 and then you double that, that's 12.8 and then you add 1.6 to that, that is 14.4.

So if you add 14.4 to 128, this person's glucose, I mean, sodium is like 142.4. So that's kind of like within the normal range. I should probably, I should probably have used a lower sodium number for my initial sodium, but at least you get the point, right? So that's generally how you calculate what their row sodium is, right? And the thing is, as you treat the decay or the HHNS, the hyponitrinia will kind of correct itself. And then remember that people that have, that are in decay or HHNS, they may be hyper, kill, mimic, perlabs, but that doesn't necessarily mean that they have adequate amounts of potassium in their bodies. In fact, a commonly tested exam association is that people that are in decay or HHNS, they may have hyper chilemia on labs, but their total body potassium stores are depleted, right? Those are again, all high yield things you want to keep in mind, right? And then you also want to remember that ketosis, right? It's not always associated with like, like decay is not the only cause of ketosis, you'll be seen on an image show for example, right? The thing is when you see a person that has ketone bodies, you know, you should also look at the, you should look at it in the context of the rest of the question, because people that are starving, people that are pregnant, people that have like hyper-emesis, gravity, people that are, you know, like big-time alcoholics, they can all have ketosis on an NVME exam, right?

So you kind of need to watch out for that, right? So don't just say, oh, it's ketone boom, and then you reflex to decay or HHNS, or you may be wrong if you actually do that, right? So you gotta be careful there. Okay, so big thing is, so how do you treat, how do you treat a decay, right? So the thing is basically if you want me to summarize it for you, basically give fluids insulin and replace electrolytes. Those are like the three big things you need to give your mind. I mean, there are some more specific things that I'm gonna talk about right now, but for the most part, if you organize it this way, you're probably in good shape, right? So like, fluids first, insulin, and then replace electrolytes, right? So what do I mean by fluids first? So typically fluids first, you give like a two-liter mamosilin bolus, okay? And usually, you know, you give that like, you give like a liter in the first or a liter in the second hour. And then the thing is, once you're done giving that, you then switch to giving those people a half-numosilin, right? So like 0.45 percent insulin, okay? So your initial fluid bolus of about two liters, you give mamosilin for that. But after that, you then start giving half-numosilin.

And one nice tool you can use is you can see, okay, like, 20 units per kilogram, and in like, 20 cc per kilogram per hour, that can be your, although that's kind of high, I mean, typically for me, I would say I probably go like 10 cc per kilogram per hour because again, it kind of depends on the person's weight, right? So, you just one of those things, you need to be mindful of what I don't, I don't really suspect that that's something that'll be tested on a shelf. So, you don't, basically, big thing, two liters of mamosilin initially, you give like a liter per hour, and then after that, you switch to half-numosilin. And there are some numbers you want to keep at the back of your mind before you can initiate insulin therapy. And I'll see probably the biggest one is the potassium, right? If a person is coming in and they're in decay or HHS, and your initial potassium is less than 3.3, you cannot study insulin therapy, okay? That's a big number you want to remember. If your person's initial key is less than 3.3, you absolutely cannot study insulin therapy. If the person's initial potassium is between 3.3 and 5.3, you can study insulin therapy, right? But the thing is the fluids you're giving them, the half-numosilin, you do need to add potassium to that fluid solution, right? So, basically, the only time that you treat a person in decay or HHS, and you don't include potassium in their fluids, is if their potassium is greater than 5.3.

If their key is greater than 5.3, that's fine, you can treat them normally, you don't need to add any potassium to the fluid, but if their potassium is less than 5.3 or greater than 3.3, you always need to put adding potassium into the half-numosilin you're getting. If it's less than 3.3, you cannot study insulin therapy. If at any time you're treating the patient, and you measure their potassium is less than 3.3, you stop the insulin therapy you've already instituted. And typically the insulin that's given in a person that's in these are diabetica issues, typically you give the insulin at the rate of 0.1 units per kilogram per hour, right? And the thing is remember there are many different kinds of insulin. The kind of insulin you use is like insulin regular, or regular insulin. Insulin regular is like the rapid activity insulin. Remember there's like the ultra-rapid activity insulin. Those are like your Lisbon, Aspart, Blue Lysine. You can use those, but that's not what is classically used on exams. I will say that the one you wish to watch for is the rapid activity insulin. If the regular insulin, that's the insulin. In fusion you're given a person that's in decay. And then some other key things to keep in mind, right? So, you know, as you're treating the person with decay, you know, you keep lowering their glucose, lowering it, lowering it.

Once he hits anything from 200 to 250, you do need to add extras to the half-numosilin in fusion they're getting because the thing is, one relatively common complication of diabetic therapies. Those patients can actually develop hypoglycemia from the insulin in fusion, right? So, once their glucose sort of drops to like the 200 to 250 range, you need to go ahead and add a extras to their, to the normal saline solution. I mean, in general, I mean to the half-numosilin solution. And then in general, there's a common question that shows up on tests. Do you give bicarb? In general, there's not much good evidence for bicarb administration in a person that's going through a diabetic emergency. So, what I mean, you know, if you read a lot of literature, you say, oh, you know, give sodium bicarb if their pH drop is less than 6.9. But in general, giving sodium bicarb doesn't really have good evidence behind it. And then, also when you hit that 200 to 250 glucose number, right? Especially like in Hichichin, that's right, for example. You do need to, you know, begin subcutaneous insulin, okay? So notice, I've been very specific here. When a person has Hichichin, and their glucose drops into the 200 to 250 range, you can go ahead and initiate a subcutaneous insulin. But for a person that's in decay, if their glucose drops into 200 to 250 range, you do need to also make sure that the anion gap is closed, right? So, what do I mean by that?

Yeah, basically the anion gap has to be 12 or less. So 12 or less. And then their glucose is in that 200 to 250 range. Before you can then say, okay, let me go ahead and initiate a subcutaneous insulin. And a common example question that shows up is when you initiate subcutaneous insulin, then you turn off the insulin like drip, like the insulin infusion, you cannot. Right? So the thing is typically when you when you start the subcutaneous insulin, you'll keep the, like, let's say you start the subcutaneous insulin at 9 a.m., right? You can turn off the insulin infusion at 11 a.m., right? At 11 a.m. or later. So again, you do not turn off the insulin infusion until after like two hours after you started the subcutaneous insulin. Again, you may see how it will define you have been very detailed with this. I promise you this stuff is very high your to know, right? And then one other thing I also I guess should mention here is that I remember that it's not, you don't want to also lower a person's glucose too fast, right? So if you're if you're dropping a person's glucose like like like crazy fast during a decay, or that can, or HHS, that can cost you a relatively dimo, right? That can cost you a very dimo, right? That can cost you a very dimo. And then I guess one other thing you also remember, right? Like it's almost like a general principle. If you correct any hyper disorder too quickly, that can cause like server like dimo, right?

So like if you think about it like hyponitrime, right? Like from from high to low the brain, right? Kind of the similar applies to hyperlipidlycemia, right? So if they give you a question about a person, you know, has been treated for decay or HHS, and then the person becomes altered, comatose, unresponsive, and think about server symptoms. And then also please do not forget that there are other things that can cause hyperlipidlycemia, right? Like if a person has like cushion syndrome, stuff like that, right? Those things can all cause hyperlipidlycemia. And then finally one thing that your friends at the MBME, you know, kind of require review is annoying how to differentiate between like three permanent causes of hypoglycemia, right? So if for example a person is like insulin, you know, maybe like a medical student that's trying to skip work or resident or you know like someone in the healthcare profession, and then they come out like a hypoglycemic crisis. Obviously, at one of those circumstances, you want to go ahead and you know, check the insulin and I mean obviously give them glucose first, fix their problems so that they don't die in front of you. But you know, you can do some testing, right? So you check the insulin levels, you'll be elevated obviously, but because they're injecting insulin from the pharmacy, right? Their CPAP type will be normal, right? Or deep or decreased, right? So that's one thing you want to keep in mind.

And then if a person has an insulin, right? Obviously for person has an insulin, they will have like increased insulin, but they also have increased CPAP type because the insulin and dodging is coming from their own bodies, right? So again, keep in to keep in mind their insulin CPAP type will be elevated. And then you may get your usual case of a person that's, you know, trying to overdose on a sulfonial urea, right? For person is trying to overdose on a sulfonial urea, they are, because remember, sulfonial urears, right? They block that ATP dependent and potassium pump that you find in that pancreatic ability cells. So when they block those things, right? That will cause the cell to deep-olarize and then calcium will rush in and then you'll squared out a ton of insulin. So people that actually like, you know, overdose on like sulfonial urears, so like gliburite, glipidide, glimipride, or people that overdose on like the make-lidinite. Remember that like make-lidinites work essentially like the sulfonial urears, but the thing is they are a lot shorter active, right? So drugs like nataglinite and repaglinite, those can cause a similar toxic germ, right? So you know, they'll have a hypoglycemia crisis. The insulin will be elevated, but because again, those drugs are like insulin secreted dogs, like the promote the release of insulin in the body, those people CPAP type will also be elevated as well.

But the key thing you want to keep at the back of your mind is that you do a secreted dog screen, right? The secreted dog screen will be positive in a person that's, you know, like overdose on a sulfonial urea and it'll be negative in a person that has like an insulinoma, okay? So that's how you tell those different conditions apart. Now one thing I want to go ahead and say is your friends at the MBA me, they me, give you a question about a person, you know, that has like a history of diabetes, and then they were working out, and then they found down blah, blah, blah, blah. Obviously for those people where you want to go ahead and they probably have like a hypoglycemia crisis, you want to go ahead and give those people like a 50% like this dextrous solution, to raise their blood glucose levels, and then after that you just feed them, right? Because food will, you know, probably give you better elevations in your blood glucose than, than just D50, but D50 is like your first step in management. If you don't have IV access, right, then one thing you can consider doing is, give I am glucagon. I am glucagon can rapidly raise a person's blood glucose levels, right? So if a person is a type 1 diabetic, obviously if you only drop the can be used in his insulin, right? So, you know, again, for those people, you know, giving glucose is fine, right? But here's one thing you need to be careful of.

If a person has like a hypoglycemia crisis, as a result of taking a softener urea, again the initial step in management is the same, right? You know, you give 50% dextrous, but one thing you really need to be mindful of is that, you cannot send those patients home immediately, right? You need to kind of watch them for a day in the emergency room, and typically on the exams, you probably also want to go ahead and give them a trial tide, because it's kind of different, like a softener urea, like some of them have, you know, pretty long half life, so they can hang around for long, right? So the person can have like a hypoglycemia episode, and then you treat it, and you're like, oh, great, their glucose has resolved. No, you cannot just wait, right? The thing is they can have another hypoglycemia episode, because the softener urea is still working, right? So typically for those people on emergency medicine, you should of course, you're not giving those people a trial tide, right? So you give them the trial tide, that can sort of shut down any further insulin release, but again, typically you have to observe those people in the emergency room for about, you know, at least a day, you know, you can maybe, you can admit them overnight to like an observatory unit or something like that. So I think that's all I'm going to say about glucose problems, although I guess another glucose problem that you could get on your exam can be a present that's in an adrenal crisis, right?

So remember that if a person has like an adrenal crisis, they can also have hypoglycemia with that, right? But the thing is, the way you would differentiate that from a, like a diabetic, like hyperglycemia crisis is people that have like an adrenal crisis, they'll instead of being hyperglycemia, they'll be hypoglycemia, that's one. They actually tend to have hyponitremia, but these people tend to like have like hyper, like you can maybe let me backtrack here for a second, right? You can already be going to see why the NBM will want to test your ability to recognize, like they will try to trick you by giving you an adrenal crisis question, and they will look an awful lot like a DKA question, right? Because many of the electrolyte abnormalities are the same with the exception of the glucose, right? So like for example, a person that's in DKA or it has hyperglycemia, a person that is an adrenal crisis has a hypoglycemia, right? But the thing is DKA is a adrenal hyponitremia, adrenal crisis is a adrenal hyponitremia, DKA can be a adrenal, like hypokillinia or hyperglymia, adrenal crisis on your exams will always be associated with hyperglymia. But DKA is associated with a metabolic acidosis, people that are adrenal crisis also have a metabolic acidosis, right? So again, make sure you can sort of differentiate those things. So you may say, okay, define. What can trigger an adrenal crisis, right? Like many things, right?

So they can give you a question about a person, you know, that has like a long history of like some autoimmune or rheumatologic disease and they run out of their medication, right? And maybe the medication is like a steroid, right? And then they stop taking it and right, and that can precipitate our problems. Or it can be a person that it can precipitate like an acute adrenal insufficiency. Or they can give you a question about a person, you know, that, you know, maybe they take steroids for like COPD or something like that, you know, like severe COPD or like severe asthma. And let's say, you know, they have like a superimposed infection, the pleases them on their like big metabolic stress, or they get like some kind of surgery that pleases them again on their big metabolic stress. Those people can, yes, even if they are still taking their steroid dose. If you don't administer like an extra dose of steroids, like a stress dose of steroids, that can trigger an adrenal crisis. Also, they can also give you a person that has a history of like some other autoimmune disease, right? So like Hashimoto's, blah, blah, blah. So essentially tell you that, okay, this person's got other sense disease that's going on there, right? So these are all things that can cause an adrenal crisis. They can even give you like a person that has, you know, like many, like many jidis, from like my sermon in jididis, right?

And then they tell you that, oh, the person now becomes like persistently hypotensive, hyperchalemic, has a metabolic acidosis, has hyponitremia, has hypoglycemia. Then all those circumstances, you want to think about what a house, Friedrich's syndrome, right? That's another thing that can classically cause an adrenal crisis on an endemic exams, right? And again, people that have an adrenal crisis, they'll have like homogenous, vomiting, they'll have all these electrolyte abnormalities, they'll be hypotensive. And they may even have eosynophilia, they give you like a CBC on the exam, right? Remember, steroids cause an hipoptosis of eosynophiles, right? So when you have like an adrenal insufficiency, then obviously you're going to be having less the hipoptosis of eosynophiles. So the person's eosynophilic control actually kind of go up. And really the way you can, you know, I mean, typically you treat these people empirically, but if you're like trying to chase after that agnostic test, the thing is you can measure their morning like cortisol, and then you measure their ECTH at the same time as well. Obviously, if a person has like a low ECTH on a low morning cortisol, then that tells you that they likely have some kind of secondary adrenal insufficiency going on. So like some problem at the level of the anterior pituitary.

But on the flip side, right, if the person has like an elevated ECTH, and then they have like a low morning cortisol, that tells you that they have a primary adrenal insufficiency, because the lack of negative feedback is making the ECTH go up, right? And typically, these people may also have like a skin hyperpigmentation, because whenever you have high levels of ECTH, remember that ECTH comes from a compound known as a pom-si, like pro opium elano quartin, right? So it gives rise to like ECTH and MSH and like bitter endorphin, right? So the thing is, that's what's called pro opio, opio, right? Bitter endorphin is an opioid melano, that's MSH quartin, that's ECTH, right? So MSH, right? If you're making a ton of ECTH, you'll make a ton of MSH, and that MSH will stimulate the melanocytes, and you have a skin hyperpigmentation, right? So that's like the classic way this stuff presents, right? So for the most part, right? So how do you treat these people? In general, you just give them like, you give them like dextrose, right? You know, you want to fix their hypoglycemic problems, and then you give them hydrochordison, right? So the thing is, your friends at the MBME, they may try to give it like hydrochordison as an answer choice, and dexamethasone as an answer choice. In general, you know, go with hydrochordison. Hydrochordison is just better, right? Because it gives you both a glucocorticoid and mineralocorticoid activity, right?

So you give hydrochordison, but if you don't say hydrochordison, as an answer, your next best answer is dexamethasone, okay? So in general, that's how you treat an adrenal crisis. And then, another, I guess, key endocrine emergency, you want to be familiar with is like a thyroid storm, right? So a thyroid storm, right? It'll be a person that, you know, has like a history of, I don't know, like gravestisies, or like, I don't know, like, I've kind of talked about this in the first email podcast that makes it like a person that has been disease, not taking the, like, skip the medications, or a person that gets like, maybe they have like some hyperthyroid disorder, and then they get like contrast for like an imaging procedure, or a person get dexamethasone, right? And then typically, these people will present with like diarrhea, they'll present like massive taguicardia, they may have a fever, or the fever will be like out of, like, the taguicardia will be out of proportion to the fever, right? So these people are like, fibro-bavaria hats are like, sleeping away, they can have like signs and symptoms of like a high-up or heart failure, right? So those people obviously have like a white pulse pressure. I want to keep this podcast to, you know, be relatively short, so I'm not going to necessarily discuss pathophysiology there. And you know, they'll be altered, they may have like a fever.

Remember, a fever is the most common in arrhythmia in a person that has like a hyperthyroid state, right? So in general, you may say, okay, so divine, like, how do I treat this person, right? I mean, like, first thing you want to make sure that you know, I mean, typically, again, you want to treat these things empirically, but if you're chasing after a lot, right? This person's TSA will obviously be low, right? The AT-40-30 will be elevated, right? So those are kind of like the big things. The reason the AT-10 is low is because you have the negative feedback, right? And in general, if a person has like thyroid, thyroid storm, right? The first thing you do is you give per per analogue, right? Per per analogue will help with the hyperadrenergic symptoms. And again, you do actually need to follow this order that I'm prescribing here. You can just like do anything you want, right? Like, you need to start with per per analogue. You'll treat the hyperadrenergic symptoms. And per per analogue also inhibits like the 5 per amguiodeunis that converts T4 to T3, so that will help on little circumstances. And then after that, you then give P-T-U, okay? They will try to trick you into giving me thymazole. Don't give me thymazole, right? The thing is, P-T-U will inhibit the synthesis of new thyroid hormone, but the thing is, P-T-U on like thymazole also has the ability to inhibit that peripheral 5 per amguiodeunis, right?

So you don't convert T4 to T3 and the patient, you know, again, like you are preventing the production of like a very almost like high grade thyroid hormone, right? So that will help the patient on little circumstances. And then after that, after you give P-T-U, you wait for an hour, right? You need to wait for an hour. And then after that, you can go ahead and institute a legal solution. You can give legal solution. Sometimes we call it SSKI. SSKI is just like a super-statury-thed solution of potassium iodide. So you essentially take advantage of the EOD-B-SDAF phenomenon. You give those people those things, right? And that will like block the photo-production of a thyroid hormone, right? And then after that, one of the things you can give is you can give hydrochlorizone, right? So typically people that have an adrenal crisis, right? They tend to, I mean, not an adrenal crisis. Fyroid storm, right? They tend to have a adrenal insufficiency. So you know, you can help that adrenal insufficiency along by giving that. But another thing you can also, that also helps there is that hydrochlorizone also has the ability to inhibit that peripheral 5-prime DIO-D-M. So you don't convert T4 to T3. And then again, that can help with the patient symptoms. And then on the flip side, right? Like on the other end of the spectrum, we have like a mix of Dima coma, right? Mix of Dima coma again. They can give you a person that has some histro of like some other autoimmune disease.

Because remember, when you have one autoimmune disease, that places you at high risk of having another autoimmune disease, right? So they can give you a person that has a histro of like, I don't know, like a... Like VD LIGO or like Prinichosinemia or like Adesins disease. And then they tell, they give you like vitals and labs. I mean, those are these persons like profoundly bradycardic, persons quality temperature is low. So they're like hypothermic. They have like decreased deptendoryflexus. They have like periobetal adema. They have like generalized non-perione adema. And they may even be altered. If you see that, try you definitely want to think about... You definitely want to think about a mix of Dima coma, right? And the thing is, unlike the labs we had for hypothyroidism, I mean for hypothyroidism, they'll have a slightly different labs, right? So their TSA should be elevated because they have like very low levels of thyroid hormone. So they have low levels of thyroid hormone. So there's no negative feedback, right? So their TSA should be elevated. Or their T43 will be decreased, right? So when a person has a mix of Dima coma, so how would you treat these people? You want to give them like level thyroid oxygen? Basically just replace their thyroid hormone. But another thing you can also typically give these people is you also again, give them hydrochlorizone. I don't know if you have noticed in the pattern here. In general, hydrochlorizone is not a bad idea.

And a person that has a mix of Dima coma, right? So again, you give them hydrochlorizone. If they have hyponitrimia, you can give them like normal saline, right? Try to avoid giving them like half normal saline, give them like normal saline, right? And then again, you replace the thyroid hormone. For the most part, you give them like level thyroid, like T4. But if the person is like super, super sick and they're like circling the drain, you can give them T3, you can give them like lyofyronin, Liotihyronin, okay? You can give those people a lyofyronin. So in general, for the most part, you also give them fluids, right? You give them fluids and if you hypoglycemic, so the normal saline, you're giving them you need to go ahead and you know, add like D5. So just again, keep things to keep at the back of your mind. And then the last thing I think I will go ahead and talk about is just different cheating as she has syndrome from her pituitary, her papal plexi. That's just something people seem to get wrong for whatever bizarre reason on NV Me exams. So the thing is she has syndrome right away will present is, it will be a woman that just delivered a kid and she has like philia to lactate after delivery. Sometimes she may be hype and you may say, okay, what can I perceive to eat this, right? Well, the thing is I think of she and syndrome as like an ischemic stroke of the pituitary.

Because think about it right when a woman is pregnant, you know, she produces all these hormones, one of those hormones comes from somewhere, right? It comes from the term pituitary. So the entire pituitary, like when there goes like a massive hypertrophy, why a person is pregnant, right? So it's like very dependent on blood supply and also like very susceptible to like hypotension or a ton of blood loss. So those people if they like infect, like have like an ischemic injury, right? Like because like, oh, they have like birth and it's like bloody, they lose a ton of blood, then that can infect the pituitary gland, right? So those people, you know, get into trouble, right? So like they'll have like signs and symptoms of pituitary and soficiency, right? So, you know, they will not produce prolactin, so they will have problems lactating. They may have like an adrenal crisis because they're not making any CTH. They may be hypo thyroid because they're not producing a TSH, right? So those are all things that can present on exams. And another, the classic test that you can use is very unusual, but you can do like the TRH stimulation test, right? So because typically if you give a present TRH, remember, another name for TRH like thyroid dropping, releasing hormone is a prolactin, releasing factor, right? So failure of a person is prolactin to arise with TRH augmentation is essentially diagnostic of a pituitary insufficiency on NV Me exams, right?

And then the difference between shi-han syndrome and pituitary epilepsy, the person that's got pituitary epilepsy, the thing is, I think of it more as like, as against like the ischemic stroke of the pituitary that on the line shi-han syndrome, pituitary epilepsy is more of like a hemorrhagic stroke of the pituitary, right? So, I almost think of it as like a sub-rachnid hemorrhagic of the pituitary. So you, you may see okay, define how this present on an exam, right? So these people usually have like, you know, like sodium headache, you may have like visual field deficits, because the thing is these people they are bleeding into the pituitary glands, right? So, that increased pressure from the blood can compress the cavernous sinus, so they have like visual field deficits, or you can also even compress like the optic chaiazine, right? And then these people tend to have like adrenaline, insufficiency, other pituitary symptoms. So you may see okay, what can cause this? Well, the thing that can cause this is, if a person has like a preexisting like pituitary tumor, like an adenoma, for whatever reason like pituitary adenoma is bleed at like a rate like almost like fivefold more compared to other brain tumors, right? So you can get into like serious, serious, serious trouble.

So, I mean, typically you treat like the assigns and symptoms of like pituitary insufficiency, try to control the blood pressure, if you're elevated, or usually these people are like hypotensive and stuff like that. For the most part, the money, the pituitary apoplex is probably not something you should expect to see on an MBA exam. So I think I'm going to go ahead and stop here, as I do at the end of every podcast, I do offer one or one tutoring for a ton of exams, step one, step two CK, step two C, step three, pre clinical medical exams, 30-ish-elf exams. If you're a medicine resident, I tell you, for the EBI and boards, the medicine-entering exam. And then if you're, I do this thing called longitudinal tutoring, where if you're like a first-second or 30-a-metre student, I tutor you for like your block-on-shelf exams, but at the same time I tutor you for your upcoming USMLA exams. And then I do this like USMLA booster courses, it's like 10 hours for step two CK and step three, or 20 hours for step one. And again, if you're interested in that, just let me know, and I'll be happy to appoint you in the right direction. I've kind of talked about it, I'm not even in other podcasts. And then if you're a medicine resident, so like an ERAS application or a college student applying to a med school, so like an AMCAZAP, I do offer like coaching for like, you know, the application process like application aid aid aid, personal statements, mock interviews, rec letters.

Again, I've been on the admissions committee of the top two med school for a year. I've worked with tons and tons of people that have applied through the ERAS process. Most of the people I worked with have much of their first choices. So again, I've been quite successful there. And then finally, if you have like a college student buddy that needs to do it for like Gen Cam, O Cam, Physics, Bio Cam, Histology, Physiology, I'd offer tutoring for all those things. So have a wonderful rest of your day. I'll see you in the next podcast. God bless you. Thank you.

Focus on the bicarbonate level; profoundly depleted bicarb suggests acidosis regardless of glucose number.

Due to absolute insulin deficiency, preventing inhibition of gluconeogenesis and stimulating ketone body production.

Initial potassium must be greater than 3.3 mEq/L; if < 3.3, do not start insulin.

Hydrocortisone, because it provides both glucocorticoid and mineralocorticoid activity.

Visual field deficits due to increased pressure compressing the cavernous sinus.

Myxedema coma.

T1 D has absolute insulin deficiency leading to uncontrolled gluconeogenesis; T2 D typically has enough residual insulin to inhibit gluconeogenesis, thus preventing severe acidosis.

The secretagogue screen (positive).

Fluids (Normal Saline bolus), Insulin, and Electrolyte replacement.

ACTH (and consequently MSH).

Ischemic tends to affect the pituitary gland itself; hemorrhagic often causes visual field deficits due to cavernous sinus compression.

Thyroid storm.

T1 D has absolute insulin deficiency leading to uncontrolled gluconeogenesis; T2 D typically has enough residual insulin to inhibit gluconeogenesis, thus preventing severe acidosis.

The secretagogue screen (positive).

Fluids (Normal Saline bolus), Insulin, and Electrolyte replacement.

ACTH (and consequently MSH).

Ischemic tends to affect the pituitary gland itself; hemorrhagic often causes visual field deficits due to cavernous sinus compression.

Thyroid storm.