DIP Episode 303 - Diabetes and The USMLEs Part 3 (Final Part)

Okay, welcome. My name is Divine. This is episode 303 of the Divine Intervention Podcasts. And this podcast I'm going to be finishing up our discussion of diabetes and then we'll be done with this. This should be a relatively short one. So again we've talked about diabetes, we've talked about the different types, we've talked about different pathways, we've talked about different physiologies, we've talked about different micro associations, renal associations, fluid dynamics associations, right? Again I'll encourage you. Really listen to part one and two. Again you'll learn so much from those podcasts. Again I know the accord diabetes podcast but they discuss a lot more than diabetes, right? So one thing I just want to say though is that you should keep in mind is so let's just get right to it. So again to these just to kind of clean up what I've discussed in the first two podcasts, although they're for the most part being the information. So first thing I want to say is what is this anti-hypertensive that we try to avoid in people that have diabetes? Well I hope you're telling me better blockers, right? Better blockers they're not necessarily the best for a person that has diabetes, right? Because if you think about it, better blockers they can blunt the neurod like opinic symptoms you can get with diabetes, right? So for persons that are diabetic, right? And let's say they become hypoglycymic, right?

For many reasons you know you can be because they took a ton of insulin or they took insulin and then they worked out, right? Maybe wouldn't they should have taken a smaller dose of insulin? Or let's say it's a type 2 diabetic, right? That took a sophomore year or year, right? Or took a miglid in it, like repaglinite, not take lintite. Remember those things have a very strong association with hypoglycemia, right? So they took those things and then you notice that oh well they were exercising and then they passed out, right? That's gonna be, you know, like hypoglycemia that made them pass out, right? But again usually when a person's glucose is running low, I mean think about if you're fast for a couple of hours or you're not eating for a couple of hours, you'll be sweating, you'll be tremoloce, everything. Those are adrenergic symptoms, right? I mean those are essentially your contradictory hormones like epinephrine for example saying okay guys we got to get some footing here, right? Because remember epinephrine is one of those contradictory hormones. It works through a G-pertine comporter receptor, actually a stimulator G-pertine comporter receptor like epinephrine, right? So beta blockers, they blunch those responses, right? Because they block your ability to respond to that epinephrine. So that's why again beta blockers are not great for diabetics. And to be honest with you that's not all.

Another reason why beta blockers are not great for diabetics is because they actually, as so she thought about worsening, like beta blockers are just not great for people that have insulin-related problems, so glucose-related problems, right? They're not necessarily the best in those circumstances. And then one thing you want to keep at the back of your mind is what kind of hyponitrymia is found in people that are, that are, let's say they're going through like a diabetic emergency, but I really hope you're telling me that oh wow divine these people tend to have like a false hyponitrym in fact sometimes it's called a hyper or smaller hyponitrym, right? Hyper or smaller hyponitrym, hyper or smaller hyponitrym, right? So why is that the case? Well we know that the equation for serum or similarity is two times your sodium, right? Plus your glucose over 18 plus your B-U-N over 2.8. That's the formula. Now the thing is when a person has normal blood glucose, right? Glucose over 18. Normal glucose is you know between 90 to 100. So let's just say 90 to make the numbers work well, right? 90 divided by 18 is 5. Well two times your sodium, your sodium is usually around 135, that's like 270. So if you notice the amount being contributed on the normal blood glucose standards is very negligible, right? It's not a big deal. But let's say a person goes into a DKA or HHS and their blood glucose becomes like a thousand.

Well a thousand divided by 18 from being my math correctly is just under 96. No, come on, that's terrible. It's just under 56, right? It's just under 56, sorry about my bad math there, just under 56. That definitely becomes a big contributor at that time, right? So in that case when a person is in DK or HHS, their blood glucose goes up, right? So they are serenmost malariety if you're calculating. Again using that formula you described. You'll go up. So those people's serenmost malariety goes up and then they have high puny trimia. But is it a real high puny trimia? Not really, right? Because again remember when you have that buildup of glucose in your bloodstream, that's going to pull water out of your cells, right? And again if you remember from general chemistry in college, right? Concentration is master divided by volume. If the mass of sodium in your body is staying constant, but the volume of your bloodstream, you know, which is essentially like the solvent for the sodium is going up, then you're basically diluting that sodium, right? Sometimes people call it a dilutional high puny trimia. And again on MBM exams is actually high you to know how to do the correction, so let me just run you through an example here. So let's see a person's blood glucose is a thousand, and you're like, wow, this person's sodium is one, this person's sodium is, I don't know, like 120 according to my measurements, right? Should you freak out? No, you should not, right?

Because if I let's use a blood glucose of my of a, yeah, let's use a blood glucose of a thousand why not? Right? So, excuse me, so the way you do the math is you're basically subtract the 100 from the total blood glucose, right? So the total blood glucose is a thousand. If you subtract the 100, you're left with 900, right? 900 is literally 9 times 100, at least this is the way I do it. So 900 is literally 9 times 100, right? So it's like there's 900s in 900. So you just take that 9 and multiply by 1.6, and if I'm doing my math well, so 9 multiplied by 1.6, I know that 1.6 times 10 is 16, so if we dock 1.6 from that, that should put us right at 14.4. So that correction of 14.4, go ahead and add it to the original sodium that you measured 120. So the sodium is roughly 134.4, right? So if you're rounded down, you know, because it's less than 1.5, you get 134, right? So that's the corrected sodium, which is obviously normal, right? Now remember, when people are also in these diabetic emergencies, especially in DK, they do have hyperkalemia, right? You know, you can see their blood glucose, I mean, you see their blood potassium concentration, oh wow, you're like, wow, this is so bad, right? They have hyperkalemia, but the thing is, the total body potassium is actually low. So what actually causes that hyperkalemia? Well, again, say for example, if you're in DK, your blood is very acidic, right? If your blood is very acidic, your body will say, okay, you know what?

Let's try to put some of those hydrogen ions inside the cell, right? But again, to maintain electron neutrality, as those hydrogen ions are entering the cell, potassium will come out in reverse, right? Potassium will come out in reverse, and when potassium comes out in reverse, right? You have hyperkalemia, that's one. Second thing is, when a person is in DK or Hichichin-Hen-Hen-Hen, they're not getting any insulin effect, right? And remember that one of the jobs of insulin is that it increases the activity of the sodium potassium ETP-SPOMP. Well, if your sodium potassium ETP-SPOMP is not working, right? You're not going to be bringing sodium out of the cell, but importantly, you're not going to be putting potassium into the cell. So potassium will hang out extracellularly, right? So that will also cause hyperkalemia, right? That will also cause hyperkalemia. But that high level of potassium in their bloodstream is actually also living by osmotic diuresis. Again, high glucose in your urine, your dry water, it also draws that potassium along for the right. So this is just one of these high old things to keep in mind, right? So in general, how do we treat these diabetic emergencies, DK, Hichichin, as does it matter? What do you do? Well, your first step on an in-beam exam is always to give fluids, right? Always, always, always give fluids, right? Again, those people can be they're very volume depleted and the fluid you give them just give them normal saving, right?

Again, I know for whatever bizarre is in medicine, students tend to get very caught up in, oh, should I give lactated rangers? Should I give, which is fine? There's nothing wrong with that. But for the most part, I would say like almost like 99% of the time, the right fluid to give to people on in-beam exam is normal saving. There's, you know, weird exception to that though. If a person has just had like a large volume parasyntesis or you're like an in-stitial-reduzised patient, right? But usually it would be an in-stitial-reduzised patient in the setting of large volume parasyntesis. You know, sometimes in a large volume parasyntesis you can pull up to 10 liters of fluid from someone, definitely seeing that happen. In that case, right, if you want to maintain because those fluid shifts right, can cause, you know, profound hypotension, keeping failure and stuff like that, which you obviously don't want. So, the way you can kind of, you know, try to prevent that is you can give albuming, right? Give albuming because people that have liver disease, unless they've gone through the large volume parasyntesis, right? If you just give them straight up normal saving, these people, their liver's don't work. So guess what? They are not making protein. So the oncotic pressures are in the toilet very, very low, right?

So for these people, if you give them fluids, because there is no protein to hold it in the vascular tree, they will just literally extra vasito this fluid and they'll have more and more of a given. So if you want to actually keep the fluid in your vascular tree, they give them fluid that has protein in it. Sometimes they call this fluid colloid, but basically it's albuming. You give that, it would jack up the oncotic pressures in their bloodstream, it will keep water in the bloodstream, right? And then those people will be fine. So just something you want to keep out of your mind for, for exams. Now the thing is, so I said, if you're treating DKHHNS, right? The first thing you're going to do is you're going to give fluids. In this case, that fluid is going to be normal ceiling, right? So you're going to give normal ceiling and don't forget, right? Again, they can even give you a shock question of pressing DK or HHNS. Again, because people have profoundly volume depleted, right? These people have a kind of hypervolimic shock, right? So I'm pressing a hypervolimic shock. What's true of their preload? Well, I hope you tell me that their preload is low, right? So their preload is low. Their cardiac output is also going to be low, because there's literally like no gas in the tank. If you're not sending them to the heart, I don't know, the heart can not just conjure blood from nowhere, right? So their preload is going to be low. Their cardiac output is going to be low, right?

And to their preload is going to be low, their cardiac output is going to be low, right? And again, because there's just no gas in the tank, the aridicule pressure, which is your central venous pressure, their left-itule pressure, which is your pulmonary capillary wedge pressure, those will both be low, right? And again, because their blood pressure is really low, the body is like, okay, let's try to see if we can maintain pressures, at least proficient of the vital organs, right? So they will have an increase in the systemic muscular resistance, right? So again, basically those values for hypervolimic shock will obtain a person that has decay or or Hichichens, right? So again, you give no more saline first, right? And then the other thing you give is insulin. And again, the insulin you give is insulin regular, right? Remember, that's the only insulin that is capable of being given IV. I believe I talked about that in episode three or one, right? So there's something you keep at the back of your mind for on exams, right? And then you also need to pay attention to these people's potassium, right? So I know that people always review these complex algorithms and blah, blah, blah, blah, blah, blah, and they're like, oh no, what do I do? What do I do? How do I memorize this? Right? Especially for those taking step two, see case step three. Basically, them tissue and easy trick. Just remember the range 3.3 to 5.5. That's it. 3.3 to 5.5, right?

So if you're treating a person that's in decay or Hichichens, and say, you notice that, oh wow, their potassium is more than 5.5. Well, what are you supposed to do? You don't need to add any potassium to the fluids that they're getting. You know, those will probably have adequate amounts of potassium to kind of tidy them over. Now, if they're within the range, so if they are more than, so notice it's a range 3.3 to 5.5. If you're more than 5.5, you don't need to add potassium to the fluids. If you're between 3.3 and 5.5, you don't need to add potassium to the fluids you're giving them, right? But if the potassium is less than 3.3 at baseline, you want to give them insulin. That's not a good idea, right? In fact, if a person is being treated for decay, Hichichens, and the potassium ends up being less than 3.3, you need to go ahead and stop the insulin in fusion. Maybe like divine. Why? Well, let me explain. The reason you stop that insulin in fusion is, again, remember one of the things I said. One of the jobs of insulin is that it increases the activity of the sodium potassium ETP spawn, right? So if that pump starts working great, in a person that already has hypochylemia, you're going to be driving more and more potassium into cells. That's going to even worsen presence hypochylemia and they can die. So you obviously don't want that, right? You obviously don't want that.

So if your case is more than 5.5, you don't need to add potassium to the fluids and insulin they're getting. If the case within range 3.3 to 5.5, right? You need to add potassium to the fluid and insulin they're getting. If the case is less than 3.3, you need to stop the insulin in fusion. Keep giving them fluids. Stop the insulin in fusion. Replanage the potassium when it gets about 3.3 again. Maybe a few points above that. You can then start giving them insulin again. So it's a higher thing to know, right? And then what if they give you a question about a person that is being treated for decay, Hichichens, and the person gets an arrhythmia and dies or something. And you don't see hypochylemia as an answer. What should you go with? Especially in these people that you know they got very large amounts of insulin. What should you go with? Like again, battery me and you die. I hope you and you're asking for an electrolyte of normality. I would really hope you're thinking about hypophosphatemia, right? I really hope you're thinking about hypophosphatemia. To be honest with you, essentially the thing that killed this person is a modified form of a refidant syndrome. You'd be like, really? Well, let me explain. Refidant syndrome is something we're classically finding anorexics, right? You know, put a habit in the sodders. They've not eaten for a long time. And then you start feeding them. That's why you're supposed to feed them slowly and steadily.

If you feed them quickly, the body will be like, okay, I haven't seen food for a long time. Let's go ahead and make a ton of insulin. So that's why, because your cells, they'll be like, wow, we haven't seen food. I mean, think about it if you're fasted for like seven, eight days straight, right? You're really hungry at the end. Anything that's placed before you eat it with gusto, right? You'll grab that thing, you eat it, eat it, eat it, eat it, eat it big time, right? That's the exact same thing that happens to your cells, right? 20, not seen food for a while, right? They're like, oh, we gotta eat. And again, what is the hormone that helps your cells eat? It's literally insulin. Just think of insulin as the fast food for your body, right? It makes them take up that glucose, right? So whenever you're pressing stats, you're feeding after a long fast, there is hyperinsulinemia, your release a ton of insulin. That insulin, your release a ton of, would drive things into cells. Just think of insulin as something that drives things into cells, drives glucose into cells, drives amino acids into cells, drives potassium into cells through the sodium potassium ATP and trams phosphate into cells, right? So that phosphate can be driven into cells so hard that the person gets hypophosphatemia. You may be like divine. Why do I care about this hypophosphatemia? Well, hypophosphatemia will make it hard for ATP to be available to the heart and the person can get an arrhythmia and die.

In fact, let me tell you this, this is very high yield. The most common cause of death in patients that are undergoing refidings, that, you know, that are going through refidings syndrome is hypophosphatemia, right? Low phosphate is the most common cause of death in people that have a refidings syndrome, right? So the thing is when a person has diabetes, right? And they're in GKHHNS, they have this massive hyperglycemia, right? Both of your cells are literally not, it's like you have food in your presence, but your hands are tight, you can't touch it because you don't have insulin to help you take up that food, right? So when these people start getting insulin, right? They'll start driving, driving, driving things in your cells, right? So again, the potassium can go down precipitously, cause hypokillinia, but the phosphate can also go down precipitously and cause hypophosphatemia, right? So that's something you actually want to keep at the back of your mind. In fact, if you're managing patients that have GKHHNS, you better watch the potassium, you better watch the phosphate, right? So you don't get burned. So how do people, in, to be honest with you, right? Like, they give you a question about a person that hasn't elevated creatinine, right? And the NDKHHNS, what should you be thinking about as the cause of the elevated creatinine? I really hope you're telling me that all these people probably have like an acute kidney injury, right? So kind of prearinal EKI, right?

Why is it a prearinal EKI? Again, these people have volume down, right? So again, I would hope you're telling me that, oh, wow, they have BU into creatinine, it'll be greater than, we greater than 20, right? Again, remember, the BUN rises faster than the creatinine for many reasons, because when you're volume down, your EDH goes up, an EDH does not just help you reabsorb water. EDH also absorbs your reabsorb your rea, right? That's one thing that you don't see many resources, but it's actually true. So as your rea is being reabsorbed that an accelerated clip, right? Your BUN will rise faster than your creatinine, so your BUN into creatinine ratio will be more than 20, right? And obviously, your urine sodium will be, you know, will be low as well, because you're trying to keep as much of it as possible, right? And your fractional extrusion of sodium, again, will be less than, you know, usually 2% or thereabouts, right? And your urine or smallarity will be really high, right? Because again, you're trying to keep as much water as is humanly possible, although having a ton of glucose in your, in the lumen of your nephrons makes that a little difficult. So a few quick topics, I just want to discuss here, so how do we diagnose diabetes? Well, we actually diagnose diabetes in multiple ways, right? So one way is, if a person comes in with the classic signs of hyperglycemia, you know, polydipsia, polyurea, polyphagia, right?

They have the classic symptoms and you just measure their glucose, right? Random non-fastening glucose. If it's more than or equal to 200, right? Milligrams for this liter, they have diabetes, right? So if a person's glucose is 200, they have diabetes if they present with these signs, right? So that's one diagnostic criteria. Another classic one is fasting, right? So the fasting plasma glucose, if it is greater than or equal to 126. So again, 126, the number is included, right? So fasting, ordering by fasting means you're basically not eating for eight hours. That's how it's defined in the world of, in the world of medicine, right? And then another classic diagnostic test you can use is you can do the hemoglobin A1 C, if your hemoglobin A1 C is more than 6.5%. So more than or equal to 6.5%. So 6.5% is included. It means the person has diabetes, right? And then another thing you can also do is you can do the world glucose tolerance test, right? So the world glucose tolerance test, essentially you give the person like a 75 gram glucose load, right? Give them that 75 gram glucose load and then you check their glucose, two hours, their blood glucose two hours later. If their blood glucose is greater than or equal to 200 milligrams per desk later, they do have diabetes, right? They do have diabetes. So again, 200 the number is included.

And to be honest with you of all these, because again, this can be an immediate question of all these diagnostic whatever tests, the most sensitive one is actually the world glucose tolerance test, right? It's used in research purposes and things of that nature. And again, remember if that hemoglobin A1 C, I kind of meet this integration I believe yesterday in episode three or two, but that hemoglobin A1 C again is not going to be the best test you should you should basically not select it in a person that has like some kind of red blood cell disorder, right? Like here it's just like doses. Your cells are if your red blood cells are dynathanax and they're either clip, you may get a falsely depressed hemoglobin A1 C, right? If you're red, because remember again, hemoglobin A1 C is literally something you measure based, it's kind of like a red blood cell based measure, right? So again, if a person has like sickle cell disease or they have hair registers like doses or hair injury and empty side doses or some kind of autoimmune hemolytic anemia measuring the hemoglobin A1 C is maybe the smartest idea in the world. I mean, it certainly will not be a smart idea on an NV Me exam, right? So one thing I want to say is that to make these diagnoses of diabetes, these tests, you actually need to, you actually need to repeat them on a subsequent day, right? So basically like you can make the diagnosis of diabetes by just doing these tests to ones. No, no, no, you gotta do them twice, right?

To confirm the diagnosis of our diabetes again, because when you do a test twice, right? You're almost like increasing the sensitivity and specificity in your sense, right? Because you know, if you do it once, you may just be catching the person at the wrong end of the spectrum or just something where it is happening their lives, they are very stressed. So the accountability of hormones are really high. So because of that, their blood glucose is transiently high and stuff like that, right? So I mean, most many many med students, they are definitely stressed, I can tell you that, especially like right before much week or right before they take these, you're similarly exempt, right? So that's why you, again, you have to essentially do two measurements with the same criteria. If it bears out positive on both, then the person does have diabetes. Now one thing I want to say is that you want to keep in mind is, you know, not just diabetes, but something that previously back in the day, we used to call pre-diabetes. In fact, these days, I believe it's called like impaired glucose tolerance, right? So you do need to know the numbers that go with those, right? Especially for these different diagnostic tests I've talked about, right? So we say that the fasting plasma glucose of of greater than or equal to 126 m per deciliter means per se has diabetes.

Well, the thing is, if you're between like roughly 110 to 125 with your fasting plasma glucose, that's something called impaired glucose tolerance. The error of glucose tolerance tests, right? I said that, oh, if for diabetes, we say that, oh, you know, 75 gram glucose, low twars later, check their blood glucose. If it's greater than or equal to 200 m per deciliter, right? The person has diabetes. If you check it twars later, you notice that, oh, wow, it's between 140 and 199, right? So 190 is included, right? Then the person has impaired glucose tolerance. And then for the A1 C criteria, for persons who don't believe in A1 C is between 5.7 and 6.4%, then those people, you know, they also have impaired glucose tolerance, right? So that's something you want to keep at the back of your mind on exams, right? And then one other thing on any of the exams, they love to talk about with diabetes is they love to talk about this whole concept of gestational diabetes, right? And gestational diabetes is something I believe, you know, some of you remember me talking about, I believe it was either episode 301 or episode 302. And I believed for that, I talked about, I believe for that, I talked about human placental lactogen. It's a diabetes, a genic hormone, right? And it causes insulin resistance, right? And again, obviously that's going to be a good thing for baby because you don't want baby to starve, right? You want baby to have enough glucose to be able to feed.

So that's why human placental lactogen is released, right? But again, many people that have gestational diabetes, they actually have a glucokinism mutations. It's just one of these weird weird associations that your friends at the MBM is, they kind of expect you to know, right? So just keep that at the back of your mind if I review. If they ask for like the mechanism behind people getting gestational diabetes, if you don't see human placental lactogen as an answer, I strongly encourage you to actually pick the answer that says that they have a glucokinism mutation, right? Now one thing I want to say so that I don't forget, between DKA and HCHNS that many people screw up is this whole concept of, because I know many met schools in the country. In fact, many resources they teach that, you know, if your blood glucose is above a certain number, you're in HCHNS, if your blood glucose is less than a certain number is DKA. So like, I think some people use 400, some use 500, some people say if your blood glucose is more than 600, you're in HCHNS not DKA. I'll tell you this right now, that's an awful thing to do clinically and an awful thing to do on exams, right? On MBM is at least, I'm not talking about clinical care in this podcast, on MBM exams if a person has diabetes, right?

It doesn't, it literally doesn't matter what their glucose is, if they're in a diabetic emergency, literally doesn't matter what their glucose is, the thing that tells you the correct diagnosis on an MBM exam is what their bicarb is. If their bicarb is low, they have DKA. If their bicarb is roughly normal or normal, they have HCHNS. So a person can have a glucose of 300 and be in HCHNS on MBM exams, right? Again, look at the bicarb. If a person's glucose is 1000 and their bicarb is 10, then DKA doesn't matter what their glucose is. If a person's glucose is 250 and their bicarb is 23 or 22, those people have I in HCHNS. Just something you want to keep at the back of your mind. Again, obviously they're going to be exhibiting those symptoms of being in a diabetic crisis. Again, just stop very, very high autonofri exams, right? So let's go back to the gestational diabetes, right? So gestational diabetes, how do we screen for it? So usually screen right around 24 weeks on MBM exams, right? Usually between 24 and 28 weeks, right? And for the most part, the thing you do is you give a 50 gram and again, to be honest with you, these numbers, they are not particularly high autonofri exams.

I'll just see them for completeness sake because I know some people listen to this podcast, they kind of like details, but you know, give them, and actually many times I like to emphasize details, but again, the vast majority of the details I highlight are very high autonofri, this one particularly that I'll say is probably not high autonofri. So, so 50 grams of, you know, they get 50 grams of glucose, and then you check their glucose level an hour later, right? If your glucose level is more than 140, right? It constitutes a positive, a positive screen, right? And if the person's screen is positive, then you follow it up with like a three hour glucose measure, right? You do a three hour glucose or tolerance test, but again, that's kind of like a different thing. Again, I don't think these numbers are particularly important, so I'm just going to skip that, right? So, the thing is, why are they so strict? Because again, you know, why are people so strict and like, oh, let's diagnose a gestational diabetes? The reason you make the diagnosis early is because you can have deleterious effects on the baby, right? The thing is, many times, right, when a woman has a lot of glucose in her bloodstream, right? When she has gestational diabetes, the baby is the one that's going to, I mean, she's going to have some problems, but the baby is also going to have a lot of problems, right? First thing is first, she's going to have problems with delivery, right?

In fact, there's an increased rate of C-sections, right? Again, that can be an easy question that can throw an bien-bim exam. There's an increased rate of C-sections in infants of diabetic moms, right? Because, again, those kids are huge. Those kids are like 10 pounders, 11 pounders, right? Those kids have macrosumine. So you may be like, okay, define, why do they have macrosumine again? The thing is, one thing many people don't understand is that insulin literally is a growth factor, right? Insulin literally is a growth factor. In fact, insulin sort of acts like growth hormone. I mean, think about it, growth hormone, right? After growth hormone is released, what does it do? It increases your production of IGF1. Well, what do you think IGF1 stands for? Insulin like a growth factor one, right? Insulin like growth factor one. So the thing is insulin is a growth factor. In fact, insulin uses a tyrosine kinase, right? Insulin uses a tyrosine kinase. If a mom is thinking, insulin uses a receptor tyrosine kinase, right? Again, remember, receptor tyrosine kinase is different from a non-receptor tyrosine kinase. Although, to be honest with you, that non-receptor tyrosine kinase term is almost like a misnomer because there's an actual receptor involved. It's just not a tyrosine kinase. It's just a receptor that is associated with a tyrosine kinase. I believe that's something that you see like for prolactin. For example, but again, that's not the goal of this podcast.

I'm going to keep going. But again, the thing is, I want to establish the fact that insulin is a growth factor, right? So insulin, again, it increases fatty acid synthesis, right? It increases fatty acid synthesis. Remember, insulin increases the activity of acetylquic orboxylys. That's one. It increases the activity of fatty acid synthase, believe it or not, that's an enzyme. It increases the activity of lipoprotein lipids, right? So that you can break down the triglycerides that exist in the bloodstream, intumonase, siglyceryl and two-fri-fadi acids. You can get them into the tip of the site and then remake the triglycerate, right? So the thing is insulin increases the fat that is stored in the babies' adipose tissue. Insulin, again, like I said, it drives things into cells. It also drives amino acid into muscle, right? So the thing is insulin definitely makes the baby bigger, right? So it causes a macrosomnia, right? Insulin absolutely, absolutely causes macrosomnia, right? So the baby is big. And another thing that insulin causes, right, is respiratory distress syndrome, right? So we know that the biggest risk factor for respiratory distress syndrome when in-beaming exams is being born prematurely, right? But if you see respiratory distress syndrome in a term kid, right? In a term unit, I really, really want you to think about that unit being an infant of a diabetic mom, right? And again, what's the mechanism there?

The thing is insulin actually inhibits the synthesis of surfactant, right? So if the child has, because again, maybe like, why is this child going to have the high insulin? Well, think about it. The blood that's flowing through the placenta, if he has a ton of glucose in it, the thing that's going to happen is the child's pancreatic beta-alect cells would be like, hmm, we're seeing a lot of glucose. What's going on, right? So those pancreatic beta-alect cells, they'll undergo hyperplegia, right? And when they undergo hyperplegia, they'll start making a ton of insulin, right? So that ton of insulin in the child is going to inhibit surfactant production in said child, right? And if inhibits surfactant production in said child, then the child is going to likely have respiratory distress syndrome, right? So, classically, on in-beaming exams, respiratory distress syndrome in a term unit is something you should look for with an infant of a diabetic mom, right? And again, when that child that's born, that source of the high glucose aka mom is gone. Well, if that source of high glucose aka mom is gone, the thing that's going to happen is it's not like the child's pancreatic beta-alect cells that are previously undergoing hyperplegia or just shrink rapidly immediately or shrink immediately, no, right? They will need to undergo like a hypoplegia to go back to like their normal levels.

But again, this is something that happens at the generic level, it's not going to be done instantaneously within hours, right? So because it's not born instantaneously, the first few days after a child, an infant of a diabetic mom is born, they will have a lot of insulin, but that high glucose source is gone. So, what do you think is going to happen to this child? The child's glucose is going to tank. And when the child's glucose tanks, the unfortunate thing that's going to happen is that the child can have hypoglycemia and can have seizures as a result of that. In fact, these kids can also have hypocalcemia, right? So, if you see seizures in an infant of a diabetic mom, I want you to think about hypoglycemic seizures or hypocalcemic seizures, right? Because again, insulin drags calcium into cells, right? And insulin again, drags glucose into cells, right? So, if you see that, you want to kind of keep that at the back of your mind on exams. And if these kids that are infants of diabetic moms have like a hard defect, holosis, stomach murmur, left-leaf lor external border, I want you to think about a VSD, VSD is actually pretty common in infants of in infants of diabetic moms. So, I guess to go ahead and wrap up quick things I just want to say. Again, don't forget that people that alcoholics, they can have hypoglycemia, right? In fact, sometimes on MBME, you can ask you, what is the mechanism behind hypoglycemia in an alcoholic?

Well, again, the thing you want to keep at the back of your mind is, again, when a person has a ton of alcohol, your body is like working over time to deal with that alcohol problem, right? So, the first thing it does is that remember alcohol ethanol in this case, right? We'll undergo oxidation by alcohol dehydrogenase first to make, what does it form? It's not acetaldehyde. So, ethanol, when it's oxidized, I know it forms an aldehyde. I don't know why the aldehyde is just not coming to mind right now. It's definitely not acetaldehyde. And what happens at the end? I know at the end, you form a city cast set after acetaldehyde dehydrogen is excellent. I know the aldehyde is ethanol, but if an ethanol is an old term, it's an old school term. I happen to remember from my disease in Nigeria, a two carbon aldehyde. I have to do some quick or organic chemistry call here. Wait, I don't know why I'm confused here. So, okay. So, we know that methanol alcohol dehydrogenase will make form out of the hydro. From out of the hydro is one carbon. And then ethanol, oh, yes, it's forming a city cast. It's resumed the acetaldehyde. Okay, okay, okay. Surreble that had to think about that there for a secondary call so it came real quick there. So, okay. So, when a person consumes a ton of ethanol, alcohol, ETOH, you form a lot of acetaldehyde. acetaldehyde is formed after alcohol dehydrogenase works. And then that acetaldehyde can undergo further oxidation to acetac acid.

Again, under the action of acetaldehyde dehydrogenase. Well, if you look at this, all these things are redox reactions. So, the alcohol, the ethanol is being converted to acetaldehyde, to acetac acid. So, that means as all those oxidations are happening, redoxions are happening at the same time. The redoxions that are happening mean you're making a ton of any pH. Any pH is the byproduct of those alcohol dehydrogenase and acetaldehyde dehydrogenase reactions. So, you may be like, hmm, divine. Why is having this high levels of any pH bad? Well, the reason it's bad is that it's going to drive the reaction where you convert pyruvate to lactate. It's literally going to keep driving that reaction, because again, remember your body normally, right? You know, converts pyruvate to lactate so that you can keep that you can keep making any pH into any pH because you need that any pH to keep the glycerol, the high three-force feed dehydrogenase step of glycolysis going. So, you have high levels of any pH, right? You're literally going to keep driving the equilibrium in the direction of lactate, lactate, lactate. Again, that's actually the mechanism behind alcoholics, having like an acetaldehyde, right? That's actually how you to know for exams. But again, because of the high any pH, the effivering, the reaction where you go from pyruvate to lactate, well, think about it.

If you keep making all this lactate and you're driving it away from pyruvate, well, you're going to have like a pyruvate deficiency, right? And when you lack pyruvate, well, guess what? You're going to lack like the first agent that's used in gluconeogenesis because remember, I believe I talked about this in episode three, oh, one, that pyruvate can be converted by pyruvate caboxylistoxaloacetite. And in that oxaloacetite can be converted by phosphino pyruvate caboxykinis or PPCK to phosphino pyruvate. So basically, you're taking away raw materials for that reaction, right? So that's obviously going to cause a problem, right? So that's when you keep that at the back of your mind on exams. And again, one thing I will say is for those of you that, you know, need help with glycogen story diseases, they do have a podcast on this, right? They do have a podcast on this. And then the final thing I want to say is if you see a person that has like certain symptom clusters, especially with endocrine disease, I want you to think about this thing called autoimmune polyglondula syndrome, right? autoimmune polyglondula syndrome. There's this transcription factor is called AIRE. And one thing it does is where you're in embryology, it helps you go to the thymus to essentially present your self antigens, right? Including like your endocrine antigens. So that in the future, you don't make autoantibodies or you don't start attacking these endocrine glands slash organs, right?

So, but if that origin is mutated again, AIRE, you'll start destroying endocrine organs. And the thing is there are two types of autoimmune polyglondula syndrome where there's a type one, is a type two. The type, the one that involves diabetes is type two, right? This one actually has a little zomodominant inheritance. And again, this is the one that has those type one diabetes, genetics susceptibilities, HLADR3, HLADR4. And again, the triad here, I think of it as person has adrenaline and sufficiency, right? They have Hashimoto's and they have type one diabetes, right? So they have a general insufficiency Hashimoto's and the type one diabetes, the type one, you know, that one is actually a little zomod recessive. And this one actually there's no relationship with like HLADR3 or the A4. If I this one has no HLADR3 relationship. And again, these people though, they still have other sense disease. So other sense disease is common to both, right? But in type one, they have like primary hypopartyroidism, right? So this is actually one of those causes of primary hypopartyroidism on NBEMES. And then they also have nucleicutinous sacchandidiasis. Now, primary hypopartyroidism, I really hope you know that there are many causes on exams, right? Again, you can get it from this type one autoimmune polyglondylist syndrome. You can get it from the George syndrome, right? If you're third and fourth far angel pouches don't form, right?

You don't form a thymus, you don't form a parathyroid, right? And then another thing should also keep in mind that causes primary hypopartyroidism. In fact, the most common causes very high yield, the most common cause of primary hypopartyroidism is if you have like third surgery that doesn't work very well, right? So you devascularize the parathyroid, so you destroy the parathyroid at the same time and then by by parathyroid and then present that season after surgery. That's like a classic NBEMES exam presentation. So I think I'm officially done with this, that it is a discussion. As I do at the end of every podcast, I draw for one and one tutoring for many exams, step one, step two, see case, step three. Preclinical med school exams, 30-ish-off exams. And again, I offer you a semily courses, again, like in about two, three weeks. I am offering a step two, see case, step three combined course. It's 20 hours long over four days, five hours each day from 11 a.m. to 4 p.m. Pacific standard time each day. Very high, of course. Very comprehensive. You know, we're going to be covering P-T surgery. I am neurology, psychoby-guine, neuro. The step one material that your friends at the NBEMES really love on step two, CK. And then those changes from November 2020, bio stats, ethics, healthcare systems, professional exam, communication skills and things of that nature, right? So again, it's a very high-yield, very high-level course. People learn a ton.

Again, I've had many people take this course that have given me very good feedback. And I've also, you know, actually done pretty well on NBEMES. And then I do have a You Tube channel, Divine Intervention, USMLE podcasts and videos. So please subscribe whenever I make a video, I post it on there. And then I have this podcast, an Apple podcasts and Google podcasts on Spotify. So you're welcome to subscribe to that. And whenever I make a new podcast, you know, you'll see, come into your podcast, you know, though remember, these podcast apps only let you see the most recent one 50. Again, I literally have no control over that. I believe it's either Word Press or podcast rule, but basically you can have more than 150 most recent podcasts. If you want everything all the way from episode one to episode three, go on the website, right? It's always going to be on the website. You're going to be able to download the podcasts on the website. You're going to be able to even listen to them straight from the website. And the website is Divine Intervention podcasts with an S.com. Divine Intervention podcasts with an S.com. So the quick life lesson I just want to talk about today is the fact that there's a difference between being right and being smart, right? There were different between being right and being smart, right? There's the difference between being right and being smart.

So the thing is again, many of you listening to this podcast know that you know, amount of faith or Christian, I mean, there's a reason why it's called Divine Intervention podcasts to start. But I feel like many times people, again, okay, let me discuss this because this is actually kind of a touchy, touchy subject. The thing is, if you're doing the right thing, that's good. You should always do the right thing. Doing the right thing should all actually is your first priority every time. But one thing should also keep in mind is try to do the right thing peacefully, right? So say, for example, you know your right on something, you know it's the right thing to do. Try to get, get, if you are getting this agreement from people, try to still get your point across to them peacefully. I feel like many people these days just because they want to get their rights, right? The fight people, they do everything whatever for it, right? The thing is again, we're called to be people of peace, not people of war, right? I mean, even there is this part of the Bible that says to follow peace with all men and holiness, right? So holiness means, you know, doing God's well, doing the right thing, right? But again, look at that. He says, follow peace with all men. Again, doing the right thing is always your first priority. So there will be sometimes where you have to disagree with people because you're doing the right thing, right?

Where people say, no, because you're doing this thing, we're going to, she studies you, we're going to put you in trouble, we're going to draw these bad things to you because you're doing the right thing. In those cases, then suffer for doing the right thing. That's totally fine. That's a different discussion, right? But the thing is you can, if for example, you're trying to show someone that, you know, this is the right way to go, what you do with love, right? You do it with calmness, you do it with gentleness. Those people will most likely see that good that you're trying to do, right? Because the thing is many people in life are generally rational, right? They'll see, okay, wow, this person is very respectful about making their points known towards, right? And then when you do those things, right? You end up winning over that person. And the person probably even starts doing the right thing, right? Again, the thing is one thing many people ignore about this life is people are great copycats. If they see something good, they want to start doing it. That's just the truth, right? People are great copycats, right? So the thing is, model would behavior and model it peacefully. Don't be a person of war. I don't know, I just feel like the current generation we live in, people just really love strife. They really, really love to fight. They really, really love to make their points known, make it known and known very, very loudly, right? No, right?

The thing is you can make a solid, strong point, but you can make it peacefully, right? So do the right thing, but try as much as this humanly possible again, as this humanly possible to follow peace with all men, right? Again, it's not always going to be possible. There will be sometimes where you have to disobey people because you are doing the right thing. There's nothing wrong with that. When the Bible says that rather will be God and disobey men, there's nothing wrong with that, right? But again, many times I feel like people always seek out doing the right thing with violence, right? With strife, with war, right? They don't seek out to do those things with peace, right? You should try to do the right thing peacefully, right? You should try to do the right thing peacefully. Okay, so I'm going to go ahead and stop here. Thank you for listening to this podcast again. This concludes the diabetes discussion. Again, I can pretty much guarantee you, essentially promise you that for those of you that listen to and understand these three podcasts, episode three, one, three, two, three, three, you'll get a lot of questions right on you. Exactly. That's just the truth of life. Okay, so see you next time in episode three, four. Have a wonderful rest of your week. God bless you. Thank you.

Beta-blockers, because they blunt adrenergic symptoms (like tremor or sweating) that occur during hypoglycemia.

Normal Saline ($\text{0.9\%}$ $\text{NaCl}$).

Metabolic acidosis drives hydrogen ions ($\text{H}^+$) into cells, and potassium ($\text{K}^+$) leaves the cell to maintain electrical neutrality.

Insulin infusion, because insulin drives $\text{K}^+$ into cells via the $\text{Na}/\text{K}$-AT Pase pump, worsening hypokalemia.

Hypophosphatemia (low phosphate), which impairs ATP availability to vital organs like the heart.

Pre-renal acute kidney injury due to volume depletion.

Metabolic acidosis drives hydrogen ions ($\text{H}^+$) into cells, and potassium ($\text{K}^+$) moves out of the cell to maintain electrical neutrality.

No. Potassium supplementation is only needed when $\text{K}^+$ falls below $3.3 \text{ mEq/L}$.

1) $\text{BUN}/\text{Cr} > 20$, 2) Low urine sodium, and 3) $\text{FeNa} < 2\%$.

Phosphate ($\text{PO}_4^{3-}$). Hypophosphatemia impairs ATP generation, leading to cardiac arrhythmias.

Macrosomia (due to insulin acting as a growth factor) and Respiratory Distress Syndrome (RDS) due to high maternal glucose stimulating hyperplasias in the fetal beta-cells, leading to excessive insulin which inhibits surfactant synthesis.

The $\text{Bicarb}$ level. Low $\text{Bicarb} \rightarrow$ DKA; Normal/Normal $\text{Bicarb} \rightarrow$ HHSN. (The glucose level itself is unreliable).

Metabolic acidosis drives hydrogen ions ($\text{H}^+$) into cells, and potassium ($\text{K}^+$) moves out of the cell to maintain electrical neutrality.

No. Potassium supplementation is only needed when $\text{K}^+$ falls below $3.3 \text{ mEq/L}$.

1) $\text{BUN}/\text{Cr} > 20$, 2) Low urine sodium, and 3) $\text{FeNa} < 2\%$.

Phosphate ($\text{PO}_4^{3-}$). Hypophosphatemia impairs ATP generation, leading to cardiac arrhythmias.

Macrosomia (due to insulin acting as a growth factor) and Respiratory Distress Syndrome (RDS) due to high maternal glucose stimulating hyperplasias in the fetal beta-cells, leading to excessive insulin which inhibits surfactant synthesis.

The $\text{Bicarb}$ level. Low $\text{Bicarb} \rightarrow$ DKA; Normal/Normal $\text{Bicarb} \rightarrow$ HHSN. (The glucose level itself is unreliable).