Ever wonder why your diabetic patients shouldn’t be eating Werther’s Originals candies? Well, we’re here to break down the ins and outs of Diabetes Mellitus, how it works in the body, and what you need to know when caring for those patients!
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Good afternoon everybody. So we get like 30 seconds that people jump and make sure everybody’s here before we get started. Hi Melissa. Hi Stacy. Hi Amber. Chris, you’re going to make me miss the Carolinas man. I used to live in South Carolina but I’m in Colorado now, so I have better mountains. All right guys. Cool. Let’s talk diabetes. Hey, it depends on the types of mountains you like, right? Mary married from Atlanta. Welcome. All right, amber, was that for diabetes? Was that, was that what that was for? Yep. Okay.
So I’m going to run a really quickly, if there’s a general path though, and then when I really want to do is just answer questions, I want you guys to tell me what it is that you struggle with. What it is that we, um, can explain better for you, where we can go with it.
So biggest thing, the first thing you’ve got to understand, this is like the linchpin for diabetes rate. Cause you have to understand what insulin is. Insulin does. So if we have our cell pay, every cell has a gate for sugar. It looks exactly like, I’m just kidding. Every cell has a gate for sugar. Okay? An insulin’s job is to basically be the key that unlocks that little gate. So if I have the insulin, the gates open, and here’s all my sugar, that sugar out here and now it can actually come through the gate into the self. So out here is my bloodstream and it is my cells. I might be in my regular tissue cells or it might be blood cells, it doesn’t matter, but just think out in your bloodstream or in yourselves. Okay? So insulin’s job is to put the sugar into the cells, open that little channel to allow it in. So you have two types of diabetes, two main types. Really, there’s like seven, but the two that you really need to understand is type one which is insulin dependent and type two which tends to not be, if they’re bad enough, they can be, but type one 100% will always be insulin dependent. So what happens in type one is their gate is closed, their gate is closed, and they don’t have enough insulin, okay? They don’t have enough insulin, they have no insulin. So if I have no insulin, then where is all of my sugar? Five, no insulin. All of my sugar stays
in the blood stream, outside of the cells, it just can’t get in. The gate is closed, the gate is locked. And I don’t have a key. That’s your type one insulin. Okay. So if I don’t have any insulin, I cannot get sugar into the cell. So this is why it becomes really extreme for your type one diabetics because they can’t manage for a little while. No, they have to have their insulin. Okay, so your type two, the difference with type two is you can get that gate open, but just not as much. Right. I’ve got, I’ve got a little bit of insulin a little bit, or my gates don’t really respond to my insulin, so I have a little bit insulin. My Gate’s kind of open and so I can get some sugars into the cell, but I can’t get all of them in. And a lot of my sugar is still gonna stay outside this cell.
Okay. So this is the difference here. I have less insulin or my gate doesn’t respond, which is called resistance. I may have an insulin resistance, so I may have the insulin, but my cells aren’t responding to it. So this is your main thing. So the number one thing to think about in diabetes is what’s happening to my blood sugar in type one it cannot go in the cell without insulin. In type two some of it gets in, but the rest of it gets stuck out cause I don’t have enough insulin or my gates won’t open. Does that make sense? So what happens if this patient doesn’t get insulin? Their body has to find an alternative source
for sugar because your cells has to have sugar to function. If I don’t have glucose, I can’t function. I can’t make energy. I cannot do what I need to do if I don’t have glucose. So when you have a type one, you have no insulin. You have to find an alternative method to get glucose, uh, for the cells to use. Okay? And so what, uh, who knows what a byproduct of that processes? Here’s an alternative process your body uses. There’s a Scottie, I’ll answer that question in just a second. There’s a, our bodies going into a certain process to be able to create glucose. Yes, thank you. My brain was like networking ketones. So it’s the Krebs cycle. It’s all these other biological cycles that happen and a byproduct of that is ketones. And what’s the problem with ketones? What are ketones create? And our buddy, how are you guys?
I’m really thirsty today. No, I’m not diabetic. I just haven’t drank enough. So ketones are acids, right? They’re Quito acids and so they create this acidotic state if we’re doing this too much, if we’re doing this too much. And so that’s why it’s so important to make sure these patients get their insulin, their supplemental insulin so that this process doesn’t happen. Do type two patients go into acidosis? Typically? No. Why? Because what did I have? They’ve got some insulin. They have enough insulin to prevent this process. Just not enough to keep their sugars at a normal level. Right. Does that part make sense? Just this part? Yes. So the question that was asked is, is there a lab value to tell if the gates won’t open? So there isn’t a specific lab value that’s going to tell you what’s actually happening to yourself. Um, there’s a test that we can do on with pancreatic enzymes to see whether or not, um, the Beta cells are working.
Um, I don’t know what those tests are called that they can cause that’s how they test to determine if it’s type one diabetes or not. But most of the time we diagnosed type one diabetes by somebody who goes into DKI because we know that DKA doesn’t happen. Um, typically in type twos. So that’s what happens. You’ll get these, these young kids, eight, nine, maybe even 13, 14. Um, my baby cousin was just diagnosed at four because she went into DKA and so that’s how they were diagnosed with their type one diabetes. It’s really sad. However, the lab value we do look at to see how their body is managing their sugars overall is what there’s a lab value we can look at that tells us how well managed blood sugars are. Yeah. Good answer guys. A1C, hemoglobin a one C and that tells us their a measurement of their average blood sugars over how much time.
Yeah, 90 days. Three months. So if somebody comes to you and says, my sugars are always good and our agency’s like nine, you’re like, no. Or maybe they’re recently good but now, so three months worth of averages and your a1c will tell you that. So that’s one thing that we look at a lot is how well are they managing. Um, but typically it’s going to be a presentation that tells us type one versus type two. Um, and they’re, I know that there’s tests they can do pancreas wise, I’m not a hundred percent sure, um, what it is, but I know it’s there. So your Beta cells are your ones that secrete your insulin. So they do some tests on that. Okay. So here’s a general issue. So the one thing I do want to cover really quickly that affects the pathophysiology of diabetes or is part of this is the major, major complications. So yes, you have hyperglycemia, you have lots and lots of sugar hanging out in your bloodstream. What’s the problem with having lots and lots of sugar hazing out in your bloodstream? What’s the problem with that? What does it cause? Hyper osmolarity. You guys are so good and it has nowhere to go. So just hanging out there, right? So no energy in the cells. Hyper osmolarities the sugar’s got nowhere to go. And so here I am, I’ve got to sell and I’ve got sugar. They’re everywhere. I got sugar everywhere. And when I have hyper osmolarity in the bloodstream, lots and lots of sugars, what is going to happen to myself?
What’s going to happen to the fluid that is inside this? So yeah, because it’s trying to fix this problem. I can’t fix it by getting the sugar into the cell. Cause I already determined that this was a diabetes problem, right? So in order to fix the problem, I’m the cert shifting fluid into the bloodstream from all of my cells, from all of my tissues out of the cell. There’s other cells out here, they’re shriveling and Trican up because they’re losing all their fluid to try to fix this hyper osmolarity. You’ll see that. So the number one problem and presentation of diabetes has to do with all of the fluid coming out of the cells into the bloodstream. So what are the three classic signs of diabetes? Y’All can lift them. Just lift them. Give me a sec and then I’ll give you a hint. They all start with the same letter.
Yeah, your three P’s. Polydypsia which is thirsty to see you. I think thirst polydypsia excess. There’s poly Phasia, excess hunger and poly urea, excess urination. So let’s look, I’m, you guys know we’re super big on Patho, right? So let’s look Polly. Uh, urea is an easy one. If I pull all this fluid into my bloodstream, where’s it going? It’s going into my kidneys and then where’s it going? Right? So I’ve pulled all this fluid into my bloodstream to try to fix the sugar issue and now I’ve got a bunch of fluid goes to my kidneys, gets filtered out and I’m peeing like crazy. Right? It makes sense. The other thing is Polly a Dipsea. I’m extra thirsty and thirsty cause I don’t have enough fluid or am I thirsty? Because the fluid is not where it belongs and it’s sending signals to my brain that I need more fluid, right? Either because I’m peeing it out or because my cells are all so dehydrated, they’re like, ah, help me give me more fluid. And so you become really thirsty. Make sense? It’s that cellular dehydration, that’s a huge problem in diabetes. Okay, so that’s the second one. Third one is polyphagia. Why am I hungry? Like what? What is happening that’s making me hungry?
Yes. I mean energy. There’s no glucose in myself. My cells are for energy and this is where I just love the human body because I could have a cell down in my, like, you know, right leg that’s like, hey, I need some energy and it tells my brain to eat, which I just think is the most fascinating thing in the world. So I have no glucose in my cells. My cells are starving. They’re also super dehydrated. So I’m now starving and drinking a ton, drinking a ton, and I’m pulling all this fluid into my bloodstream so I’m peeing like crazy. Does that make sense? They’ll see that connection. I love this. One thing I love about path though y’all is just connecting the dots of what you’re seeing. So really and truly the number one treatment process for diabetes is get their blood sugar down.
It will sort everything else out that, the other thing I want you to see here is this hyper osmolarity inside the vessels can actually cause a lot of damage to the vessels themselves. And so diabetes ends up becoming a vascular problem, becomes a vascular problem. So like all the type of osmolarity at the all this sugar where it doesn’t belong and so it can be sky’s that the sugar molecule is sharp. It’s not necessarily physical damage. Some of it’s chemicals, some of it’s fluid movement, some of it is physical. It just, it’s a little bit of everything that hyper osmolarity can cause a lot of problems. So I now have this vascular problem cause I’m damaging all of these blood vessels. And so that’s why you start to see the longterm problems like uh, nephropathy and retinopathy and neuropathies, all your offices. I can’t feel my fingers.
I can’t feel my toes. My kidneys are starting to have problems. My eyes are seeing all those really tiny, tiny vessels in your body. So the things out in your fingers, the things in your eyes, they start to really, really struggle. And so that’s why you get all those problems. So then you can’t, they can’t feel their feet. They get a little wound on their foot. What, uh, why does glucose, so then they get a wound on their foot. Wound, gets infected with glucose. Have to do with that. What does glucose have to do with infection?
What likes, yeah. Bacteria likes glucose. It eats it and loves the glucose themes on it, right? So I can’t feel my feet. I get a little wound. I’ve got tons of sugar. The bacteria go nuts. Now I’ve got a raging infection that I didn’t even know was there for a week and a half and I have a vascular problems. So I’m not getting enough perfusion and I can’t heal that wound appropriately. So this is why we start to see diabetics who are uncontrolled start to have a lot of problems with their feet, a lot of problems with their feet. They get infected, they get wounds, they can’t heal them. And even wounds anywhere else are also slow heal. Um, and so you’ll see diabetics, if they’re very uncontrolled, they’d end up with amputations of one, tow, three toes, a whole foot, whole leg. Because they’re not the, this tiny, tiny vessels that they have at the end of their feet are not managing well.
So one of the most important targets of therapy for diabetes is to keep their hemoglobin a one C low. And by low, I mean low for them. So like six and a half would be ideal for a diabetic. I’m not diabetic. My [inaudible] is 4.5 that’s appropriate for somebody who’s not diabetic. Right? So for our diabetic 6.5 and under, it’s great. It makes us happy. Right? So this makes sense. You guys had to put all these pieces together. What’s happening, why it’s happening, what’s happening in the vessels, what’s happening, what’s causing the symptoms? So ask me questions. Tons of them, I will take them. Cause I think it’s so important when it comes to disease processes to get a foundation. But then to really just like explore what happens, what do you need to do, how do we treat these patients? And I want to make sure you guys get your questions answered.
And if you don’t have questions, have something to talk about that I can talk about. I always have something.
guys. Anybody wouldn’t buy these? Would they clam. Okay. Um, yeah, so [inaudible] maybe watch a video on the day in the life of a type one diabetic. Absolutely. I guarantee you can find that on, um, on Youtube. So let me, I’m gonna just gonna drop a link really fast to the diabetes lesson. Um, and in that module there’s a lesson on diabetes, on management, on DKA, and on HHS. Okay. So questions about insulin therapy. So different types of insulin therapy. It depends on the patient. Um, all type one diabetics will be on some sort of a regular acting insulin. So regular acting insulin like a Novolog that they will take when they eat. Because normally in our bodies, when we eat our sh our insulin, our sugar goes up, our insulin goes up to bring our sugar down and then we normalize, right? So they don’t have that.
So when they eat, they need to take that regular insulin, that regular acting short acting typically not the rapid, but the short, um, regular insulin. And they’ll take that to manage when they eat. A lot of them will also take a longer acting insulin because again, we’re trying to mimic the body and what the body will do is actually give us a basal insulin, uh, level, uh, basles, um, secretion of insulin. And so that will help kind of maintain us over time. So they will also tend to take, you know, 10, 15, 20, maybe even 30 units, are they long acting insulin like lantus that they’ll take once a day to give them that Bazell rate and then they’ll take their regular insulin with their food. Um, so yeah.
I’m just looking to see if there’s other questions diagnosed with type two because yeah. So, um,
I think it was, was it Mary, I don’t wanna get your name wrong cause you don’t use an m originally diagnosed to take to your 10 years later diagnosed with latent autoimmune disease. Uh, latent autoimmune diabetes of adults. Yes. Which is a thing, this is why I said diabetes. There’s like seven types now, but the main two that you need to kind of understand. Um, so a lot of people are diagnosed with type two because they still produce insulin, but later they stopped producing insulin. So they call it type one and a half cause it starts like type two and ends up as type one. Absolutely. And that’s why I said type one is always insulin dependent. Um, those who are type two, if they progress, could become insulin dependent. Um, and so that’s where, that’s where you just have to, it’s best if you just understand what’s happening in their body. So if you discover that they are no longer producing any insulin, then they’re going to be treated more like a type one.
So Scotty’s question is can meds like invokana increased clearance of other meds as it makes you pee more? So, I don’t know specifically the answer for Invokana, but I will tell you that most medications that cause urination are not necessarily messing with, uh, clearance of medications. Um, unless those medications are renally cleared. But even then they’re usually messing with water movement or sodium movement. Um, again, I don’t know specifically about that drug so I won’t answer to that. But if the medication, like for example, a loop diuretic for example, um, it would just pull out more water, it wouldn’t mess with the actual drug clearance. Most drugs are metabolized through the liver and so then their actual function doesn’t necessarily get changed if you increase their clearance. Um, they might just need a little bit more frequent dosing or something like that, but I don’t have as much knowledge when it comes to clearance and things like that. That is a great question for a pharmacist and I guarantee you any pharmacist would love to answer that for you because they know a lot more about that. Amber, can you clarify your question for me? Help?
So insulin guys, there is um, there is a whole lesson in pharmacology course on insulin and the different types and the timings. There’s teachings in there. So definitely jump in there. Oh, I answered already. Okay, great. I’m going to try and go grab that. I’m teaching for you or that lesson.
Pharmacology. What other questions can I answer? Do you guys understand the difference between DKA and h? H M s or h? H. N. K? Anybody need a quick explanation of it? Because that’s a big thing when it comes to diabetes. Kind of understanding that, okay, so here’s that insulin lesson I was telling you about in pharmacology. So you can grab it if you want. So remember we talked about type one diabetics. They have no insulin, right? So they have to find a work around, okay. So they start finding a workaround. They start producing Quito acids and they get in this acidotic state. So in DKA, diabetic Ketoacidosis, they’re typically type one diabetics. They’re now in a ketoacidosis and their blood sugars are super high. They’re in a hyper glycaemic hyperosmolar state. Just like HHS differences, one has acidosis and one doesn’t. So then the big difference that you’ll see is the sugar levels that they’ll try to teach you.
You know, if it’s less than 600 it doesn’t matter what the exact number is. But understand that type one diabetics will tend to start showing problems and symptoms at a much lower blood sugar, 400500600 which is still really high, to be honest. It’s still really high. So 400500600 you’ll see, you’ll start to see problems with your type one diabetics and your DKA, partially because they literally have no insulin, they have no compensatory mechanism, they have no way to get energy, and now they’re in acidosis. And so now they’re sick for other reasons. They’re sick because they’re an acidosis, right? They’re vomiting, they feel awful. They’ve got fruity ketone breath, you’ve got ketones in their urine. Um, they’re possibly even confused because of all of it. Right? So because remember that cellular dehydration, if my brain cells get dehydrated, can I think straight? Nope. Right? So remember the sugars tend to be a little bit lower in DKA because they don’t have any reserve.
Okay. The big difference between decay and HMS is purely that they don’t develop ketoacidosis. There’s still hyperglycemic, they’re still hyperosmolar. So they still have severe cellular dehydration. They’re still pulling a ton of water out of the cells. Right. And they, um, but they don’t end up in ketoacidosis because they have some functioning insulin and because they have some functioning insulin, their sugars will actually get a lot higher before they start to show symptoms. So before they start to show symptoms, their sugars are in the nine hundreds, 1,011. I’ve seen a 1400 before, which is just crazy insane because they’re compensating there. They’re getting some glucose. So they’re getting some energy. They might not be as confused cause their brain is stealing whatever glucose they have. Right. The, you said brain consumes 20% of buddy water. I think he made glucose. I’m pretty sure it’s glucose actually. It might even be, I might be 80% of the glucose. So in HHS their sugars get a lot higher because they’re compensating. They have the ability to get some energy. Um,
Marisa, she had DKA twice but didn’t display any symptoms. That’s amazing. That’s amazing that your body didn’t display symptoms. I wonder if you had them but just didn’t feel or didn’t recognize them. But that’s, I’m glad that you’re okay. So, um, the question is treatment differences. Okay. And this is something that we’ve talked about a lot. Um, I think we even had a little, a whole discussion about it on our, on our Facebook forum and that’s great cause I want you guys critically thinking about this stuff in both cases. If you’re talking, what’s the first thing I do right? I’ve checked their sugar. I know this is what’s happening. The first thing I do, you’re going to start fluids. Why? Because typically fluids are easy access. They are uh, on the unit. It takes you two minutes to do. If that you, you, you get a line and you get him fluids going, right?
That’s typically the first thing you do. Um, just timeline wise because taking an insulin drip from pharmacy takes like 20 minutes. Trust me, it does. So first thing you do is start fluids. You’ve got to start managing a southerner, dehydration. You can and often do use insulin with HMS. I will tell you, I had a patient with an 1100 sugar that I got down to 300 or less with four liters of fluid and no insulin. So it is possible because they have their own insulin. We just need to compensate and kind of fix the, the major problem that’s happening, which is their cellular dehydration issues, their hyperosmolarity issues. So it’s possible to manage h, h and s without a drip or with just one dose of insulin. Um, so it’s not necessarily about circulation, it’s actually just about fixing the hyper osmolarity. So the question was do we put fluids in so the insulin can circulate?
It’s really about fixing that hyper osmolarity cause that’s what’s causing their symptoms. So we’re kind of diluting out the blood, um, and diluting that blood sugar and giving out a chance to kind of disperse and, uh, let the insulin, I do have work. Like I said, usually we’ll give them some, they might get 10 units, IB or they might get, um, some sub Q. But a lot of times we don’t put them on drips because they have some insulin that their body can use. However, do patients who go into DKA, who are type one diabetics have any insulin at all? No. So if I don’t give them insulin, they will not get better. If I could give them 30 liters of fluids and they’ll still die because we’re not fixing the problem. Okay. So I think in our lesson we talk about the priority treatment for, for DKA is insulin.
And that doesn’t necessarily mean it’s the first thing you do. Like I said, typically the first thing you do is start fluids because you can, and it’s, it’s quick and it’s easy and it’s, it’s, uh, it’ll fix some of their symptoms right away, but it doesn’t fix the problem in DKA. Okay. So we have to give them insulin. You have to give them insulin to start moving the sugars and to start, um, reversing the ketoacidosis. So fun fact, and this is just take this with you, ask the question. You do have to have, uh, orders. Um, sorry. Speaking of orders, amber said, can you get fluids related to standing orders? So typically if you’re in the Er, you might have a standing order, but most of the time you’re not going to have preexisting standing orders for fluids. You’re still going to have to have orders for that.
Um, so the question is for an NCLEX purposes, fluids or insulin. So typically if it says what’s your priority action or what’s your first thing to do, it’s going to be fluid cause it’s going to be the first thing that you do. Yeah. So we end up with a patient, they’re in acidosis and they have an anime gap, right? Because it’s all these extra assets. It’s not just the electrolytes, it’s extras. I don’t stop giving insulin until they’re no longer an acidosis until that Anna and gap is closed until they’re no longer struggling with the acidosis part of it. So that means I might get their sugars down to like one 80 and then I start them on a [inaudible] drip so I can keep giving them insulin so that I don’t bottom them out because you have to give them insulin until we reverse the whole process. Yeah. So Scotty, the question is, if you have a patient that you know is in DKA, haven’t you already gotten the sugar?
You can’t know their MDK without getting a sugar. Right. So it absolutely will depend on what’s in your question. Um, if the, if the question, so here’s an example. If the question says you have a patient with a history of type one diabetes who comes in reporting excessive, there’s nausea, vomiting, and has fruity breath, what’s your first action? Okay, well then it stuck a Sur, right? Cause you don’t have a sugary yet, right? You don’t have a sugar yet. Um, so, so absolutely getting a sugar on that person is important. I’m drawing labs probably because that finger sticks going to show you high, high probably. Um, but yes, absolutely. If you actually already know, you know the sugar, you know what’s going on, you know what the issue is and the action is, and then it’s what do you do next then fluids tends to be, so it might be insert two large bore ids, right? Cause you can’t do fluids until you do that. So just think timeline. Think realistically of like what’s really happening. Um, if the, if one of your options is insert two ards varieties versus uh, give a leader of normal Zaillian where you can’t give a leader until you’d have IBS. Right? So just think logically with that kind of stuff.
Yes. So Christopher asked, so you would give d five after the insulin has worked until the acidosis is under control? Yes. So we literally will start doing this where their insulin level, like their drip rate is really high and they’re just getting regular almost daily. Then he’ll start a sugar jet and we’ll start doing this and we’ll find a balance where we give it. We’re now, we’re giving them two units, an hour of insulin and 50 milliliters an hour of deep half on us. So we’re just keeping it balancing sugar. Yes. So we, we kind of step everything down and we kind of get them to a nice balance while we wait for the acidosis to completely clear. Yup. Great question. So can I ask what about low potassium? So why are we concerned with low potassium or potassium at all in DKA? What, how is potassium effected by this Diabetic Ketoacidosis?
So yeah, we’re always concerned about the heart if there’s a potassium problem. But why is this DKA causing a potassium problem? So when they come in with DKA, so here’s the better question. When they come in with DKA, they’ve just arrived. You’ve done nothing for them. Where’s their potassium typically? Higher load. Yeah. It’s actually usually high acidosis. Hyperkalemia always acidosis. Hyperkalemia. Remember that? So do we immediately start giving them kayexalate and all these things to get rid of their potassium? No. Why? Because what are we about to give them
fluids and insulin. And what does insulin do to potassium? What does insulin do to cassium? It lowers it because it shoves it into the cells. Same Way it shoves glucose into the cells. Insulin shoves potassium into the cells. And so I, when I have a DKA patient, I’m not worried about a high potassium until I start their insulin drip and then I watch it. So the question was what about low potassium in DKA? And the low potassium happens after you’ve given them a bunch of insulin and now their, their potassium is now three because you’ve gotten rid of all their potassium. Right? So, um, one of the major things we do when we’re treating DKA, as we watch that potassium and a lot of times we’ll actually replace, we’ll replace their potassium or maybe we’ll even put some potassium into their IB fluids so that they’re just kinda keeping that normal level and keep it where we want it to be. Yeah, it happens to pretty much every DKA patient. Mary, it’s one thing I love. This is going to sound really bad. Uh, I love DK patients because they’re predictable. Uh, and their treatment is predictable and you know exactly what to do. Fluids, watch your potassium, give them insulin, check their acidosis, give them some anti-nausea meds. It sounds like you didn’t have any symptoms, which is awesome for you. But anti-nausea is a big thing. They’re going to be vomiting with the acidosis.
Yeah. Yup. So blood gases, absolutely. That’s how we’re going to know that they are acidotic. We can also, we, a lot of times we’ll check, like I said, the anti on gap. Do you guys know what the Antionne gap is?
Okay. So the anti on gap and ion gap is you take your cat ions, which is your positive ones. So this is like sodium and you subtract your anti ions, which is your negative ones. So you subtract chloride, you subtract your bicarb and I feel like I’m missing one. Oh, mag is over here, calcium is over here. If you take all your positive ones and you subtract your negative ones and you want it to be, I want to say, no, call me on this. I want to say it’s like less than 12 is normal. Something low, lower is normal. These numbers, when you add up all the negative ones and add up, all the positive ones should be relatively close together. So then what happens is we, if we have extra acids in our body because it shoves this potassium way up, we start to see this number go way, way up.
So you could see an anion gap of like 40, um, 26 30. I’ve seen pretty high because it’s all these extra acids that are in our system. So anytime you have a high end iron gap high and I n gap equals acids. Okay. So we watched their anti on gap cause it’s way easier to get than a blood gas cause it’s just in a regular chemistry. It’s just calculated. Um, and so we watched their Anna and gaps. So as they get better, as their acidosis gets better, that Anna gap closes is what we call the gap closes and it gets lower and lower and lower. Um, to where these numbers, your positive numbers and your negative numbers added together are closer together. So close the gap. So you can do a blood gas. You absolutely will do a blood gas at the beginning cause you need to see how acidotic they are.
You will monitor that periodically. But it’s way easier and way faster to monitor your Ana and gap cause you can get it at the same time you get your glucose because it’s all on the chemistry. That makes sense. Yes. So I said having ABGs taken hurts. Absolutely. That’s why I say I like using the anti gap cause I don’t have to poke them for blood gas. So you use this [inaudible] right here in their artery, in their radial artery. And that’s where you get that abds and it’s painful. Don’t ever tell a patient this is not going to hurt. Tell them this is probably gonna hurt, but I’ll be quick. Um, potassium can burn, especially in a peripheral id. So make sure you diluted if you need to. For sure. So finger sticks. We do finger sticks once the sugar’s low enough. So remember your glucometer is only going to go up to maybe 400, four 50. Right. So sometimes I’ll still do a finger stick, but if I know they’re still 800 um, I’m just going to send off a chemistry. I’m going to send off a BMP, get a glucose level tech, my ana and gap because otherwise it’s just going to say hi. Which I knew.
No, no, no. It’s a blood draw. So the question was did is, does the Anti n d gap come with a finger prick or blood draw? It’s on the basic metabolic panel. The chemistry. So yeah, it’s a blood job. Sorry. Good question. Yup. BMP. Y’All are good questions. We’re, we’re way over here. You realize the time it was. What other questions? Any other questions I can answer for you guys real fast about diabetes or how we manage it? How we assess it?
I’m going to drop this link in here one more time for the diabetes lesson for you. Okay. So if you haven’t gone to it, you can go to it.
All right. You guys said Austin Yod. Great questions. So d I Alexander DII Diabetes insipidus is totally separate from diabetes Mellitus. It’s completely separate. Completely different. They, the only reason they have a similar name is because of the amount of [inaudible] that happens. So if you check out, I want to say it’s an hour metabolic endocrine course. So Med surge medical, like endocrine, there’s a lesson on diabetes insipidus for you. Yeah, totally different. Um,
All right. As you guys know, anybody who’s been in tutoring with us before, here is the survey for you to fill out and let us know how we’re doing. So amber, the opposite of DUI is s I a d h or a syndrome of inappropriate antidiuretic hormone. So those are, those are upsets. Good question. Yes. Those two, they’re, they’re all related to pituitary hormones. So they’re the only reason they called it diabetes insipidus when they discovered it was because of all the pm. So they rec, they compared them. Yeah. I’m the only one who gives the survey. Oh, I’m telling no, I’m just kidding. But seriously, please fill it out because it helps us get better. It helps us get better. It helps us make sure you guys are getting what you need. I did John. Forget tans forgets it’s chances. This is Chance’s baby. Bless his heart. All right guys, we all know, I love hanging out with you. I’m back sometime next week with another tutoring session of some sort, so just fill out the form. Let us know what kind of things you want to hear and what we can do to get better. All right? Love y’all. Have a great day. Go and be your best belts and as always, happy nursing.