DIP Episode 395 - The Clutch Diabetes Management Podcast

Okay, well, my name is divine. This is episode 395 of the Divine Intervention Podcast. In today's podcast, I'm going to be talking about how to manage diabetes. And this is going to be targeted more towards step two and step three. This is something that many people really struggle with on exams. And you really don't have to be in one of those categories. And if you're taking the US Emily Step Two or Step Three exams, I have a 20-hour course that's going to be coming up from the 27th of this month to the 2nd of July. It's only four hours every day from 5 to 9 pm, Pacific time. And then I have a test-taking strategy course on the 24th of this month. That's a Friday from 5 to 7 30 pm, Pacific Standard Time. For the 20-hour course, we'll skip the Wednesday of that week. So meet Monday, choose Thursday, Friday and Saturday. Again, many people have taken these courses. They've done extremely well on their exams. So if you're interested, shoot me an email and I'll give you some more information. So diabetes, obviously we know that there are two kinds of diabetes. There's type one, there's type two. People that have type one diabetes, just in general, those people, they're only going to have insulin as an option. Yes, there are some anti-diabetic oral agents that you can take. But for MDME exam purposes, just think of insulin. And also, unfortunately, people that have type two diabetes at some point, the pancreas is going to burn out.

Because if you remember, all that chronic, you know, sometimes they have problems with the pancreas. They have like hyperinsulinism, the secretion, secretion, secretion. It's almost like after a while the pancreas just kind of gives up and says, you know what, that's it. I'm not dealing with this anymore. And then, this is not having problems. And then, when the pancreas burns out, those who are going to need insulin. Another group of people that you should also keep in mind and need insulin are people that have chronic pancreatitis. Literally, your pancreas is gone. You've drank a ton of alcohol. It's burnt out of your pancreas, burnt it to a crisp. So really, the only option there at that point is going to be insulin. And typically, when you're studying people on insulin, a safe place to start is 0.5 units per kilogram. So let's say a person is a 70 kilogram person, or 70 times 0.5 is 35. So you're studying on 35 units of insulin. Does there a total daily requirement of insulin? Many times, you're going to split it 50-50. 50% will be their... their basal insulin. And then, 50% will divide it into the number of meals they have in a day. And you give them, like, so let's say, for example, they eat three meals in a day. Then you give them a third of that with each meal. So let's do the math, right? So 70 kilogram, okay, let's do 80 kilogram person, or make the math a little easy.

So an 80 kilogram person, 0.5 units per kilogram, they're a total insulin requirement of 40 units per day. So those 40 units, half of that will be basal. So they'll have 20 units of basal insulin. Basal insulin is usually stuff like large in, dead amir, deadgludeck. Those are the long-actin insulin. And then, the remaining 20, let's say they have three meals a day, you split that into three. So 20 divided by three, if I'm doing my math well, is six to thirds. So they'll have, like, 6.7 units of insulin with each meal. That's really how you divide it. Really, that's also, also, like, a pretty easy way to do it in hospitals. But again, this podcast is not about management, right? It may help you in management, but that's not the goal. Okay, so use whatever I tell you at your own, at your own discretion. Okay, so that's how you're giving insulin. Now, let's talk about the anti-diabetic agents. Again, thankfully for step two, step three, you don't need to need them in the crazy amount of detail that you need it to know for step one. But, you know, there are still some key things you want to know, right? So what's the first line treatment for diabetes? Type two diabetes is going to be made for them, right? Mettforming is pretty helpful for type two diabetes. It's a great drug. It's an amazing drug, right? And the key thing you want to remember about mettforming is that it's a big one-night. That's the drug class it belongs to. It's a big one-night. It's a big one-night.

So how does it act as a big one-night? The thing is, it basically decreases hepatic gluconeogenesis. That's kind of like the big thing you want to keep in mind. Essentially, when you take mettforming, you're going to decrease hepatic gluconeogenesis. You're going to decrease hepatic gluconeogenesis. There's a very deep mechanism on this, but I've discussed that in the past in one of my older podcasts on endocrine pharmacology. So if you want to go to step one level detail, you can consult that, right? But the key thing you want to know for exams, it decreases hepatic gluconeogenesis. And there are certain situations where you should not give mettforming. If your kidneys are bad on mbn exams, no mettforming for you. If you're getting contrast because you're getting imaging, no mettforming for you. Because literally contrast can torture kidneys, right? So you don't want to give something, if a person is taking something that can damage their kidneys, like even an amino glycoside, you need to pause those people's mettforming. Remember, mettforming can cause really bad lactic acidosis. It can actually decrease your reabsorption of vitamin B12. So if they give you a question about a person that has been on chronic pankforming therapy and they develop a mega-noblastic anemia, B12 deficiency is the cause. That's something that's pretty high to keep at the back of your mind for, for example. Mettforming can actually cause weak loss. It can cause weak loss.

It really doesn't have any strong association with hypoglycemia, right? So that's something you should also keep in mind, right? Just in general, if a person is coming into the hospital many times, you pause game at forming. Especially if you're getting surgery, right? If a person is getting surgery, you probably shouldn't be putting them on mettforming. Because surgery is a pretty big metabolic stress to the body. That can cause people to have a very powerful lactic acidosis. And then, remember, the next set of diabetes drugs are your sulfonylureus. So these ones, they are potassium channel blockers, right? They block potassium channels that will depolarize the pancreatic beta-ilate cell. When it depolarizes, voltage-gated calcium channels will open. And once those voltage-gated calcium channels open, you're going to square out a lot of insulin. You're going to square out a lot of insulin, right? So your sulfonylureus, you know, they're pretty helpful from that purpose, right? But they have a lot of side effects. They can cause weak gain. They can increase your risk of hypoglycemia, right? And it's also kind of high yield to know that many of them are sulfa drops. So the person has a sulfa allergy, getting a sulfonylureus rare, maybe not the smartest idea. And there is also a series of drugs that are pretty close to the sulfonylureus, they are called the mid-litenites. They are basically like rapid-acten sulfonylureus.

They are going to be drugs like nataglinite and repaglinite. They essentially work exactly the same way as sulfonylureus, right? Now, what are some key things to keep in mind with these sulfonylureus? If your liver is not good, you should not be on these drugs. If your kidney is not good, you should not be on these drugs, right? So if you have liver problems, kidney problems, or your heart is not very good, it's not a good idea to be on these sulfonylureus. But the big ones to know liver kidney dysfunction do not be on any of these drugs. And then, another set of drugs I want to talk about are the SGLT2 inhibitors, right? So these are drugs like they are in the inflowsing, kind of like the flowsing, the repaglinite flowsing, the way these drugs work is that they inhibit the SGLT2 transporters that we find that the proximal convoluted tubule. So think about it if you inhibit those SGLT2 transporters. You're not going to be able to reabsorb glucose in your kidneys, so you're going to let go of that glucose. That's how they work as anti-diabetic agents. But you're putting all those glucose in your urine. Can you see a problem with that? You're going to be getting a lot of UT Is, a lot of yeast infections, more UT Is. You can even get a phony, a gangrene. That's like necrotizing fasciaries of the perinium as a result of these drugs. Now, one key thing that's very high you'll to know is if your kidneys don't work, don't take an SGLT2 inhibitor.

If your kidneys do not work, do not take an SGLT2 inhibitor. And it's also going to high you to know for MD&exams that the SGLT2 inhibitors definitely improve survival in heart failure. They're definitely improve survival in heart failure. They're one of those drugs that actually have the ability to improve survival in heart failure. Now, the next group of drugs I'll talk about are the TZ Ds. Those are the thiazolidine diodes. These drugs are the glitter drugs. They all end in glitters on, rosy glitters on, pio glitters on, troglitters on, and really these drugs, the key thing to know about them is that they are p-par-gamma activators. They are p-par-gamma activators. Basically, by activating p-par-gamma, it's a transcription factor. You're going to utilize, you're going to create a lot of things that can help you with glucose utilization. Now, the big thing about these drugs is they are p-par-gamma receptors in the kidneys as well. So they cause a fluid retention. They cause fluid retention. If you have a bad heart, not a good idea to get these thiazolidine diodes. So, a person has heart failure, not a good idea to get any of these drugs. And don't forget your TZ Ds also associated with weight gain. Well, your SGLT2 inhibitors actually associated with weight loss. Your SGLT2 inhibitors actually associated with weight loss. And then, if you're looking at the next major drug class, you know, they are these GLP1 agonists.

So the GLP1 agonists, they all end in tight, exenatide, Lyraglutide. Basically, these drugs stimulate insulin production and the decreased glucagon production. So, think about it, glucagon raises your blood glucose. So you want to decrease this production. Insulin lowers your blood glucose. So you want to increase this production. So your GLP1 agonists, they all help from that perspective. They're actually really good for weight loss. They are pretty good for weight loss. One of them actually is approved for weight loss. But remember, if you have any kind of medallary thyroid cancer risk, let's say you have a me and two A or two B, it should not be on these GLP1 agonists. And also, these GLP1 agonists, they can certainly increase your risk of pancreatitis. They can increase your risk of pancreatitis. So, very close causing of these GLP1 agonists are the DPP-4 inhibitors. The dipeptidyl peptidase-4 inhibitors. They all end in gliptin, right? So, seragliptin, sacsagliptin, lena-gliptin, aloe-liptin. Basically, they prevent the degradation of GLP1. So they essentially work as a GLP1 agonist. They just do it in an indirect fashion. Again, these drugs, they have very similar contraindications or side effects as the GLP1 agonist, right? So these drugs, again, they can cause pancreatitis. If you have any methanolarythyrocancer risk, it really should not be on these drugs. It really should not be on these drugs.

So, I was saying in general, if you know the stuff I've talked about, you should be in a really good shape. You should be in a really, really good shape. Really, really good shape from a diabetes management perspective. From a diabetes management perspective. And again, don't forget your sulfonial ureas. Remember the drugs that can cause hypoglycemia. So, phonial ureas and the miglidinites, right? The drugs where if you have a bad liver or a bad kidney, you shouldn't take them. I've got to be things like your sulfonial ureas, your metformin, right? Those drugs are no more than when you have a bad liver or you have a bad kidney. If you have a bad heart, don't take a phyosolidin diet. If you have a bad kidney, don't take an SGLT2 inhibitor. Remember, metformin can also cause a lactic acidosis. Again, I just want to put out this quick higher podcast. I really hope you find it to be helpful. I really, really hope you find it to be helpful. So, thank you for listening to me. Again, I do offer one, I want you to learn for all the USMLA exams. Step 1 to step 3. Preclinical exams, 30-ish-elf exams. I also help with ear-ass applications, mock interviews, personal statements, letters of recommendation. I've done these things for years. I've, you know, thankfully gotten pretty good at it. I have many people that I've worked with that I've even graduated from. Residency. I've also been on an admissions committee in the past.

And then I also offer these review courses, the 75-hour step 2 school, that's taking place in the first two weeks of July. And then I also offer the 20-hour step 2, step 3. Obviously, these classes all apply to complex level 2 and 3. And also the MBME test-taking strategies course. Okay? Also the MBME test-taking strategies course. And then I have a new website called Divine Intervention Lifelessens.com. It's a Bible-based website. I make like two podcasts a week. They're about 10 minutes long. And I talk about, I use biblical principles to describe how to solve, you know, just classic personal problems that many people face. So, if you're interested in that, just check out the website, Divine Intervention Lifelessens.com. I actually have a podcast that's associated with it. It's called the Divine Intervention Life Lessons Podcast. You can actually find it on Apple Podcasts. So, thank you for listening to me. Have a wonderful rest of your day. God bless you. Thank you.

Insulin.

Pancreatic burnout (advanced T2 DM) or chronic pancreatitis.

50% for basal insulin and 50% divided among mealtime doses.

Decreases hepatic gluconeogenesis.

Severe kidney dysfunction (CKD) or recent contrast imaging/renal insult.

Sulfonylureas; Risk of hypoglycemia.

The proximal convoluted tubule in the kidney.

Liraglutide, Exenatide (Agonists); Sitagliptin (Gliptin).

Decreases hepatic gluconeogenesis.

Thiazolidinediones (TZ Ds).

TZ Ds (Thiazolidinediones).

Metformin and SGLT2 Inhibitors.

Stimulate insulin production and decrease glucagon production.

Weight gain (and risk of sulfa allergy).

GLP-1 Agonists and DPP-4 Inhibitors.

Decreases hepatic gluconeogenesis.

Thiazolidinediones (TZ Ds).

TZ Ds (Thiazolidinediones).

Metformin and SGLT2 Inhibitors.

Stimulate insulin production and decrease glucagon production.

Weight gain (and risk of sulfa allergy).

GLP-1 Agonists and DPP-4 Inhibitors.