Cram The Pance - S1E2 Diabetes cram session!

Episode Date: January 2, 2021

Going over type 1 diabetes, type 2 diabetes, type 1 and type 2 diabetes medications, DKA, HHS, Somogyi phenomenon, Dawn phenomenon. All you need to know for your PANCE, EOR and exams in 20 minutes!►Paypal Donation Link: https://bit.ly/3dxmTql--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

All right. So this podcast, we're going to be doing focusing on endocrine. And I'm going to be focusing on diabetes, the meds, the diseases and certain things that I think you need to know for your boards, your EORs and for your exams in school. Again, I'm focusing on the important things. I think you need to know the high yield and going off the NCCPA blueprint. So let's start with type 1 diabetes. You need to know that this is beta cell destruction. Pancreas is no longer making insulin. And it's going to be most common in children and young adults, normally under 30 years of old, 30 years of age. Doesn't always have. to be though. As far as etiology, there's a couple of different types. There's type 1A. This is by far your most common. This is going to be autoimmune. You're going to see positive Gat antibodies, is isle antibodies. But again, this is the one you need to focus on because this is the most common. There's also type 1B, non-autoimmune, idiopathic, stronger hereditary component, but not very common. And I would not focus on that one. Type 1A is your most common. The patient is going to be presenting almost always with polyurea, polydipsypcia, polyphagia. the patient is going to have this excessive hunger in eating because they have all this glucose in the body, but none of it is getting into the cell.

So the body thinks it's pretty much starving. So they're going to be eating a lot. They're going to be peeing a lot. They're going to be drinking a lot. They're going to be dehydrated. They may even present with DCA. As far as diagnosing, you need one of these to diagnose diabetes. And this is the same with type one or type two. So you need either a fasting plasma glucose of 126 or higher on two separate occasions. You can also have a two-hour glucose tolerance test of 200 or higher. an A1C of 6.5% or higher, or a random blood glucose of 200 or higher in a symptomatic patient. So they're 200 or higher and they're peeing a lot, they're drinking a lot, losing weight, whatever it is. You need to have those symptoms along with the 200 or higher.

So one of those to diagnose treatment for type 1 diabetes is going to be insulin. Don't go crazy on this. They're not. I really don't think they're going to test you on all the different types. Remember the fast acting is LISPRO, ASPART, takes 5 to 15 minutes to start acting. intermediate is NPH, not used as often. And then your long acting is going to be either detamere, glargine, deglodec. Those are all your 24 out, 12 to 24 hour insulins.

Don't go crazy on those, though. Just know that type 1 diabetics need insulin. They can't be using any of the oral medications. So a couple other things I think are important to know. There's something called the Samogiai phenomenon. This is going to be a patient that has low blood sugar overnight that's followed by rebound high blood sugar. So nocturnal hypoglycemia, followed by rebound hyperglycemia. So low blood sugar is overnight. In the morning, they spike up because the body has been releasing all of these hormones, cortisol, growth hormones that kind of counteract this low blood sugar they had overnight. So then when they wake up in the morning, they eat something. They give insulin. Their blood sugar goes crazy high because of all of this insulin resistance they have from all of these different hormones that were released from the low blood sugar. Dawn phenomenon is similar, but their overnight blood sugar is normal. And then they have these surge in hormones around 2 a.m. to 8 a.m. And this is in a lot of diabetes.

patients. And again, that surge of hormones in the morning hours is going to cause its insulin resistance. And you're going to have some high blood sugars in the morning because of that. Just know the basics on those. I wouldn't go too crazy. A way to remember them is somogiae is you can remember that as so moch insulin with M-O-C, S-O-M-O-O-M-T insulin because you're going low. Don, remember down insulin instead of dawn. Think of down insulin. All right. So type two diabetes. This is the one you need to focus on. This is going to be insulin resistance and impaired insulin secretion. As far as the risk, by far the biggest one, the one you need to know and the one I think everybody knows is going to be patients most likely going to be obese or overweight.

90% of type 2 diabetics are overweight. Genetic and environmental factors also play a, you know, a role here. And type 2 diabetes has a much higher genetic component than type 1. So much in fact that I know my endocrinology practice and a lot of other ones. If you don't have anybody else in the family, if you're type 2 diabetic and nobody else has it, a lot of times we'll invest other causes like chemochromatosis, Cushings, because it is so commonly, you know, passed down. As far as a patient, they're going to present the same way as a type 1 diabetic, sometimes a little bit further on because they can have it longer. It's a much more insidious onset. So they might have polyurea, polydipsy, polyphasia, but they might also have some

wounds that aren't healing. They may have infections that aren't resolving UTIs, yeast, infections, things like that may be seen. As far as treatment, you're always going to start with lifestyle changes unless this person comes in with like a 12A1C and they're just completely out of control. But most patients, you'll start with lifestyle, diet exercise. If that doesn't work, you need to remember your first line is always going to be metformin. Always start with metformin unless they have some contraindication like a, you know, renal failure or something like that. But start with lifestyle and then after that metformant and then you can go to anything else you want because they can't really ask you, well, what are you going to go to after metformin?

that's not going to be a question because it's not fair and it's not how it works. So first line lifestyle, then the first line medication, first line pharmacological agent is going to be metformin almost always. And then you can focus on your other agents, your TZDs, your GLP ones and things like that. I'll go over the meds towards the end of the podcast. So next I'm going to go to diabetic ketoacidosis. Most common in type 1 diabetics, you're not going to see in type 2s very often at all because in type 2 you still have some insulin left in most patients.

And that insulin prevents, um, this actual, the ketoacidosis in the body, the insulin enables them to still be able to have the energy from the glucose, get it into the cells and prevent this breakdown of fats and things like that. So most common in type 1 diabetics, it's almost always who you'll see it in. It's a consequence of insulin deficiency and counterregulatory hormones. As far as the causes, you need to remember the five eyes, five eyes for the causes of diabetic ketoacidosis. Infection is your first eye and by far your most common. So think of a patient coming in with a UTI, pneumonia causing this. The next eye is is eczemia like a CVA or a TIA. Infarkin, think of a patient coming in with an MI.

Ignorance is another one in another eye and that's somebody just, you know, not being compliant with their medication. They're not taking their insulin for a number of days. And then also intoxication. A patient may be, you know, drink too much alcohol and they're having these really crazy out of control blood sugars. Another eye, too, to add on a sixth eye, and sometimes I use it in place of intoxication because it isn't as common, but infant, that's because the patient's pregnant, which may be bringing this on. But remember those first five eyes.

Those are the important ones. If you don't remember any of them, you only want to remember one, just remember infection, because that's a huge one. And then it's just basically a general stress in the body, something that's going on. The patient is going to present with the knowledge of vomiting, polyurea, polydipcia, abdominal pain, as far as on the physical exam, a big thing you should remember is that fruity acetone breath. Acetone is one of the primary ketones of the body actually generates in DCA, and that's why you have that smell on their breath.

There's this acetone smell. They're going to have kusmal or they may have kusmal respirations. Remember, they're in metabolic acidosis. So the lungs are trying to compensate. The body's trying to blow off all that excess CO2. So they may be having kusmal respirations. It could be tagacartic, takipnic. Again, they're dehydrated and their body's going through this stress. So you may see that as well.

As far as diagnosing, blood glucose is normally over 250. It's not extremely high like we'll see later in HHS, but it is normally pretty high above 250. Their pH, their arterial pH, this is very important. It's going to be less than 7.30. Their bicarb is also going to be low because remember again, this is a metabolic acidosis. Remember Rome, respiratory opposite, metabolic exact. both the pH and the bicarb are going down exact. So metabolic acidosis, less than 7.30 bicarb less than 22. And this is a high-an-gap, high-an-gap metabolic acidosis. It's one of the mud piles, if you've learned that.

And then you're also going to see positive ketones in the urine. One of the things to remember, like I said, it's a high-an-gap. When you're actually treating this patient in the real world in the ER, you want to focus, not so much on getting the blood sugar down, but you want to focus on closing that gap. The treatment isn't completed until you close that gap. And that should be your primary treatment focus. As far as treating these patients, the way you'll remember this, remember this patient's really dehydrated. They're really thirsty. So remember sips, Sips, like they're taking sips of water because they're thirsty because they're dehydrated. So sips. What that stands for

is saline S, insulin, I, potassium, P, and S search for underlying cause. I don't want to go too crazy into each one of these, but I want to make little notes because these are important. The saline is going to be isotonic at first, but then once their blood glucose drops less than 250, you don't want them going low, so you're going to add dextro. So you add D5. As far as the insulin, you're only going to give them regular insulin. You're not going to give them the long acting because it's going to take forever. That would not be very smart. So regular insulin. The only time you're not going to give insulin is if their potassium is less than 3.3 because remember, what does insulin do? Insulin is used in hyperkalemia because it drives potassium into the cell.

So if their potassium is less than 3.3, you give them insulin, that's not going to be so good. They're going to become hypokalemic. You're going to have a lot of problems. So give them regular insulin unless their potassium is less than 3.3. And then once their potassium goes above 3.3, start giving them insulin. As far as potassium, it doesn't really matter what their potassium levels are. They're almost always going to be potassium deficient. It's just part of this, part of DCA.

So you're going to give them potassium unless their potassium is above 5.3, then you don't want them to become hypercalimic. But you normally will give potassium unless it's above 5.3. Let's move on to hyperosmolar, hyperglycemic state, HHS. This is going to be most common in type 2 diabetics, has a much higher mortality rate. The etiologies are pretty much the same as in DCA, infection, MVA, CBA. as far as the patho behind this, they're going to have some sort of illness where they're not drinking enough fluids, they're not keeping hydrated, and they're going to become severely dehydrated. Again, you're not normally going to see this with ketosis because the patient has insulin

in the body. They need to be completely absent of insulin to actually get to DCA. So that's important to remember. The patient is going to present similar to the way they did in DCA, so I don't want to drag that out. But a lot of times these patients, because they're so sick, they might. might have some altered mental status and things like that. And remember, their blood sugar is going to be much higher than a DCA. Normally, it's going to be over 600. So as far as diagnosing blood sugar is going to be above 600 in a lot of cases, they're going to have an increased osmilarity.

That's going to be above 3.20. And they're going to have an absence of acidosis. So their, their pH will probably be normal above 7.30 in most cases. Treatment, again, remember, sips, saline, insulin, potassium, search for underlying cause. And I don't think I mentioned that earlier, but obviously something's causing DKA and HHS, so you need to search for whatever that underlying cause is and treat that as well. So remember HHS, most common type 2 diabetics, blood sugar is going to be really high, but their pH is actually going to be normal. They're normally not going to be acedotic. So moving on, I wanted to also focus on the type 2 diabetes medications because these are important to know. We'll start with your first line medication, your metformin, which falls under the class of bigwinides.

It works by lowering the glucose from the liver and inhibits gluconeogenesis. So when you're fasting, your liver pumps out all this sugar to give you some form of energy since you don't have food in your body. This actually slows that down and it inhibits gluconeogenesis. So your fasting blood sugar will lower because you're not getting all this excess glucose from the liver. It's usually your first line med. Why?

Because it's been around so long. It's been around since the 1950s. It doesn't cause low blood sugar. It's weight neutral so you don't gain weight on it. It decreases your A1C pretty significantly by about 1.5%. And it can even decrease your cardiovascular risk. And it's dirt cheap because it's been around so long. So it's really just a great first line med.

It's cheap. It works well. It doesn't make you gain weight. It doesn't cause low blood sugars. So that's why it's your first line med. As far as your adverse drug reactions, the most common by far is going to be GI. Diarrhea. I see this in so many of my patients.

We can kind of counteract this or combat it by using the extended reliance. least and things like that. But remember, metformin diarrhea. That's your biggest one. The other really big one, too, is lactic acidosis. And that's why we don't give it in patients who have a GFR. Depending on if you're first starting them, if their GFR is less than 45, you won't start it. If you've already started treatment, once it hits 30, you'll discontinue it. So lactic acidosis, like I said, is a big one with metformin. And why does this happen? Metformin actually inhibits, like I stated before, gluconeogenesis from the liver. and it does that by blocking pyruvate carboxylase. And a deficiency in pyruvate carboxylase actually inhibits the ability to clean up lactic

acidosis in the body or lactic acid in the body and allows a buildup. So just remember, I went too far with that. It shouldn't have given you all that extra stuff. But remember, metformin can actually cause lactic acidosis and something you need to look out for. And that's something you need to actually think about when you're giving the patient iodinated contrast, like in CAT scan, because CAT scan can, and, reduce an acute kidney injury and can lead to lactic acidosis if they're taking metformin.

So remember, if they're having a CAT scan, they're giving iodineate contrast, you need to stop the metformin about 48 hours beforehand. Another thing, too, that you might see that they might test you on is vitamin B12 deficiency, which metformin can cause. Normally, it's only on patients who have been taking it a long time, normally over 10 years. As far as the contraindications, remember renal impairment is really important, less than 45. You shouldn't start them if they're already on it. You want to stop them once they hit less than 30 GFR. And then, of course, you want to stop the metformin before I didn't need a contrast.

And hepatic impairment is important as well because if the patient has a liver that's not functioning properly, well, this medication is working on the liver. So you don't want to give it to somebody who has hepatic impairment. Sorenic impairment on your big contraindications. Moving on to sulfoniorias, you really should only focus on the second generation ones, gliburide, glypid, and glomepyde. They all end in rye. or zide, zide or ride, or, you know, just IDE. Two things I think you should remember, glomepiride is going to be your longer half-life. It's going to be the one that lasts sometimes up to 24 hours.

And I remember that because glomapride has an em in it and just makes me think of molasses. Low as molasses. Glypazide is going to be your fast acting normally about eight to ten hours. And then glypozide has a z in it. So I think of zippy, fast, zippy short acting. Their first gens, I wouldn't worry about those. They're very rarely used, if at all. the only thing I would remember, one of the first gens called chlorpromide can actually cause hyponatremia.

So it can actually be used as a treatment for diabetes insipidus. Otherwise, don't even think about first gens. We don't use them anymore. And they shouldn't really be testing you on these. As far as the MOA mechanism of action, it's an insulin secretagogue. So it actually mimics the effects of glucose on the body. And it stimulates beta cells to release insulin into the body. because of this, you can actually see low blood sugars in it because it's actually making the body

secrete insulin. So that leads me on to one of your biggest side effects or your ADRs, and that's hypoglycemia. Patients can definitely go low with this medication. Another thing is weight gain. You can actually gain weight on this. And then finally, there's actually an increased risk of cardiovascular events, which is kind of going to make you realize why we don't use this medication very often. Really, the only reason I ever use it in practice is if a patient can't really afford other medications, other classes, because this is, again, a really cheap medication. It does work pretty well at lowering the A1C. But again, low blood sugars, weight gain, increased risk of cardiovascular events, not going to be top of my list because of these things. But it is cheap. So for certain patients,

it is one of the options that we have. Moving on to megalinides, they all end in glenide, G-L-I-N-I-D. There's two different kinds, repaglinide and the taglinide. These are also insulin secretagogues. They make the beta-cell secretives. insulin. So they work similar to sulfoniorias, but they're not a sulfon urea. So they don't have the sulfur components. So you can use it in patients with sulfa allergies. The main thing with these is they have a much faster onset than the sulfonurias. About 30 minutes. So they're more for meal time. You're going to give this to a patient who's, you know, every day at they have dinner, their blood sugar goes super high and you just want to combat that one area. You can give them

megalitinide. These aren't used very often. They can, of course, cause low blood sugar. but not as much as sulfon urea is because they have a much shorter half-life. They can also cause weight gain. So again, these aren't one of the ones that you're going to ask, probably be asked a lot of questions about and they're not used much in practice. Moving on to a medication that we use even less so than these, this is going to be your TZDs. To pronounce it, I'll give it a shot,

thia zolidiones. That's why we call them TZDs. We barely ever use these. They're actually banned in France and Germany and in Europe. up, they're just not used very often because they have a lot of bad things going on with them. But I'll go over them real quick. As far as the mechanism of action, they actually increase insulin sensitivity in certain zones of the body. The way I remember this is the two medications are called peoglitazone and rosy glitazone. They both end in zone. Glitazone. So I remember

GL and glitone or Glii in glitone, glucose lost in the zone. So Piolytosone, Zyglitazone, and that's because this increases insulin sensitivity and glucose absorption in certain zones of the body, adipose muscle liver. So when you see rosyglittazone or Piaglotidazone, think of glucose lost in the zone in certain zones of the body. That's how it works. So rosy glittosone, when I think of rosyglytosone, I think of roses and I think of Valentine's Day and I think of heart, which makes me think that rosyglytosone actually increases cardiovascular events. And as far as peeoglyazone, I think of p-o-glitone, pee, like peeing, and that makes me think of the bladder, and that makes me remember that P-oglitazone can actually increase your risk of bladder cancer,

making you wonder why we use these meds at all, which we very rarely do. So as far as contraindications, you don't want to use these in heart failure. They can actually increase the risk. You don't want to use an interpatient with history of bladder cancer or liver disease. It can actually increase hepatotoxicity. Again, all these terrible side effects, this is why we barely ever use these medications, if at all. So remember, rosy glittazone, roses, Valentine's Day, heart makes you think of the increased risk of cardiovascular events. Poglidazone, p, bladder, increased risk of bladder cancer.

That's about all you need to remember for these. So moving on to alpha glucosidase inhibitors, there's acarbos and miglitol. How they work is they delay intestinal GI absorption. But when they do this, they cause a lot of GA problems. Flatul and styria, they can even cause hepatitis. This is another one we don't use much. I don't think you should remember too much about these. Just remember acarbos, amygletal, or alpha-glucosidase inhibitors,

and they cause a lot of flatulence, diarrhea, and hepatitis, and they delay intestinal GI absorption. Moving on to some of the meds that we actually use a lot more commonly, glugogon-like peptide 1 receptor agonis, or GLP1, RA. So these are going to be loraglotide, Zanatide and Dulaglutide. These all end in Tide, T-I-D-E, and Tide detergent. I'm sure we all know about Tide detergent.

The way I remember this one is G-L-P-1. G-L-P stands for G-L-Londry pods. I don't know if you've ever seen those laundry pods about, you know, I don't think there's a YouTube video of kids eating them. But so gooey-la-londry pods, G-L-P-1, and then think about Luraglutide, Xenetide, they all end in Tide. So think of Tide-Goo-E-Londry-Londry-Py. It'll help you remember the class and the medications that are inside of them.

So GLP1 receptor agonists, these are almost all once a week injectables. Some of them are once a day. They have one new one. It's called ribelsis. That's actually oral. But otherwise, it's pretty new. I think they should only be testing you on the fact that this is an injectable. It's once a week.

It's a non-insulin injectable. So the way it works, it actually mimics something in the body called an incritin. So it works on different parts of the body. I don't think you should know everything, but I'll just go over a real quick. quick. So it slows gastric emptying. It decreases glucagon secretion from the liver. It stimulates pancreates. It stimulates release of insulin. This is glucose dependent, though. So that's why it doesn't cause a lot of hypoglycemia. So it's only going to do this if you're eating food. And it tells your brain you're full, so which helps in weight loss. So it can decrease weight. It actually

decreases cardiovascular events because it increases myocardial contractility. That's one of the things the GP1 can actually do in the body and it decreases ischemic injury. So it decreases cardiovascular events. It decreases cardiovascular mortality. And it can help patients lose weight and it doesn't cause hypoglycemia. So this is a great medication. It has a lot of great things going for it. As far as the most common side effects you're going to see from this, nausea is almost by far one of the biggest ones. So GI problems. Pancreatitis is also another possible side effect you can see from this, but the big one is going to be GI problems, nausea in particular. As far as contraindications, this actually has a black box warning for medullary thyroid carcinoma. So either a family history

of medullary thyroid carcinoma or men 1 or 2A or the patient having medullary thyroid carcinoma. So any history in the patient or the family do not give this medication. It's a black box warning. Also, a history of pancreatitis or gastroporosis is going to be a contraindic. medication and that's because this actually slows gastric emptying. So you don't want to give this in a patient that's gastroporesis. And then pancreatitis too because this can increase the risk. So moving on to DPP4 inhibitors. DPP4 inhibitors are similar to GLP1s. They actually, in their dipeptitopetal peptides, DPP4 inhibitors, DPP4, what it does is that actually it, it inhibits or it actually degrades the glp1 so if you inhibit d pp4 you stop the degradation of g lp1s

and it's going to lead to all the same things i went over for the glp ones the medications in this class are cidoglyptin liniglipton and saxaglipton the way i remember this is they all end in lipton lip lip t i and then d pp4 this is better if you can see a visual aid which i have on my youtube page but so lipton i think of DPP4 and I think of dip just add an eye to the DPP. So I think of dip, the dip that people put in their front lip that comes in those little tins. So DPP, think of dip. Then you see lip, you're putting the dip in your front lip and it comes in a tin. Again, I have a much better visual aid, but try to think about that in your head as you're driving or listening to this. So the good thing about DPP4 inhibitors, unlike GLP1 agonists, they are actually.

oral. It's once a day medication. So this is a lot better for some patients that don't want to do injectables. But they don't work as well as GLP1 agonists. They're not as strong. They really only target the post-pranial glucose. They don't, whereas GLP1 agonists actually affect both the post-pranial glucose and the fasting. So as far as what you should know for DPP4s, know that it can actually cause pancreatitis. It can cause hepatitis. It's weight neutral, so it shouldn't make patients gain weight and there's not too much else I would know about these medications. Finally, SGLT2 inhibitors, this is a big one. This is used a lot.

So these all end in flozen. Empagloflosen, cantagal flozen, dapeglozun. And I hear the word flozen at the end and I think of flowing, flowing, flozen. And I think of that's because this is actually flowing the glucose through the kidneys out of the body. So glucose flowing out, floes in. So what it actually does is it lowers the threshold of the sodium glucose co-transporter, the SGLT2, and it inhibits reabsorption of glucose through inhibition of the SGLT2.

So the body normally tries to retain glucose. The body's pretty efficient. So when glucose is coming out through the kidneys, the kidney through the SGLT2 will actually pull this glucose back in. So what an SGL2 inhibitor does is inhibits this process. And instead of the body reabsorbing the glucose, it actually comes out through the kidneys and you pee it out. So when you think about that, you're having all this excess glucose through the urine. This can obviously increase your risk of UTIs and yeast infections because what

is bacteria feed off of and that's glucose. So you have an increased risk of UTIs and yeast infections. That's the big one to know with this. That's all I'd know. There's a bunch of other things that are possible. One of the medications can actually increase your risk of amputation. here's the u-glaxemic dkA but the one i would focus on for your exams is uti and yeast infections um so as far as some of the positives here it can actually decrease your cardiovascular risk um it increases the risk of heart or decreases the risk of heart failure especially in epict of flosen um it can decrease weight and it can actually decrease your blood pressure it can decrease the systolic by about five to ten points and it actually acts as a mild diuretic

so in some cases patients may need to stop their hydrochlorothyside or other medicine medications because this works pretty well doing that. And that's pretty much it. As far as the diabetes medications, I think that's the main stuff you should know for the meds and for the diseases. Again, I'm going to be releasing some other stuff for endocrinology, focusing on some other different diseases and pathologies. I hope you enjoyed the podcast. If you have any comments or questions for me, let me know or ways you feel like I can improve. Thanks again and good luck on your exams.