DIP Episode 302 - Diabetes and The USMLEs Part 2 (+ 20 hr Step 2CK/3/NBME Test Taking Strategies Course Reminder)

Okay, welcome. My name is Divine. This is episode 302 of the Divine intervention podcast. And in this podcast I'm going to be continuing the topic that we started in episode 301, Diabetes on the USME Lies. Again, as I've said, I know this is a diabetes podcast. But as you probably know from other podcasts, I love to make integrations. Diabetes is just a great topic for making lots of integrations. Because the thing is when you master those integrations, when you see these contexts as you're learning, you then just become way better at mastering the information. So that's one thing I'm going to focus on again. And hopefully I can finish it up today, but if I can't, so and by the way, today's podcast is not going to be as long as the previous one. If I can finish it up today, I'll make a final podcast and that will complete that diabetes trilogy. But let's see if we're just, we just need a part one and a part two, right? So again, today's task is to kind of clean up some of the things I talked about last time and also talk about some things I did not talk about. And then we kind of go from there, right? But again, there are many ways you may be surprised at on an ambient exam. 10% of the questions can be related to diabetes in some way, right? But again, it may not be diabetes diabetes, they are testing the question. It just be something that is peripherally related, right? So again, it's just a matter of just again, that's why you see these podcasts are kind of long.

And then for those of you that are taking the step two, see key step three exam that are listening to this. I remember I have a course. First, I have an MBME test taking strategies course, the 27th of this month is two and a half hours. Very high yield. You'll learn systematic ways of reading questions, of answering questions, of not falling for MBME traps. Even for questions that you don't know what's going on with those, right? Like how do you approach those questions? I'll teach all those tips and tricks and techniques as we go along in the course. And then from the 20th of April to the first of May, we'll be having the 20 hour step two, see key step three course again before it was 10 hours. It evolved to 16 and a half hours, but now it's 20 hours, right? Because again, I just want to include more material, especially the stuff, the step one material that your friends at the MBME have studied carrying quite a bit about and things of that nature. Okay. So let's just jump right into it. Again, we kind of talked about the IB Ds last time. We talked about how it causes lots and lots and lots of problems, right? We know that diabetes is the thing that causes, in fact, it is like one of the most common, if not the most common cause of like blindness in the US, right? Causes blindness, cause a lot of keeping problems, a lot of nerve problems, right? In fact, many people that have diabetes, right, they end up unfortunately losing the extremities, right?

Because remember diabetes can cause problems with sensation and the person can get like a bad infection of the lower extremities and then they lose their, they lose, you know, they have like auto-emputations and you know, bad things like that happen, right? And one thing I think I want to say about diabetes, remember people that have diabetes, diabetes is actually an immunocompromised state. So these people, they typically actually get the short end of the stick with regards to infection, right? For example, a classic Mbimi question, maybe a person that came in with, you know, flunk pain, CV tenderness, fever, right? And then they tell you that, oh, they perform a urinalysis and they see white blood cell cast, they see white blood cells, they see bacteria, right? And obviously you're like, okay, this person likely has pylonophritis, right? And you're like, okay, let's go ahead and give this person IV-safe traxone. Remember when you're treating pylonophritis, you don't use, you don't use back treatment in Bimis for that. You use that IV-safe traxone or you use an IV fluoroquinolone, right? That's how you treat pylonophritis in Bimis. So you treat the person, but then you notice that, wow. 40, 24, 48 hours after therapy, I'll say 48 hours to be on the safe side. The person is not getting better, the person continues to have fever and all that badness, right? And then usually on the exam, they will see what is your next best step in management, right?

And usually it's going to be in a diabetic. If you see stuff like that, you want to go ahead and get a CT scan of the abdomen, right? Because again, the person unfortunately may have a very bad complication of pylonophritis, right? So they may have this thing called like a demetelio.org demisi, this, see a fluid collection around the cortex of the kidney, right? That's a perinephric abscess, right? That means to be incised and drained. It's actually an emergency. Another thing you see demetelio that, oh, you're seeing gas bubbles in the walls of the kidney, right? That's, remember, gas, emphysema, right? That's emphysema, pylonophritis. That's actually a surgical emergency. You need to call, I think, a transglon surgeon. So the person can get an emergency and infrector, right? If not, the person will die, right? So again, diabetics, it's almost like they get like the advanced form of almost infections or like, if an infection can go bad, it really goes bad in a diabetic, right? And remember, these people can also get like mucomicosis, right? So they can tell you that, oh, it's a diabetic, has facial pain, sinus pain, right? Or they can even tell you the person has a frontal headache. If you see that, because remember, mucomicosis, it actually loves to go and torture persons frontal lobes of their brain. That's why it's a surgical emergency. Something where you have to de-breed extensively. And then in addition to that, you have to give those people lymphotaricin B, right?

You need to give those people lymphotaricin B. And then even diabetics, right? Again, the ones that usually have like neck fasch, right? So like, remember, you can have neck fasch in the perineum. They can have this thing called a phonies gangrene, right? That's basically like a fancy term phonic retising fasciitis of the perineum, right? So those are things you kind of need to give out the back of your mind with diabetics. Even your friends at the Mbmed care that you know that, oh, you know, what if they tell you that, again, you're seeing like gas-bought-lessy, a person who presents with red-up, a quadrant pain, and very high-fever's, and is a diabetic. And you're seeing like gas bubbles in the wall of their gold blather, right? I would really hope you're thinking about like gangrenous, colysis-titis, right? Again, that's very life-threatening, right? It's something that you need to fix, and you need to fix relatively quickly, so that the patient doesn't die, right? And then again, if I remember last time, we did talk about type 1 and type 2 diabetes, right? And again, we talked about how type 2 diabetes, they have a lot of insulin resistance, right? So some of the receptor may not be working, right? So remember, insulin uses a tyrosine-kindness receptor, right? So if that tyrosine-kindness receptor is not working, it's almost like having nephrogenic diabetes in cipitis.

It's like, oh, there's ADHD around, but you have a V2 receptor problem that can be caused by like lithium or hypercalcemia, or the mechocycline or anything of that sort. But in diabetes, again, it's a tyrosine-kindness receptor that doesn't work. Or in some cases, some people, again, there are many genetic things that cause a tyrosine-kindness diabetes, and I think it can also be just your glute 4 receptors don't work, right? Remember, your insulin-dependent tissues use glute 4 receptors, right? So like your adipose cells, your muscle cells, they use insulin, right? In fact, the way I remember that is I remember just we cannot put 4em, right? We cannot put 4em, right? So glute 4 for 8 adipose and m-mossal, right? So again, if you have a glute 4 problem, right, then you're not going to be able to your muscle cells and your adipose cells, which make up a big chunk of your body, right? They will not be able to respond to insulin, unfortunately, right? And again, still going off of that receptor enzyme problem, right? We talked about materially onset diabetes of the young last time, right? We said that it's a disorder where you may have like a glucaquianis receptor defect, right? And again, we talked about how if you have a glucaquianis receptor defect, then your glucose sensing is going to be all screwed up, right? So you may not release insulin in your...

You may not release insulin at all, or you may not release insulin adequate amounts to hyperglycemia, because again, in a normal person at a block glucose of like 120 milligrams per this liter, you may release adequate amounts of insulin, right? But again, in a normal person, if you have a glucaquianis problem, then that glucose will not be... Because remember, glucaquianis we find it in the pancreatic beta-ilets, right? So if we don't sense things appropriately, we will not convert that glucose to glucose 6-fos-feet, and then that glucose 6-fos-feet cannot help us make ATP in the pancreatic beta cell, right? So that we can close those potassium channels and see creating insulin, right? In fact, materially onset diabetes of the young for the most part is in here, if it is in an autosomodominant fashion, right? So in here, there are autosomodominant fashion, right? And again, today's topic, again, we're going to make some integrations here and there. So what if they give you a question about 32-year-old woman, you know, they tell you that she has been having irregular menses, at BMI's 33, right? So she is obese, and then they tell you something about how, you know, again, her appearance come very regularly, and she has been trying to have kids with a husband, she's not making any headway, right? And then they tell you that, you know, she has like these velvet illusions on her skin, and you know, she...

She has like signs of hyperindrogenism, I really hope in those circumstances you're thinking about PCOS, right? PCOS, polycystic ovarian syndrome, remember, it has a very strong association with people having diabetes. In fact, many of those people when they have diabetes, you give them metformin, and for some of those people, just giving them metformin alone, maybe the thing that means, make them become... Make them become pregnant, right? I mean, obviously, for potassium, PCOS, I want to try to get them pregnant, you can give them things like... You can give them letharzoid, right? Or you can give them plumifin, right? You can give any of those things, but metformin actually has been reported to help some of these women taking, right? So the thing is insulin actually plays a big role in the pathophysiology of PCOS. Again, I just don't have time to discuss that today, so I'm just going to keep going, right? And then one other thing your friends at the MBME love to test is they love to test how people that have diabetes, right? They have hypertension. What kind of thing are you supposed to do to them in terms of treatment? Well, I hope you're saying that, oh, divine, we're going to give them an ACE inhibitor, right? Because again, remember diabetes torches a presence kidneys. In fact, diabetes, if I'm not mistaken, is one of the most common causes, if not the most common cause of chronic renal failure in the US, right?

So you can kind of leave that off or slow down the progression of kidney damage with an ACE inhibitor, right? And again, we know how that should work, because remembering diabetes, the thing that happens, and I'll talk about this in more detail in a bit, right? You have this non-inzymatic glycosylation, preferentially of the effrayin materials. If that happens, right? That thing of non-inzymatic glycosylation of the effrayin materials has been tantamount to constriction of the effrayin materials. If you constrict the effrayin materials in the hydrostatic pressures in your glomerular capillaries is going to go up. And if that goes up, your GFR is going to be high. So you may be like divine. This is great. My GFR is always high. What's the thing? What's the problem with that? Well, let me tell you this. There's definitely going to be a problem with that, because if that happens, again, your GFR should, your body tries to modulate your GFR in responses, in response to changes in effray natural perfusion, right? Well, your GFR is not always high. Your GFR is always high, right? Then you're going to be filtering all the time, filtering hard, filtering hard, filtering hard. The thing is that filtering hard over time will cause something that is known as hyperfiltration injury, right? And that can damage the glomerulus, right? That can damage the glomerulus.

And when you're damaged the glomerulus in that way, then the pressing is, you know, they're going to go into chronic renal failure, right? And the thing that really happens with ACE inhibitors is, angiotensin 2 is a very powerful constrictor of the effrayin materials. So if you give an ACE inhibitor, you'll decrease the production of angiotensin 2. And if you do that, then you ultimately cause a dilation of the effrayin material, right? And by dilating the effrayin material, you're going to increase drainage from the glomerular capillaries. And if you do that, you're essentially lowering the pressure, lowering the hydrostatic pressures in the glomerular capillaries. And that's going to, you know, help. That's going to prevent that hyperfiltration or slow down the risk of that hyperfiltration of injury, right? And then, and then remember in the abedics, right? Again, remember these people, again, the half hyperglycemia, the half-high glucose. Remember glucose is an all-dose sugar. If you remember from organic chemistry in college glucose is an all-dose sugar. It's not a keto sugar. Well, it so happens that there is an enzyme known as all-dose reductase that operates in the body, right? In fact, we find it in a bunch of, you know, a bunch of cells, right? We find them in the eyes, we find them in the retina, we find them in the kidneys, right? We find them in shuan cells, right? So all those reductase, what it does when glucose, because of hyperglycemia, right?

Because, again, I said something that when a person has diabetes, especially like type 2 diabetes, and they have insulin resistance, or again, they have an insulin deficiency. Those insulin-dependent cells, right? Those cells that depend on insulin to take up glucose like your adipose cells and your skeletal myocytes, they're not able to take up glucose. Well, guess what? They are insulin-dependent cells, but surprise, surprise, they are insulin-independent cells, right? So the thing is, whenever there is an insulin deficiency of this insulin resistance, those insulin-independent cells will then start taking up glucose on their own, because they're just more available for them, right? So many of these insulin-independent cells, right, like the eyes, like your retina, like your shuan cells, like your nephronos, they're taking that glucose, that glucose is covered by all those reductase to serve the top, right? Now, the thing is, that's sorbitol. Some tissues in the body actually have the ability to deal with it, right? Some tissues have this enzyme called sorbitol dehydrogenase, that can convert that sorbitol to fructose, right? And then that fructose could potentially diffuse out of the cell. But the thing is, many of these tissues, right, actually don't have sorbitol dehydrogenase. So one of the glucose is converted by all those reductase to sorbitol, that sorbitol hangs out in those things.

And sorbitol is extremely osmoticly active, it's going to pull water into those things, like the lens of the eye, right? That can cause cataracts, that's why diabetes is one of the biggest risk factors for cataracts, right? So it brings in that water, and you know, it kind of messes up the lens, right? So it can mess up the lens of the eye, right? So the person can have like blurry vision, right? Again, it can mess up your shuan cells, right? And again, remember your shuan cells are the cells that help you with my lineage in your peripheral nervous system. Well, that doesn't work very well anymore when a person has hyperglycemia, right? Again, you can notice these are not adipose cells, these are normal so cells, these are insulin independent cells. They get a bigger than normal supply of glucose, because those insulin dependent cells, like your adipose cells and your skeletal myocytes, and no longer working anymore, right? So again, this should also, let me bring in an integration here with galactose problems, right? So whenever you see a child having a galactose metabolic issue, many of these kids also tend to have cataracts, right? Again, the reason they have cataracts is because galactose is also an old-dose sugar, right? So just like all those reducties can act on glucose and convert it to sorbitol. All those reducties can act on galactose and convert it to galactitol, right? Galactitol is also smutically active, right? So that's why those kids get cataracts, right?

So remember, people can get either galactokinesis deficiency, which is less severe, right? Or they can get a classic galactosemia, right? Galactos one phosphate-urideotransfer is deficiency, and they can get in trouble. But usually they get cataracts, right? Usually they get cataracts. And again, some of you may be like, oh, why those galactokinesis deficiency? Why is it less severe than essential galactoseemia? Well, the thing is, galactokinesis deficiency means you cannot convert galactose, right? Two galactose one phosphate. So you'll be like, oh, the vine is that so bad? Well, the thing is, it's not so bad, because galactose is a six carbon sugar and hexokinesis, right? Has the ability, almost like non-specifically, to convert six carbon sugars to their phosphate-urideotransfer, right? So hexokines can pick up some of the slug that's sticking out by galactokinesis, same thing with fructose, right? Again, essential fructoseuria, not a big deal, right? Because again, well, it's a big deal, but it's not that bad, because again, that hexokinesis can help you deal with that fructose problem. But again, if you notice people that have fructose metabolic disorders, they don't have those cataract problems. Well, why does that make sense? Again, if you remember from organic chemistry in college, fructose is a keto sugar, right? Glucos and galactose are all those sugars. All those sugars have the ability to be acted on by all those reductives. But fructose is a keto sugar.

And as far as I know, there's no such thing as keto's reductives in the body. So those things cannot fructose really, it's going to have a hard time completing the lens of the eye or whatever, right? So those people usually end up not having too many problems, right? So again, back to this whole issue of non-inzymatic glycosylation, right? So again, this non-inzymatic glycosylation, again, it literally doesn't need any enzymes, right? Whenever you have high amounts of glucose around, glucose combined with amino acids, right? You can have this condensation reaction. Because remember, amino acids are sort of kind of basic. Glucos is sort of kind of more acidic than them, right? So you can have a condensation reaction, right? And you have this non-inzymatic glycosylation happening, right? And again, when that happens, it will begin to damage the eyes, right? It will damage the retina. It will damage neurons, right? Again, because it's killing shwan cells. And then it's going to damage the kidneys as well, right? In fact, many times when you have this non-inzymatic glycosylation happening, it creates something that's called an advanced glycosylation product, right? Or some people call it advanced glycosylation end products, right? The thing with those things is they are very destructive, right? So like those things when they begin to insert in the membranes of things, right? Or they begin to shop in the basement membranes of things. They make those things leaky, right?

They make those things leaky, right? So that's one of the reasons why people that have diabetic nephrapathy, they have a lot of microabulinaria, right? And again, these things can make blood vessel walls more leaky, right? So again, all these bad stuff from your bloodstream can begin to leak into your blood vessel walls and cause this thing called hyaline, arteriolo sclerosis, right? So again, and remember, people can also get that diabetic nephrapathy and classically on end-bmm means, right? Don't forget that that's associated with those chemo steel, right? Kiwm, ES TiEL, TIEL, yes? Chemo steel, well-synmodules, right? On histology, right? So that's something you want to give at the back of your mind on end-bmm exams. In fact, one nice integration that your friends at the end-bmm make is, and I'll talk about this some more with how we screen people for diabetes, right? They may try to see that, they may give you a patient with like hair ditches for your cytosis, or hair ditches for a lip docis and say, you know, this person, if you want to screen them for diabetes or whatever, what can we do? Well, I would really hope that you are saying to not, I really hope you don't pick the answer that says to check the hemoglobin A1 C, because you may get falsely decreased results, right? Whenever you have some disorder, where your blood cells are dying at a rapid clip, right? The A1 C is very likely not going to be accurate in those people, right?

Because again, remember, your hemoglobin A1 C is actually one of these examples of an advanced glycosylation and product, right? So the thing is, it gives you like a very good proxy for what your glucose control has been like within the last three months, right? So if for some reason, a person has something that's killing their blood cells very quickly, let's say like sickle cell disease, or like hair ditches for a cytosis, or hair ditch for a lip docis, or let's say a person has some kind of autoimmune hemolytic anemia, in those circumstances, measuring those people's hemoglobin A1 C is actually not product, right? It's not product, right? So again, that's a very nice way to integrate hemoglobin A1 C on an immune exam, right? And again, please don't forget, right? People that have diabetes, what's the most common cause of death in these people? Well, I really, really hope you're telling me that, oh, divine, these people, the most common cause of death in them, it's going to be an MI, right? It's going to be a myocardial infraction, and usually when people have diabetes, they actually tend to have their like not classic MI symptoms, right? So they can, especially when women, right? So they may not have the chest pain, or they may have like nausea instead of chest pain, right? So again, whenever you see a diabetic, and they have abnormal symptoms, I'm saying this for people that are going to be comrades in the future.

One of the smart things you can do is you just go ahead and check their troponins. You, you don't cover quite a number of surprises across your career. If you, if you did that, right? And again, diabetes, again, like I said, it can cause retinopathy, right? Because again, of that sobrietyle business, and they're actually two kinds of retinopathy. You need to keep at the back of your mind for imbim exams, right? So you want to keep in mind that there's such a thing as non-proliferative retinopathy and proliferative retinopathy. And the thing is you actually do need to be able to differentiate between these two on a fondoscopic exam on imbimines, right? So if a person has non-proliferative retinopathy, right? Remember, they'll form all these micronutrients, right? So the imbimines, they'll give you these buzzwords in the question, or they may give you these buzzwords as answers. You do need to be able to recognize them, right? So in the case of non-proliferative retinopathy, remember, again, you'll have these micronutrients, right? You'll have these flame hemorrhages, you'll have these exudites. Those are buzzwords you need to remember. But for the proliferative retinopathy, right? The key key term you want to remember on your exam is neo-vascularization, right? Neo-vascularization because you're trying to form all these new blood vessels, for whatever bizarre reason, right? In fact, these new blood vessels, as you begin to form them, form them, form them.

They can begin to talk on the person's retina, and that can cause retina detachment. Retina detachment is a relatively common complication of diabetes on imbimines, right? And usually when these people have these micronutrients, they may say, oh, how do you treat them on an imbimines exam? Well, you can do things like photo-quagulation. Photo-quagulation is probably the big buzzword. You want to keep at the back of your mind on imbimines, right? And then, don't forget, as well, I think maybe I almost forgot to say this. But in terms of the back complications, right? Like usually, the first thing that gets torched in a person that has diabetes is actually the eye, right? So those people, they get retina-pathy first, and then, that retina-pathy basically is way more common, right? Then those people get in neuropathy, which is way more common, then those people get in neuropathy, right? So just remember, eyes first followed by neurons followed by kidneys, right? So eyes first followed by neurons followed by kidneys, right? And then, again, many of these people that have diabetes, unfortunately, they can develop like peripheral neuropathy, right? So those can cause them to begin to have all these neuropathic ulcers, right? They can have problems with their reflexes, they can have all these things. And usually, when a person has diabetes, if they're trying to get you to treat their neuropathic pain on an imbimines exam, I'd hope you're saying, oh, you know what?

Let's use an SNRI, right? Remember, you can use an SNRI, like, block the teen, for example, in these people, right? You can use a tricyclic antidepressant, right? Non-triptyline, image-triptyline, you can use GABA-pentin, you can use pre-gabbaline for these folks, right? And again, remember, diabetes, if you- again, because maybe like the vine, this neuropathy is not a big deal, it's just the lower extremities. No, it's not just the lower extremities. It can also affect your GI tract, right? Remember, there are many neurons that constitute your enteric nervous system. If those neurons don't work very well, you're going to have diabetic gastroperaces, right? And typically, diabetic gastroperaces, how do we treat it? Well, I would hope you're saying, oh, define you know what we can use dopamine antagonists like metoclopromide. Well, unfortunately, that metoclopromide can cause drug induced Parkinsonism, right? In fact, if they give you on your elliptic malignant stout presentation, in a person that has diabetes, right? You want to think about metoclopromide as the treatment for diabetic gastroperaces that's causing those problems, right? Because again, it's essentially an anti-psychotic. It's a dopamine receptor antagonist, right? And then remember, you can also use strict diabetic gastroperaces with erythromycin, right? Remember, that's a motiline receptor agonist so that you can have more flux through your GI tract. And then remember, diabetics, right?

Again, on ambient exams, they can also have like neurogenic bladder, right? So remember, neurogenic bladder is the thing that's known as overflowing continents. So those people, the trussor muscles don't sense adequately when the bladder is full, right? So those people, if you check their pulse void residual, it'll be very, very high. It'll be in the hundreds of milliliters on an ambient exam, right? In fact, they can give you a question about a diabetic, right? That has like an iridescharge, has a very painful pain. Right? If you see stuff like that, I want you to think about not just because I know when people say, oh, iridescharge, the pain I was hurting, or let me think about otitis extrerna. Well, the thing is, if you see a diabetic on an ambient exam that has otitis extrerna, I want you to think about malignant otitis extrerna, right? Again, many of these things I'm saying now, maybe like divine these things cannot be important. Until you then see them on an ambient exam and then you're like, oh, wait, this stuff is actually high yield, right? Malignant otitis extrerna is floridly high yield to know for ambient exams, right? And remember, we usually treat this with a fluorocrylonal, right? When we're sure that it's fluorocrylonal, we can treat it with acetic acid, right? Usually these people, they tend to get like systemic therapy. This is because usually a regular otitis extrerna, you can just put like acetic acid eardrop, so whatever, they'll be fine.

But for people that have malignant otitis extrerna, usually want to give them like IV antibiotics of some sort, right? And then remember that people that also have diabetes, one thing that can happen to them, right? So they can give you a question about a diabetic, and this diabetic has like peripheral arterial disease, right? They tell you that, oh, you know, you walk one block and it's like that hurting until you rest for a while, and then you'll get better, right? Well, obviously for person has PD, the first thing you're going to do is you're going to go ahead and check there, what is it called? Check their ankle-breach healing decks, right? So if the ankle-breach healing deck is less than 0.9, well, you're kind of out of luck there, person has peripheral arterial disease. But guess what? What if you measure a person's ankle-breach healing decks and it's like 1.5? It's like much greater than normal, right? If you see that, that doesn't mean that they don't have PD. Remember, when people have diabetes, they can classify their blood vessels, right? In fact, this is what is known as monk oberg, monk oberg, calcific sclerosis, right? So if they classify their blood vessels, that's going to cause you to get falsely elevated ankle blood pressure readings, right? So usually for those people, what's going to be your next best-tempered management?

You're going to measure the toe-breach healing decks, and that will give you a more accurate measure of these people having peripheral arterial disease, right? So again, diabetes is not the best thing in the world. And again, just because I need to run to an engagement, I'm going to go ahead and pause here. But again, I will say this. The next podcast I will make, I will probably hopefully make it something very, very soon, or probably within the next few hours or days at the most, is going to be diabetes and the USM and this part three. Once I'm done with that, we'll be done with diabetes. And you'll have a very complete thorough understanding of diabetes. Basically, in that podcast, I'm going to be talking about some, again, integrations with some other genetic syndromes and diabetes, with the management of diabetes, complications. I'll talk about how diabetes is that, nothing in the first place. I'll talk about it in pregnant women, right? So again, stay tuned for that episode. I think it's something you'll find to be really helpful. And then, as I do at the end of every podcast, I do offer one or one tutoring. For many exams, step one, step two, CK, step three, pre-clinical medical exams, 30-ish-off exams. If you're a medicine resident, actually, you should offer the medicine boards and internal medicine training exam. So if you need tutoring for any of those things, feel free to reach out to me. And again, as you've seen, I have step two, CK and step three courses.

For step one, I do offer actually a personal life step one course. It's one on one, although, again, in the future, I would offer very likely offer group groups, step one courses. But for now, I'm just doing the personalized one on one step one course. So if you're interested in any of those things, the personalized step one course, it's kind of tailored to your needs. It can be 20 hours, it can be 30, it can be 40 hours, just kind of depending on what your knowledge piece looks like. So if that's something you're interested in, feel free to reach out to me. And I'll be happy to give you some more information on that. And then, please subscribe to the website, divine intervention podcasts with an S dot com. Whenever I make a new podcast episode, I always uploaded there. And if I make a new podcast episode, if you're subscribed to the website, you will get an email notification. And I do also have a You Tube channel. It's called divine intervention, USMLE podcasts and videos. I'll say that again, divine intervention, USMLE podcasts and videos. The thing is, you know, sometimes some people make these like mock off You Tube channels. So that's something you want to be careful of. If you want my real content, think about divine intervention, USMLE podcasts and videos. So please subscribe whenever I make a video, you'll see there. And I also have these podcasts on Apple podcasts on Google podcasts on Spotify. So again, you can see the most recent 150 podcasts on those.

Again, some people may be like, what divine this is episode 302. Where are the other, where were we find the other episodes? The place you'll find the other episodes will be on the website. Every episode from episode one, all the way to 302 is there. You can download it from there. You can listen to it there. Again, I unfortunately can put more than 150. I think it's either Word Press rule or podcasting, whatever rules. So it's literally out of my hands. I've literally tried everything else and it just doesn't work. So again, if you're looking for everything from episode one, feel free to get in there. And then one other thing I would say is, if you want to know, because many people have this question already, like divine, how do I know what podcast to listen to for Step One, what podcast to listen to for Step Two, Step Three, what podcast to listen to for Susu-Su and Susu-Su, and Shelf, whatever. What I would encourage you to do is go to the website, divineinterventionpodcast.com. Click on the header that says exam topics list. That will lead you to a spreadsheet that has all the, what is it called? All the different subjects and how they are broken down. So I think that's something that we help for. I break it down for Step One, all the disciplines tested on Step One and all the relevant podcasts for each of those. Step Two, Step Three, all the different disciplines, all the different shelf exams. I break it down one by one. And I put the episode numbers.

And then you can just go back to the website and in the search box in the upper right corner, just typing the episode on the topic, boom, and it takes you right to that instead of scrolling, scrolling, scrolling, and stuff like that. So, thank you for listening. I hope you got in something from this podcast. And again, there will be the final part. I think one more podcast should tackle all of our diabetes needs and then we'll go from there. So thank you for listening to me. God bless you. Have a wonderful and safety and remain blessed. Shalom.

Eyes $\rightarrow$ Neurons $\rightarrow$ Kidneys.

Neovascularization (formation of new, fragile blood vessels).

Aldose reductase.

IV fluoroquinolone or IV ceftriaxone (avoiding oral trimethoprim-sulfamethoxazole).

Dopamine antagonists (e.g., metoclopramide) or Motilin receptor agonists (e.g., erythromycin).

Non-proliferative shows microaneurysms/exudates; Proliferative shows neovascularization.

Non-enzymatic glycosylation $\rightarrow$ Advanced Glycation End Products (AG Es) $\rightarrow$ Microalbuminuria and Hyaline arteriolosclerosis.

Calcification can cause falsely elevated readings; use Toe-Brachial Index (TBI) instead.

Cataracts, due to sorbitol accumulation.

Glucagon receptor defect in pancreatic beta cells, impairing ATP generation and insulin release.

Microaneurysms, flame hemorrhages, exudates.

Because these conditions cause rapid blood cell turnover, making the A1c measurement inaccurate.

Non-enzymatic glycosylation $\rightarrow$ Advanced Glycation End Products (AG Es) $\rightarrow$ Microalbuminuria and Hyaline arteriolosclerosis.

Calcification can cause falsely elevated readings; use Toe-Brachial Index (TBI) instead.

Cataracts, due to sorbitol accumulation.

Glucagon receptor defect in pancreatic beta cells, impairing ATP generation and insulin release.

Microaneurysms, flame hemorrhages, exudates.

Because these conditions cause rapid blood cell turnover, making the A1c measurement inaccurate.