DIP Episode 293 - NBME Gastroenterology Series 1 (for all USMLEs)

Welcome, my name is Divine. This is another USMLP podcast and I believe if I'm not mistaken that this is episode 293. So we'll be starting a review series for the USML exams. I mean this is going to be useful to anyone taking anywhere from step one, all the way to step three. It's going to be a review of Gastroenterology, although some things I would say will be more active to people that are studying for step one. But again, I think if you're studying for any of the USML exams, you should find this to be pretty, pretty helpful. So we'll just make this in short bits and pieces, but we're going to just keep chugging along. Okay? So this is again a episode 293. So let's just get right into it. Right? The thing with Gastroenterology that's, you know, it's pretty annoying is there's really not much, you know, like farm or fizz behind it. It's mostly just a lot of pathologies. But again, the thing is if you pay attention, I'm going to use a lot of pieces, a lot of vignettes to highlight many of the core concepts. And then I'm going to try to mix some integrations across multiple disciplines. Right? Again, a lot of it is also, excuse me, a lot of it is also a pattern recognition. Right? So just again, just things to keep in mind. But again, I don't think it's going to be too daunting. It's pretty straightforward if you know if you kind of understand what's going on.

And again, if there is understanding that's necessary for a particular area, or is available for a particular area, chances are probably, probably go over it. Right? So the thing is, let's just start with some anatomy and embryology. Right? So the thing is for those of you that are taking step one, right? So this is not applicable to people taking step two, seek is step three. Well, if you're going into a surgery rotation, demipimpy on this and a surgery surgery rotation, right? But remember, you want to make sure you know your layers of the abdominal wall. Right? Again, it's just something that's pretty, pretty high, you know? Right? Remember, if you start from the skin, right? From your skin, you have your superficial fascia. Right? And they remember your superficial fascia includes your compass and your scarper fascia. Right? And then you go to your bleak muscles. Right? So obviously the one that should come first should be the external bleak muscle. And then after that, you should have the internal bleak muscle. Right? And then after that, you have like transversus abdominis, you have your transversalis fascia. Right? And then you have your extra peritoneal fascia and then get to the paritoneal peritoneal. Right? So again, it's not too hard to memorize, right? Again, skin superficial fascia. And then remember, your superficial fascia has two parts, right? Compres fascia and scarper fascia. Right? And then you're going to your bleak muscles.

Obviously the one that should come first should be external before internal bleak. Right? And then you have your two teas, right? You have your transversus abdominis. And if you're going in alphabetical order, it kind of helps. Right? Transversus abdominis. And then transversalis fascia. Right? And then after that, you go to your extra peritoneal fascia and then boom, you go to your parito peritoneal. Right? Remember, your visor peritoneal is the thing that directly lines the walls of your GI organs. Right? And obviously your GI tract, you know, has three parts. Right? There's the foregoth, there's the midgoth, there's the hindgoth. Basically, if you wanted to divide them up, your foregoth basically extends all the way up to the ligament of trites. And then, so that's a part, obviously a part of the duodenum. And then from that part of the duodenum, if you go all the way to the proximal two thirds of the transversus colon, that's your midgoth. Right? And then everything from the distal third of your transversus colon all the way to like your rectum is going to be your your hindgoth. Right? So again, your foregoth again, basically the first half of your duodenum, your stomach is there, your liver, basically all those things are on the stomach and the intestines are pretty much foregothed derived. Right? So remember again, like your duodenum, your stomach, your liver, your gobladder, your suffogas, right? Those are all called part of the foregoth. Right?

And again, remember these things are all derived from endoderm for the most part on endemic exams. And don't forget, right? Your celiac trunk is the blood supply, right? Your celiac trunk trunk is the blood supply for your foregoth. I remember I made a podcast, I think it's one of my podcasts in the 100s, maybe like 180, something or whatever. I would encourage you to listen to it, I call it like the vascular podcast. Basically, I go into the high blood vessels and the way your friends at the NV Me love to integrate those things. And then remember again, like I said again, I'm going to be doing like some kind of targeted repetition so that it's easy to remember these factors that I'm discussing. Again, anatomy and embryology, unfortunately, a lot of it is just a lot of memorization. But remember your midgoth, right? It goes from your distal to adnum, right? To the proximal two thirds of the transversus colon. And remember, the blood supply of this, right? Is your superior mesenteric artery, right? Your superior mesenteric artery is a big, big, big, big, big blood supply, right? And one thing your friends at the NV Me can do, right, is they can give you a question about a person that has a history of e-fib, right? Or the person had a recent MI. And then they tell you that all this person has sodium onset, severe abdominal pain, right? And it's very non-specific, right? And the person even have signs of periodonitis. And they're asking you for the diagnosis.

Well, I hope you're thinking about acute mesenteric ischemia, right? So the thing that pretty much happened is that these people essentially deform the clot in the heart because they have e-fib. Remember, the left e-fib is kind of quivering at that point, right? So they have a recent MI deform the clot in one of the ventricle. And then that thing flex off, goes into the systemic circulation and occludes the superior mesenteric artery, right? The most common cause is very high, though. The most commonly impaired vessel, blood vessel in a person that acutement is enteric artery. Well, when acutement is enteric ischemia is actually going to be the superior mesenteric artery, right? And again, you notice the symptoms are acute. It's not something that arises over weeks, over a month. Now, right? If it's over weeks, it's over a month, then it's not going to be acutement is enteric ischemia, right? So again, don't forget in MBME questions, pay attention to your timelines. That's usually a smart thing to do. And then remember, your hind guts, right? Again, basically is everything from, again, your distal third of the transverse colon all the way to the rectum, right? And again, we're talking about this transverse colon so much. I remember that the transverse colon, they can give you a question about a person that, you know, recently completed antibiotic therapy for some disorder, right?

And then you notice that this person has been having like CV abdominal pain, as we have a lot, having a lot of diarrhea, right? If you see that, I would really hope you're thinking about C-difcolitis, right? Now, the thing is, how do C-difcolitis relate to the transverse colon? Well, they can give you a question about a person that has C-difcolitis or they can even make this a question about a person that has like all C-difcolitis. And they tell you that all this person, even Chagas disease, believe it or not, right? Chagas disease can also cause this complication. And they'll tell you that the person for the last like few hours has been having like very CV abdominal pain. And then they'll tell you that they obtain like an abdominal x-ray and you'll notice that the person has a marked dilution of the transverse colon, right? They tell you that, oh, it's more than six centimeters in diameter. If you see that, I really hope you're thinking about toxic mega-colon, right? I hope you're thinking about toxic mega-colon. Remember toxic mega-colon is a well-established complication of C-difcolitis. It's a well-established complication of alternative colitis is a well-established complication on N-B-M exams of tripe and osomacruzia. Remember, T-cruzia causes big problems, right? It can cause ecalysia, it can cause a diluted suffogust, right? It can cause a diluted cardiomyopathy, right? So that can present as heart failure with reduced ejection fraction.

It can cause herchprone's disease because it can destroy your nerve-plex eye in the distal colon, right? And remember, the transverse colon is sort of kind of tamed in towards the distal colon, right? So they can give you a question about a person that has toxic mega-colon from South America, right? If you see stuff like that, I want you to think about Chagas disease caused by again tripe and osomacruzia, right? And then remember again, as I said that the distal third of the transverse colon all the way to the rectum has the infirmizent, is the hind gott. Remember, it has the infirmizent area artery as it blood supply, right? And then the thing is the organs of your gott is not like they're just some mesh mesh and that's just going to sandwich into your GI tract. No, that's ridiculous, right? Or like, oh, like someone just opened your belly, tossed a bunch of organs there, no, no, no, no. Those organs, I kind of think of it as, you know, for those of you listening to this stuff, to this podcast that are from Africa, right? You probably know, you know, you know, washer and dryer, I mean, who, at least I remember when I was little, I could afford a washer and dryer. But I know for a fact that, you know, whenever I would wash clothes, right?

Again, even when a wall has the washing machine, so you hand wash your clothes, you hand wash those clothes, you want them to dry, you basically have ropes that are outside your home, and then you literally put those clothes on those ropes and then you put like pegs or pins on them to pretty much hold them to those ropes so that they can dry, you know, under the sun or whatever, right? So, the thing is your GI organs almost have like ropes that are suspending them, right? Those ropes are called mezzanteri, right? Those ropes are called mezzanteri. Those, the mezzanteri that supplies your, the mezzanteri that suspends your GI tract, those ropes that suspends the different organs of your GI tract, they actually derived from mezzoderm. That's very high you to know, in fact one factoid that your friends at the NV Me love to test a lot is that the falseiform ligament, remember the falseiform ligament, F-A-L-C-I-F-R-M, right? That, you know, is kind of around the liver, right? It's actually derived from a ventral mezzanteri, right? So again, don't forget, a tear supply of your foregoth is the cilia cardory, right? A tear supply of your midgoth is the superior mezzanteri cardory, and then a tear supply of your hindgoth is the inferior, so foregoth is your cilia cardory, midgoth is your superior mezzanteri cardory, and then hindgoth is your inferior mezzanteri cardory, right? And remember that ultimately all of your goth drains into the liver, right? Through the Pot-O-V, right?

Drives into your liver through the Pot-O-V, and don't forget that again, the fact that all your got, like your foregoth midgoth hindgoth for the most part, drains into the liver that can tell you why people that have carstenoid syndrome, right? If they have just the GI malign, if they have the malignancy just in the GI tract, usually in the appendix or in the small intestine, they won't have symptoms, right? Because again, all those parts of the GI tract, they all drain into the Pot-O-V, when you drain into the Pot-O-V, the liver has the ability to metabolize that serotonin, right? And metabolize that serotonin, right? So it will not be able to make it to the right side of the heart. So those people for the most part will not have any significant symptoms. But then, if that malignancy methods the sizes to the liver, right? Then that promptly becomes a problem, right? Because you've essentially bypassed that Pot-O-V circulation, so you bypassed the metabolic activity of the liver. So those people can then begin to have right-sided heart symptoms, right? And remember, usually, those right-sided heart symptoms will be things like tracospid regurg and pulmonic stenosis, right? There's a nice, non-monic there tips that is in many resources that you can use to memorize that, right? So like the TI is for tracospid insufficiency, and then the PS is for pulmonica stenosis, right? So again, these are just all high-yield things to keep at the back of your mind.

And then another little tip bit of an atomic old detail, right? Like your retroperitoneal organs, you know, you kind of need to know these things, right? So remember your retroperitoneal organs, I think, like your, you know, there's this nomonic that I love using, sadbucker, many of us have heard of this, right? So remember, your superinol glands, right? Your adrenal glands are retroperitoneal organs. And then your yoder and your inferior venechiva, right? Those are both retroperitoneal organs as well. Your doodnam, but it's not every part of the doodnam, it's the second and the third parts of the doodnam, right? That are retroperitoneal, right? And then remember your pancreas, your ureters, right? Your ureters, your colon, again, not every part of your colon, it's your ascending and your descending colon that are retroperitoneal, right? And then your kidneys are also retroperitoneal, again, they are kind of in the back of the body, right? That's why we, whenever we're checking for a kidney infection or a kidney stone, we can try to check a CV tenderness, right? Cost of a tuberlangu tenderness by literally tapping on the person's back, right? So the kidneys are in the back, right? They are retroperitoneal organs. And then your soft August and your rectum are also retroperitoneal organs, right? So what are some high yield things, your friends, that the enemy love to test with regards to the term retroperitoneal?

Well, the first thing is you've got to know what these organs are, right? But then the second thing that pops up quite a bit on exams is they can give you a question about a person that, you know, presented with a myocardial infarction. And then the person had to get some kind of, you know, had to be taken to the cath lab, went for some cardiac catheterization. And then they tell you that, ooh, that they inserted something, you know, through the presence like arm or whatever, right? You know, to do the cardiac cath, or they may have done like, uh, actually, let me tell you this, because if you're doing a cardiac cath, you can go in through the radial arteries, but another thing which, you know, many people don't do, right? Or you can go through the femoral arteries, right? So many times people do a femoral puncture to, um, to do a cardiac cath, right? Because, you know, if you go through the femoral arteries, you can sneak it all the way to the yoder, and then go through the yodic sinus and go to the coronary arteries, right? That's how people do cardiac cath, right? And then they tell you that, oh, after, like a few hours after this cardiac cath, or a few days after, but usually it's a few hours after, the person becomes like profoundly hypotensive, the presence of him who glubin is dropping significantly, and then they are asking you for your diagnosis. If you see that, I really want you to think about a retroperitoneal bleed, okay?

You want to think about a retroperitoneal bleed. Remember, the yoder is a retroperitoneal organ, right? So the thing that potentially most have happened, most of you, most of happen is, you may have punctured the yoder, right? And if you punctured the yoder, it's not going to end very well for a person, right? So the person can have a retroperitoneal bleed. So for those of you that are taking step two, see, step three, let me say, oh, what's your next step in management? The next step for you is to perform CT angiography, right? And that's going to show you the bleed. And then you can actually do like some embolization, so you can try to control the bleed angiographically, right? That's something that's usually done by interventional radiology in the railroad, right? So again, just things to keep in mind. And then, I'm definitely also going to keep at the back of your mind is, you can give your question about a person that has like, we love to test this weird association between IGG4 related diseases and GI pathologies, right? If you see that, don't forget retroperitoneal fibrosis. Retroperitoneal fibrosis is one of those weird bizarre things that also happens in people that have IGG4 related disease. IGG4 related disease is just disease where people for some reason, they have fibrosis of weird organs in the body, they have like weird autoimmune problems, right? And when you check those people's serum, they have elevated levels of a specific kind of IGG called IGG4, right?

So those people, they can have retroperitoneal fibrosis. That's a high yield association to know. Another thing they can also have is they can have autoimmune pancreatitis, right? So those antibodies can begin to attack the pancreas, right? They can also make autoantibodies against their gallbladders, right? So they can have like an autoimmune colicistitis, right? And then it's very high yield to know that these people, they can actually give you a question where they tell you that this person has a painless rock heart thyroid. Now, say that again, this person has a painless rock heart thyroid. If you see that, I want you to think about right delves, thyroiditis, right? Right? Right delves, thyroiditis, right? Delves, thyroiditis. That's a very classic pathology that's common in people that have, in people that have IGG4 relief data disease, right? Now, for those of you that are taking step one, right? Again, what are some other weird things they love to test with? Like again, like anatomy and stuff of the GI tract. And again, I would like to introduce some step 2-seeking integrations. That's why you see I'm just calling this a gastroenterology review, right? So like, you'll be useful for anyone studying from step one all the way to step three.

I feel like for those of you taking step 2-seeking step three, if you actually kind of listen to these step one parts, it will help you understand quite a bit of pathophysiology so that the stuff you're learning for step 2-seeking step 3 will become like a joke to you. It will become like very easy because you actually understand like what in the world is going on. And as you're seeing, we're going to keep making a lot of integrations, right? So it's almost like I'm just calling across everything all the way from step one to step three. But again, it will be useful for anyone that's in Med School that's going to be taking any of these, you'll see my exams. And for those of you that are taking step one, some of this step 2-seeking step three stuff that I'm supposedly mentioning, believe it or not, some of those things I've studied showing up on the Morrison exams because again, step one, you're trying to make it as clinical as possible, right? Because that's the big, bigger issue. I mean, people have had with it that, oh, it's just a memorization-based exam, doesn't have much clinical relevance, blah, blah, blah, blah, blah, right? It does have clinical relevance, right? And as you'll see, if you learn the clinical context behind many of these pathologies, a lot of it is just a lot easier for you to pick up. And again, it will also benefit you as you kind of rolling to your third year. Okay, your clinical rotation.

So how do we reabsorb many of these keep, I mean, I'm not going to talk about how you reabsorb every single thing, right? But let's talk about some key high-yield things that are reabsorbing the GI truck, right? So the first one has carbs, right? So we know that digestion of carbohydrates begins in the mouth, right? We know it all starts in the mouth with civari amylies, right? So again, this is what is one way your friends at the end of the meal love to go after this concept. Well, they love to go after this concept in scene. If you can pick the most sensitive test, like the more, let me put it this with the more sensitive lab marker for the diagnosis of acupuncturitis, right? So remember, in pancreatitis, acupuncturitis, the presence amylies will be elevated. And the presence light piece will also be elevated, right? So which one is more sensitive? It's going to be the light piece, right? Because again, remember light piece pretty much comes from your pancreas for the most part, although it can come from all the parts of your body, but the pancreas is the big one. Would amylies can be elevated for many different reasons, right? So it may be elevated because you have acupuncturitis, but it can also be elevated because you have a lot of vomiting, right? So they can give you a question about a person that has anorexia nervosa and say, oh, which of the following will be most likely elevated in this patient? Pick amylies, right?

Pick amylies because people that have anorexia nervosa, right? You know, if they puke as their preferred method of getting rid of nutrients and stuff, right? The amylies is going to go up, right? So again, remember amylies can come from the saliva from your salivary glands, but you can also come from your pancreas, right? But light piece is more specific in the diagnosis of acupuncturitis, right? So, vocal hydrics, right? Remember, you begin that digestion in the mouth with salivary amylies, and then when you get to the small intestine, right, we have these dysaccharidesis, right? The dysaccharidesis, you literally find them on the brush border of the small intestine. They essentially break down these dysaccharides to monosaccharides, right? They break down these dysaccharides to monosaccharides. So what's one pathology of friends that the MIMI can introduce here? Well, they can give you a question about a person that has a lot of bloating and a lot of diarrhea that is temporarily associated with the consumption of food, right? That is temporarily associated with the consumption of food. If you see that, you want to think about a lactase deficiency. I'll say that again, if you see that you want to think about a lactase deficiency, right? Remember lactase deficiency, these people usually not have any physical exam abnormalities, they will not have any lab abnormalities.

If you see physical exam or lab abnormalities, that excludes lactase deficiency as your diagnosis on an MIMI exam, right? So that can be lactase deficiency, and sometimes you can have like almost like an acquired lactase deficiency, after they have like a really, really bad gastroenteritis on an MIMI exam, so again, remember those dysaccharides is you find them on the surface of the GI tractor, you find them on your brushboarder, you find them around your microv-line, right? So they literally break down those dysaccharides to monosaccharides, right? And then one of the things that your friends at the MIMI can integrate on MIMI exams is there is a particular kind of dysaccharides that is known as alpha glucosides, right? It's known as alpha glucosides. So what's the deal with alpha glucosides? The thing with alpha glucosides is that it's a dysaccharides that helps you break down some of your carbohydrates, but the thing is they some pharmacology associated with it, right? Especially if you're trying to treat a person that has diabetes, you cannot really prevent them from reabsorbing that type of dysaccharide, right? You can prevent them from reabsorbing that type of dysaccharide, right? So if you, because remember your body cannot reabsorb dysaccharides, it can only reabsorb monosaccharides, right? So if you inhibited a dysaccharides, then that glucose or whatever, or hung out in your GI tract in the lumen of your GI tract.

And then, I mean, the the dysaccharide will hang out in the lumen of your GI tract and those dysaccharides, right, they have a ton of OH groups, a lot of hydroxy groups, so they are very osmotically active, right? So because you're osmotically active, they're going to draw a lot of water into the lumen of the GI tract. So you know, you're pretty much preventing reabsorption of sugar. So that's good for diabetes, right? But you're going to really begin to see that those things can cause some other problems, right? I mean, those people like this, you don't want to see close to them on a plane ride, you don't want to see close to them on a train or something, right? Because those people, they're almost like biological weapons in and of themselves, right? I mean, they are farting on all these things, right? Because they're pretty much going to have a diarrhea, they're going to have flatulence on all those things, right? So what are the diabetes drugs that work as alpha glucosides inhibitors? The alpha glucosides inhibitors, you should be thinking about things like acarbose and miglitol, right? Acarbose, ACAR, BOSE, acarbose and miglitol, those are alpha glucosides inhibitors that are used to treat diabetes, right? So we said that, okay, so let's kind of get back on track here, right? So we said that these dysaccharides is they break the dysaccharides into monosaccharides, right? So how do you reabsorb that stuff, right? Well, on the epics, right? The lumen, right?

The lumen side of the GI tract, right? Remember, we have SGLT transporters, right? Those SGLT transporters, they work for all monosaccharides. But on that epics, there is actually a specific kind of transporter that helps you reabsorb fructose, right? The helps you reabsorb fructose. Remember, fructose is actually reabsorbed on the epics, on the epical surface of the entire sites of the GI tract, right? By glut 5 transporters, right? By glut 5 transporters. Remember, glut 5 transporters are also found in sperm, right? Remember sperm uses fructose as its source of energy, because it has to swim pretty energetically to get into that woman, right? And then also remember that those SGLT transporters, we don't just find them in the GI tract, we don't just find them on the surface of the entire sites of the GI tract, we can also find them in the nephra, right? Especially at the level of the proximal convoluted tubules. If you want to get a lot more specific here, you'll find them at the level of the, you find the SGLT two isoform, right? On the epics of the proximal convoluted tubules, right? So obviously, those SGLT two transporters, what are they, right? So their SGLT literally means sodium glucose links transporter, right? Sodium glucose links transporter, right? So what's the high-yield thing your friends at the MBM will have to test here across all the USML Es?

Well remember that first of, I guess maybe for people that are taking step one, the fact that it's a sodium glucose links transporter, that means it's a transporter that takes advantage of the gradient energy of sodium to reabsorb glucose, right? It takes advantage of the gradient energy of sodium to reabsorb glucose. So what's that gradient energy, right? Remember, the sodium potassium ATP is pumped, what it helps us do is it helps us pump three sodiums out of a cell and brings two potassiums into the cell, right? So it takes out three sodiums, brings in two potassiums. So the thing is sodium is primarily an extracellular ion. So the thing is when sodium flows from outside the cell like the lumen of the, of the proximal convoluted tubule of the urine side, all the way to the inside, right? It's flowing down its gradient. You can use that gradient, right? To move glucose against this concentration gradient from the lumen of the GI, from the lumen sorry of the, like the urine side of the proximal tubule, all the way to the intracellular space of the proximal convoluted tubule cells, right? So that's an example of secondary active transport. That's a high-yield concept that your friends at the NB may love to test, right? So the thing is if you wanted to be a diabetes drug, it probably makes sense that you can inhibit this SGLT2 transporter, right? So you can inhibit those transporters, right? You can use drugs the or ending flossing, right?

So drugs like canagly flosing, that pagly flosing, and pagly flosing, right? Those are SGLT2 inhibitors that can help you pretty much reabsorb it, I mean inhibit the SGLT2 transporter, right? So that you don't reabsorb that glucose, right? And that those drugs actually work pretty well. But again, you can really begin to see what the side effects of the drug can be, right? It can literally be something along the lines of, because think about it, all that sugar that's in your urine. Remember this bacteria in your urine just starts, right? Obviously, you're going to have a great party. You're pretty much going to be organizing things given for these bacteria, because so far all the sugar you're putting in your urine, right? So urinary tract infections are key key key side effects of these drugs. In fact, the person that's diabetic, right? They can have like necrotizing fasciitis around like their, you know, like around your perinium from this drug, right? So they can have like phony's gangrene. Remember phony's gangrene? F-O-U-R, N-I-E-R, right? Phony years gangrene is basically neck fasci of a presence, a so necrotizing fasciitis of a person's perinium, right? So that's a very well established complication of these S-J-O-T-2 inhibitors. So that's something you want to keep keep at the back of your mind. You can even get like candidol, like vaginal infections and things like that, right?

So remember candidol infections, real cottage cheese appearance, peach of the vaginal secretions will be less than 4.5, right? So again, you just want to keep those things at the back of your mind on the exams. So again, let's go back to the enterocytes, right? of the GI tract for carbary absorption, right? So we said carbs, right? On the epical surface, again, we said all the monosaccharides, the area absorbed through S-J-L-T transporers, right? On the apex of the enterocytes of the GI tract. And then remember, for fructose, specifically on the apex, again, notice there's a big difference between the apex. The apex is the site facing the lumen. The basal site is the site that's facing the, that's facing like your blood vessels, right? So essentially the thing that happens is, again, apex S-J-L-T transporers help you reabsorb all monosaccharides. And then, glute 5 transporers, again, on the apex, specifically helps you reabsorb fructose, right? But on the basal surface, we have these glute 2 transporers, right? These glute 2 transporers, they are the things that show to all your monosaccharides, all clued in fructose to the bloodstream, okay? On the basal surface, the glute 2 transporers, right? Now, I said that for carbs, you can only reabsorb monosaccharides. That's kind of different for proteins, right? The thing is for proteins, you actually have the ability to reabsorb dipeptides and tripeptides in the lumen of the GI tract, right? So how those protein digestion happen?

Well, the first thing that happens is, you know, the pH of the stomach is pretty low, right? And it's around two, because of those parietal cells that's making like a ton of acid through that hydrogen potassium anti-porer, right? Remember, that's the thing that's inhibited by your pertin pump inhibitor, like omega-pursol, S-O-M-Pursol, and so-Pursol, Pantopursol, right? All those presoles, right? So that LOSTOMA-P, right, you know, helps with the conversion of pepsinogen, which comes from chief cells to pepsin, right? And then pepsin in the stomach, right? Remember, pepsinogen is the zymogen form, but pepsin is the active form, right? So that pepsin, its job is basically, we'll bring down proteins into amino acids, right? You'll bring down those proteins into amino acids, and, you know, if you bring down those proteins into amino acids, you can reabsorb them in the entire site. This is actually one pathway of protein reabsorption, right? So, and remember, the kinds of amino acids that you have actually kind of depends on how they are reabsorbed, right? So the thing is, if you have like a neutral amino acid or a basic amino acid, that's actually reabsorbed by faceted diffusion, right? So it diffuses down, but it does that in a faceted fashion, right? So that means you need some kind of transporter to make that happen, right? But then for all that kinds of amino acids, right?

So basically, all the kinds of amino acids that are not neutral, that are not basic, are you actually use a like sodium linked transport, right? So again, that gradient energy of sodium is really used a lot in secondary active transport of autonomous stuff in the GI tract, right? But then remember, protein digestion does not just only start in the stomach, you know, you can also have some stuff happen in the small intestine, right? So how does that happen, right? So remember, the pancreas, right, can one of its enzymes, it can release something called tripsinogen, right? It can release tripsinogen again, that's a zymogen, so obviously it's going to be inactive. The thing with that tripsinogen is, it can be converted by an enzyme known as enterocainase, and enterocainase will convert tripsinogen to tripsin. And then tripsin can actually help you digest protein, but one of the major things that your friends at the MBM love to test that tripsin does is that it actually activates two other enzymes, it activates an enzyme called a caboxypeptidase, it also activates peptidase, right? That tells you that, oh, this is something that probably breaks peptide bonds, and then chymotripsinogen is another zymogen that it also activates, right? And those things again help you break down proteins into amino acids. But again, remember, this tripsinogen will come from the pancreas or come through the blood and through the sphincter of ody.

So again, just how you know all those are how you think with regards to carbs and proteins, I guess I can also talk about fat absorption. I'll just talk about that and then I'm going to go ahead and stop because I want to keep these to roughly 30 minutes. So although I also talk about a step one course at the end, that I'm holding on the 5th to the 9th of April next month, it's a 40 hour course, but let's finish this off first. So the fats, right? So how do we deal with fats? The thing is fats actually partially broken down in the antram of the GI tract, right? But that's a minor pathway. What's the big thing that happens? Remember, your eye cells in the duodenum, right? You release an enzyme known as CCK, colicisto, chinin, right? Colicisto, right? So coli, that means it's something that targets that goes after your gallbladder, right? So it goes to the gallbladder, right? So one of CCK basically has two jobs. First thing is it goes to your gallbladder, tells you gallbladder, okay, let's contract, quick, quick, quick, quick, quick, quick, quick, quick, quick, right? And then you square out bile, right? Square out bile. But another thing it also does is it goes to your pancreas, right? CCK tells your pancreas to make lipids, right? To make lipids, to make lipids. I'll say that again, CCK goes to your pancreas and tells you to make lipids. It's very high you to know, for example, right?

And we can see why when people have like colinolethyases, they try to avoid eating because if they eat those eye cells into the duodenum will see that fat and then they're going to secret colicisto chinin and then that's going to cause, again, your gallbladder contract, then your gallbladder contract on those rocks and that's not going to be a very pleasant experience, right? The person is going to have a ton of pain, right? The person will basically be eating like a limit until they can get that gallbladder removed, right? So what does lipids do? Remember, lipids, you know, it converts triglycerides, remember triglycerides, right? Literally look at the name triglyceride, right? Traglyceride. It is basically glycerol, which is an alcohol, right? That has three hydroxy groups, right? For those of you that, you know, affectionately love organic chemistry, glycerol is essentially from non-stickian propane 1, 2, 3 trial, right? I used to teach anterior actually a ton of organic chemistry, but love all chemids are pretty fun subject. But that's a different conversation. But it contains glycerol, right? But instead of those OH groups, right? You strip of those hydrogen ions and then you put a ton of fatty acids, right? So triglycerides are basically glycerol and 3 fatty acids, right? So the lipids converts it to monoacylglycerol and 2, 3 fatty acids, right? So that means one of the fatty acids are still connected to the glycerol backbone, right?

But then you form 2, 3 fatty acids, right? So when you say 2, 3 fatty acids, right? Those things form my cells, right? So the MICE double LES, right? Those my cells, the thing that helps you, you know, kind of form them is bound, right? And then again, these fatty is absorbed by the interocytes. But the thing is, because the thing is that triglyceride cannot be reabsorbed, right? But if you have monoacylglycerol and these 3 fatty acids absolutely, they can be reabsorbed, right? So they are reabsorbed by the interocytes of the G-Extra. But the thing is once they get reabsorbed by the interocytes of the G-Extra, guess what? They're going to be re-meeting to triglycerides, right? So it's almost like you break them down, right? So that they can go through, right? And then after you break them down so they can go through, right? They then re-meeting to triglycerides inside the interocytes of the G-Extra. That's actually done in the smooth endoplasmic reticulum of the interocytes of the G-Extra. Again, it's just some of these small annoying nagging details that your friends at the MDME, they love to test an exam, right? So they're remedi into these triglycerides in the smooth endoplasmic reticulum, right? So smooth endoplasmic reticulum is actually expressed pretty heavily in the interocytes of the G-Extra. So and then as they're remedi into triglycerides in the smooth endoplasmic reticulum, your reverendoplasmic reticulum does not sit around, right?

Your reverendoplasmic reticulum, remember the fact that it's rough endoplasmic reticulum means it's endoplasmic reticulum, that is studied with ribosomes, right? So at this point you've transcribed, you've translated the gene for epobye 48. And in that epobye 48, you know, binds up with those triglycerides, right? And you form chylomicrons. And in those chylomicrons, right? They go into those lymphatic vessels, they go into those lacteels, L-A-C-T-E-A-T-E-A-L-S, right? So they go into those lacteels, they are absorbing into the lymphatics, right? They go into the circulation, and then those things go to your peripheral cells, right? And then you have all this stuff that happens with our cholesterol, our metabolism with our L-Cat, E-Cat, epo-A1, epo-C2, yada, yada, yada, right? So I think I'm going to go ahead and stop here. And then again, I said, I will speak to the courses I have coming up again, for those of you who have been studying for step one, I have a 40-hour course that's coming up early next month. It's from the fifth to the ninth of April. It's a 5-D course, right? It's 40 hours, it's eight hours each day. Very high-yield course, again, you'll learn a ton, review about 4,000 concepts. Actually, it's going to be actually very likely more than that, about 4,000 concepts that are tested on the US and the US step one exam.

And again, for those of you that are either at the end of your dedicated period and you're about to take your exam, it'll be a very, very good way to just pull everything together for you in 5 days, over 40 hours, right? It's eight hours each day. Very intensive course. For those of you that are going into your dedicated periods, right? Again, in 40 hours, you'll pull everything together and it'll help you walk into your dedicated period with a very solid understanding of stuff, right? So what's the thing that's unique about this course compared with other courses that are available? Because again, I know there's a lot of step one courses available. The thing that makes my courses unique is one, as many of you have seen from my podcast, I'm very good at integrating things across multiple disciplines. So that's something that's going to be happening a lot during the course, too. I love to go with context. Again, I'm not just going to be giving you, like, again, you see, like a lot of what we did today was anatomy and embryology, right? But did you see me just spend my time just giving you factoids, factoids, factoids, factoids without context? No, no, no, no, no, no, I don't do that, right? So for me, I'm a very big, big, big believer in giving people context and giving people an understanding, right? So I will not just teach you concepts, I will teach you those concepts in the context of how they will be tested on the USML exams, right? So I'll give you that context.

I'll make different integrations, right? And a lot of what I'm going to be going over that, I'm going to be going over clinical cases, I'm going to be going over vignettes, right? Again, that will highlight those contexts that your friends at the NV Me love to go after. And obviously, I will spend a lot of time explaining pathophysiology, right? Again, I don't like just teaching people facts, I'm going to do a lot of explaining, right? So that you'll come away with a very solid understanding of stuff, right? And then for those of you that are taking step two, see key step three, they're going to have a 16 and a half hour course taking place from the 25th to the 27th of this month, right? Of April. I mean, sorry, of March. And then on the 24th, I obviously have an NV Me test-taking strategy course that goes for two and a half hours. So if you're interested in any of these courses, just shoot me an email through the website and I'll give you information on it, I'll give you information on payments, on how to pay and all that stuff. I want you to make payments. You'll be interested for the course. The course will be a group course. It'll be held over Zoom. And then please subscribe to the website, divineinterventionpodcast.com. And then also, I have these podcasts on Google podcasts, on Apple podcasts, on Spotify. If you want to please subscribe to them. I also have a You Tube channel where I have a bunch of videos, divine intervention, USML podcast and videos.

Please feel free to subscribe to those again, any bit of support, positive feedback, definitely, definitely helps. And also just any corrections or things you would like me to change definitely helps. So I want to go over and life less and real quick today. And this was actually something that I talked about in church yesterday, right? So, you know, the grace of God, I get opportunities to preach in church because I, as you can see from this podcast, obviously, love teaching. So, you know, I love to teach in church. So, you know, one thing I talked about in church yesterday, but I think it's pretty applicable to to med students, right? Is people that are in healthcare is the value of immediate obedience, right? So you see people, they keep kicking things down the curb, kicking things down the curb, kicking things down the curb, kicking things down the curb, right? And then as you keep kicking things down the curb, you're like, man, how am I, how do I keep feeling? How do I keep not succeeding in life? How do I keep getting stressed? The thing is many times the stress that people go through in life, it kind of created for themselves. Again, don't get me wrong, you know, people falling to unfortunate circumstances, you know, they lose a loved one, COVID-19 happens, you know, weird stuff happens. That's understandable. But I will tell you this again, just having worked with thousands of students in my lifetime, I've seen this step.

A lot of people, they postpone things, they keep postponing, postponing, postponing, postponing, postponing. They don't do things at the right time, right? The thing is if you do the right thing at the right time, you can achieve greatness with little stress, right? With relatively little stress, that's just a truth, right? Or you see people, the weight still the last minute, they are studying for step one, the weight still, their schools dedicated period, and then they wonder how they are studying off and they are getting scores in the 150s, on envy me practice exams. Again, it breaks my heart when I see people go through all these problems because these are things that are largely avoidable, right? So for example, take for example, for me, right? When did I get into medical school? You know, I got into Johns Hopkins, you know, by the grace of God in 2014, right? You know, I kind of had this figure in out phase of life, you know, or studying anatomy, blah, blah, blah, blah, blah, you know, it's kind of intense, at Hopkins then, anatomy was seven weeks, right? And not having seven weeks with dissections and everything is pretty brutal, right? Or do I learn to come from those from an anatomy course? It was a very first-rate course. But the thing is, I've got to figure things out, you know, kind of like the first few months of med school. I think it was like four months. I was like, you know, let me just kind of get my feet on them and all that stuff.

If I'm not mistaken from January of 2015, which was like, midway through my first year, I started studying for step one day, right? I started doing just a long-duty, no studying, right? I studied just, you know, on a, I mean, did I do every day? No, but I was pretty consistent in what I was doing. I studied pretty consistently for months, right? So when I was a school administrator at CCSE exam, I was already doing really well. I was already above the average step one score on my CCSE exam just to start literally, right? So the thing is, and obviously, right, like my degree period was very relatively cautious compared to what I see some people go through, right? All these things happened because I just chose, right? And these are things, right? Like, again, your life is defined quite a bit by your choices. It's not really defined by your background. I tell people this, don't, there's this famous Nigerian musician that said this thing. It's a gospel musician. Don't let your background put your back to the ground, right? So the thing is your background should not determine how far you're going live, right? It's really like some of the choices you make that really determine how far you're going live, right? And one of those good choices I'm encouraging you to take today, right? Is to do the right thing at the right time, right? Do the right thing at the right time.

If you will be at the right time, if you do the right thing, when you're supposed to do it, not like on a delayed schedule, right? Not procrastinating. You'll likely be able to succeed again with ease, right? Again, like, to be honest with you, many of my USMD exams, it was not the three, four weeks before my exams that really made any big difference. No, the big difference had been made because in the place of doing the right thing at the right time, right? In the place of deliberation, I'd need longitudinal commitments. And then I got the benefits of those things, right? So again, I know maybe like, man, the fine, you keep your up, your up, your up, your up and over the step, but you may say, why is it important to do the right thing at the right time? Well, the thing is, it really helps your mental health, right? You're not always stressed because you see a lot of med students, mental health crisis. Again, for many different reasons, and again, I'm not here to judge anybody, right? Again, people go through, I mean, I've worked with med students that I've had lots of losses of loved ones and all these things. That's true. But one thing that really contributes to stress amongst medical students and healthcare professionals is they don't do the right thing at the right time, right? And the thing is when you're stressed, right? You're not going to be mentally okay. That's the truth. When you're stressed, you're not going to be mentally okay.

It causes things like people becoming obese because of all that cortisol, right? And you remember cortisol is literally a stress hormone, right? So the thing is, but when you're at ease, when you're relaxed, because you've done the right thing at the right time, because you've done things in longitudinal fashion, because you've made long-term, long-range commitments, then you're not freaking out all the time, right? Again, did med school stress me out? Absolutely did. I'm not going to lie. Med school, especially med school, at Johns Hopkins, was really stressful. Although again, by the way, it was a great experience. If you get accepted at Johns Hopkins, you should probably go there. It's a great med school. I mean, I definitely see the benefits in my life right now, but that's a different conversation. But basically, because I was not as stressed, right? I did not start panicking. I did not start becoming depressed or any of those things, right? Just because I did the right thing at the right time. Again, if I mean mistakes in my life, yes, am I a perfect person? No, right? Again, remember, I'm a human being, I'm not Superman or whatever some people think. I am. No. I'm pretty basic, not more human being, like all of you, right? But many of you, you can avoid many of some of these things that really stress people, right? Because there are many stressors in Mexico where you can avoid some of them by just doing the right thing at the right time, right?

Doing the right thing at the right time, right? Start early, do the right thing, obey immediately, do the right thing immediately, right? Don't keep waiting, right? Even the Bible says that now is the time of salvation. Not 10 years from now. It says now. Today, if you hear my voice, right? Right? So now is the time of salvation, right? So do that thing now. Start preparing for a step one now. Start preparing for step two, see key now. Start preparing for step three now. Start preparing for your residency and training exams now, if you are a resident, right? So like just all these things, it will just help your life, right? And help you be successful. So thank you for listening to me up away. I hope you found this podcast to be helpful. I'll see you in the next series. So again, this is Gus Renorologist in series one. Thank you for listening. God bless you. Goodbye.

Embolic occlusion of the superior mesenteric artery (SMA), often due to cardiac sources like atrial fibrillation or recent MI.

The midgut (proximal two-thirds of transverse colon to distal duodenum) is supplied by the Superior Mesenteric Artery (SMA).

Re-esterified triglycerides (in smooth ER), Apo B-48, and phospholipids.

Lactose deficiency (Lactase deficiency).

The Inferior Vena Cava (IVC) and/or the aorta.

Retroperitoneal fibrosis, Autoimmune pancreatitis, and Dry/Delve's thyroiditis.

To reabsorb glucose from the filtrate (urine) back into the bloodstream via secondary active transport, utilizing the sodium gradient.

The Falciform ligament.

Skin $\rightarrow$ Superficial Fascia (Camper/Scarpa) $\rightarrow$ External Oblique $\rightarrow$ Internal Oblique $\rightarrow$ Transversus Abdominis $\rightarrow$ Transversalis Fascia $\rightarrow$ Extraperitoneal Fascia $\rightarrow$ Pariapitoneal Peritoneum.

The stomach uses pepsin to break proteins into amino acids; the small intestine uses pancreatic enzymes (like trypsin) which activate other proteases (e.g., carboxypeptidase, chymotrypsin).

Marked dilation of the transverse colon, typically exceeding 6 cm in diameter.

To reabsorb glucose from the filtrate (urine) back into the bloodstream via secondary active transport, utilizing the sodium gradient.

The Falciform ligament.

Skin $\rightarrow$ Superficial Fascia (Camper/Scarpa) $\rightarrow$ External Oblique $\rightarrow$ Internal Oblique $\rightarrow$ Transversus Abdominis $\rightarrow$ Transversalis Fascia $\rightarrow$ Extraperitoneal Fascia $\rightarrow$ Pariapitoneal Peritoneum.

The stomach uses pepsin to break proteins into amino acids; the small intestine uses pancreatic enzymes (like trypsin) which activate other proteases (e.g., carboxypeptidase, chymotrypsin).

Marked dilation of the transverse colon, typically exceeding 6 cm in diameter.