DIP Episode 185 - Updated USMLE Step 1 GI Review Series 1

Okay, welcome. My name is Divine. This is episode 185 of the Divine Intervention Podcast. And in this podcast, I'm going to be focusing on a gastroenterology review for the USML step one exam. I've made an intro podcast in the past, but I'm going to make this my first to like mainstream one. And then you'll be in a series and then we'll be done with a little bit of cheer. So let's get right into it. So what if you get a question about a 45 year old guy and they tell you that this guy has hypercowsimia and this guy has been having a, you know, these like severe episodes of like a big gastric pain that is not necessarily radiating to the back. And then the MBS asks you, what other finding would you most likely observe on a physical exit like one further exam and testing? What answer should you go with? Well, I will hope you go with hyperprolectimia, right? So this person has classic MN1 syndrome, right? So the thing is MN1 syndrome. Remember, it's a triad, right? And the way I think about it, it's a triad like you remember, it has parapan pit, right? So parapan pit, the parastands for parathyroid hyperplegia. So that's the classic presentation of primary hyperparathyroidism in those folks. And then two is these people tend to have pituitary adenomas. The most common one will be a prolactinoma. And then three, these people also tend to have, so parapan pit, so pituitary adenomas.

And then they can have pancreatic neuroendocrine tumors of which a gastronoma is the most common, right? So that's the thing that's causing the peptic ulcer disease in this patient, right? Although another thing that could also be causing peptic ulcer disease in this patient is hypercalcemia, because hypercalcemia actually increases the release of gastric. And that can ultimately cause a production of more gastric acid, right? And that can increase the presence risk of peptic ulcer disease, right? Well, this person has a gastronoma. I remember a gastronoma literally is a tumor that secretes gastric, right? And when you secret gastric, as I'll talk about shortly, you'll have an increase in your gastric acid secretion and you'll have things of that nature. So let's, I guess maybe talk somewhere about this, right? So how is gastric acid secreted? Well, obviously gastric acid comes from, comes from a parietal cells, right? Remember parietal cells, we find them in the stomach and those parietal cells, the secret to high yield things you want to know for the purposes of the USML exams, the secret like hydrogen ions, right? Through like a hydrogen potassium antiporter that you find on their surfaces. And the thing is, it's actually very high yield to know that that hydrogen potassium antiporter is an ATP. You may say, okay, divine. Why is it an ATP?

Well, it's an ATP is it because it uses ATP and it uses ATP because you're getting potassium into the cell against this concentration ingredient. Remember potassium is primarily an intracellular ion. So the thing is if you want to bring even more potassium into the cell, then you're essentially moving them in a green against the ingredient. And if you're moving, sorry, excuse me, if you're moving them in against the ingredient, right, you need ATP for that. So that antiporter takes potassium into the into the parietal cell and then it brings hydrogen ions out. So that's how you get the acidity of the stomach. And then another high yield thing that's secreted by your parietal cells is intrinsic factor. Intraseg factor is what is used together with vitamin B12 to help you essentially reabsorb vitamin B12 at the level of the terminal Ilya. So how do we ultimately release gastric acid? Well, the thing is it all starts with the vagus nerve. So the vagus nerve actually can release something known as gastrin-releasing peptide, okay? That gastrin-releasing peptide will literally act on G cells that you find in the antrum of the stomach and then those G cells will make gastrin, right? And then that gastrin, it can do multiple things. One thing you can do is it can talk to your parietal cells directly to go ahead and make acid. Another thing you can do is it can also talk to a certain kind of cell known as the enterochromophine-like cell.

The enterochromophine-like cell is in fact this is actually the main mechanism that gastrin helps with causing acid release in the stomach. So gastrin will bind to receptors on the surfaces of the enterochromophine-like cells. I'll call them ECL cells going forward and then those ECL cells will then release histamine and then that histamine will act on H2 receptors that will find on the parietal cells. Remember, those are G protein-copyred receptors. If you want to be a little more specific, they are G stimulatory, so Gs, G protein-copyred receptors, that will increase the activity of a denolite cyclase and that will cause acid secretion. So it should make sense that if you want to shut down acid secretion, one thing you can actually do is to give a H2 blocker, a H2 histamine receptor blocker, like a drug like famodidine or anidine or cymedidine, remember cymedidine is an inhibitor of cytochromp 450. So when you inhibit those H2 receptors, then you essentially inhibiting that ECL cell, mediated release of acid. So that's one of how you'll think to know. Another how you'll think to sort of keep at the back of your mind with all this acid secretion is that the vagus nerve can also directly stimulate most granic and three receptors that we find on the surface of parietal cells and if you stimulate those most granic and three receptors, then that can also increase the release of acid in the GI tract. So let's back up here for a second.

So what are the key things that cause acid secretion? We said that the vagus nerve can directly stimulate most granic and three receptors on parietal cells, that's one. Second thing we said is that the vagus nerve can release something known as gastrin-releasing peptide, which will act on the G cells that we find in the antrom of the stomach and then those G cells release gastrin. Now we said that gastrin can directly stimulate parietal cells. That's a smaller mechanism, but the more bigger mechanism is that gastrin can also act on ECL cells, which then in turn release histamine and in that histamine acts on H2 receptors and then that promotes the release of acid from parietal cells. This pathway is very high to make sure you understand. Now the thing is on these parietal cells, we also have receptors that are sensitive to Prosteglandins, okay? The thing is those receptors though are also G protein-copyred receptors, but they are inhibitory G protein-copyred receptors. So the thing that happens is when Prosteglandins bind to those GI-based G protein-copyred receptors, that will decrease the amount of adenylocyclyce that prevents the parietal cell and that will show down the release of acid, right? So this is one of the reasons why taking an insect can cause pepticoster disease, because when you take an insect, insects and inhibitors of cox of cycloxygenies, and cycloxygenies is involved in the production of Prosteglandins.

So if you take an insect, you inhibit cox, you have less synthesis of Prosteglandins. If you have less synthesis of Prosteglandins, you have less activation of those inhibitory G protein-copyred receptors that you find on the surfaces of parietal cells, and that will cause an increased release of acid, and that can predispose the person to having pepticoster disease. So that's the mechanism behind insects increasing a person's risk of pepticoster disease. And if you notice, I said that those are that hydrogen potassium ETP is pumped that you find on the luminal surface of a parietal cell, right? I said again, that's the primary transporter that's responsible, not transporter, but primary pump responsible for the production of acid in the stomach. The thing is you can actually make antibodies against that pump, or you can make antibodies against the parietal cell as a whole, or you can make antibodies against intrinsic factor, and that's the pathophysiology behind pronissious anemia, right? Because think about it, if you knock the parietal cells out of circulation, and you no longer make intrinsic factor, then you will not have the marriage partner of vitamin B12 to have the ability to reabsorb B12 at the level of the terminal area. That's one high yield thing to know there. Second high yield thing to know there is that we have a class of drugs that actually work by inhibiting that hydrogen potassium antipotor, they are known as the proton pumping inhibitors, right?

Because literally that hydrogen potassium antipotor is a proton pump. So if you have a drug that inhibits that pump, it should make sense that it's known as a proton pumping inhibitor, a PPI. So the thing is those PPI's didn't inhibit that pump, and those drugs all end in the prezole. So they are very easy to recognize on exams, right? So drugs like Omeprozole, Lansoprozole, Esomeprzole, Pantoprozole, those are all PPI's and they all work by inhibiting NAPROTOMP, that you find on the surface of parietal cells. And then again, kind of time back to what I mentioned initially, talking about a person that had anemia in one. Remember, anemia in one, they can have pancreatic neuroinduclein tumors, well one of the pancreatic neuroinduclein tumors they can have is a gastronoma. Remember, that's something known as the Zolinger-Elicin Syndrome. One classic presentation of the Zolinger-Elicin Syndrome on NV Me exams is they'll talk about a person that has ulcers, but they'll tell you that this person has ulcers in the jidruna. When a person has peptic ulcer disease, it is extremely unusual to have ulcers that are that distal. So if you see like distal ulcers in the small intestine, EKE the jidruna, or like a distal, doodinal ulcer, you want to think about Zolinger-Elicin Syndrome as a possibility theology.

And really, the way you treat a gastronoma is obviously you want to remove the tumor, but some other measures you can also explore right, obviously, is to give a PPI, because ultimately the thing that's causing many of your symptoms, right, is the fact that you have the gastron coming from the gastronoma, stimulating the parade of cell directly, and also stimulating the entire chromatin like cell to cause problems. So if you have the ability to inhibit that end gateway, of acid secretion in the GI tract, EKE the proton pump, then you can fix that presents our problems. Another drug you can also give is you can actually give oxygenate. So, chiro tide, it's a somato-studying analogue, what the thing it does is that it essentially inhibits the secretion of many things in the GI tract, and it can directly stop the parade of cells from making acid, and it can also directly stop the G cells. So these are all high yield important things to know for the purposes of exams. So again, make sure you can sort of put all these things together, and one other thing I guess I will mention that's kind of important that many people do not realize is that. Remember that many people think in fact this is one common ploy, the MME plays on people. They will try to get you to think that G cells that make gastric, because again remember I said oh it's the vagus nerve of parasympathetic system that stimulates G cells to secret gastric, right?

So the MME will try to trick into picking acetylcholine as the direct stimulant of G cells to make gastric, resist that temptation on your exams. Gastring secretion from the G cells is promoted very specifically by gastring releasing peptide. So it's the vagus nerve that is actually making that gastring releasing peptide that is then stimulating those G cells. So again, very high yield, very important to make sure you actually understand what's going on with that. So what are some I guess other important things that kind of happen in the stomach, right? So remember that the stomach also has chief cells. Those chief cells they make a particular zymogen known as Pepsi no gene, okay? So Pepsi no gene, right? It's the zymogen form of an enzyme known as Pepsi. The thing is that Pepsi is the thing that actually helps you start protein digestion. So protein digestion actually starts in the stomach, right? And it happens under the action of Pepsi. But the thing is those chief cells do not make direct Pepsi, they make Pepsi no gene. And then that Pepsi no gene when it's exposed to the low pH environment of the stomach, it's then cleaved from the zymogen form to the active form known as Pepsi. And then you have protein digestion. And then remember that we also have some cells in the stomach, right? Like sometimes they call them just mucosos cells. Those mucosos cells they make a bicarb. And that bicarb will help you protect the GI mucose, will help you protect the GI mucose.

I mean, stomach mucosa from erosion, right? Because again, the pH of the stomach is like two. It's very, very acidic, right? So the thing is you need a bicarb to kind of help you with, to kind of help you with that process. So that bicarb comes from just certain mucosos cells that directly make bicarb to coat the lining of the stomach so that again you don't essentially like denude your stomach mucosa. And from a histological perspective, it's very high you to know that your stomach is made of simple columna epithelium, okay? The thing is the histology of the GI tract in general is very, very high you to know for the purposes of the USML exams, right? So your stomach has simple columna epithelium, okay? The stomach has simple columna epithelium. So really for the most part, those are kind of like the big things that are secreted in the stomach. And remember, like I said, if a person has pernicious anemia, you're not making intrinsic factor, you'll get a B2 O deficiency. And obviously, a B2 O deficiency can cause lots and lots of problems, right? Like people with B2 O deficiency, they can get like a peripheral neuropathy, right? And when you have a B2 O deficiency, remember, that will also elevate your levels of homocysteine, right? And then if you also have a B2 O deficiency, remember B12 is a co-factor for the enzyme known as methylmalonoco-A-mutease. So if you have a deficiency of B12, methylmalonoco-A-mutease will not work.

So you lose the ability to convert methylmalonoco-A to succino-CoA. So that's why a methylmalonica-sedemia is patholomonic on NVM exams of a B12 deficiency. And then you should also not forget that a B12 deficiency can also cause amygdala-blastic anemia because you're kind of missing of DNA synthesis, right? So if you're not able to make DNA, then you can get into trouble with amygdala-blastic anemia. And classic period, I don't know, bloodsmen, you'll see the classically described hypersegmented neutrophils with that. And then one final thing that a person can also get with a B12 deficiency is that they will get something known as a subacute combined degeneration of the spinal cord, okay? A subacute combined degeneration of the spinal cord, basically your lateral corticospinal tract will be screwed up. So those people will have like opameron neurons symptoms. And then another thing that will be screwed up is the dorsal columns, right? Your dorsal column median, let me discuss system. So you have problems with like fine touch, vibratory sense and perceptive sense, okay? So again, those are all high your things to know in relation to vitamin B12. Now, one other thing your friends at the NV Me kind of expect you to know with regards to the GI tract, especially since I've kind of talked about the stomach, is just kind of knowing the blood supply. I've probably said this at NOSM in multiple podcasts, but this is just something that people find as a bear to memorize.

To be perfectly honest with you, the easiest way to learn this stuff is just to draw it out. If you draw it out and go over it a couple of times, it will stick in your mind, okay? Draw it out a couple of times, it will stick in your mind. So the thing is your GI tract, embryologically is divided into three major groups. We have the foregots, we have the midgot, and we have the hindgot. So you may see, oh, divine, what mix of the foregot? Well, the things that make up the foregot are things like your stomach, your duodenum, right? At least like the first and second parts of the duodenum. Essentially everything in your duodenum up until the ligament of trites, or you can see maybe the ampoule of water if you want to, either one it really doesn't matter, but up until that level, that's your foregot. Your foregot also includes things like your gallbladder, your liver, your spleen, and some like your softness for the most part, you can also technically call that foregot, okay? So that's something that's very high you have to know. And then your midgot is everything from like the rest of your duodenum, that does not include your foregot to the proximal two-thirds of the transverse colon, okay? And then your hindgot is everything from the distal end, basically from the spleenic flexure to the upper third of the rectum, that's your hindgot. So why is it important to differentiate things like this?

It's important to differentiate things like that because your foregot has a specific blood supply, it's the cilia cardry, your midgot has a specific blood supply, it's the superior misenteric cardry, and your hindgot has a specific blood supply, it's the inferior misenteric cardry. Remember it's very high you to know that the inferior misenteric cardry is the blood supply to the hindgot. And remember that your hindgot ends just at the pectinic line, the pectinic line is basically like takes up like the upper third of the rectum, okay? So the upper third of the rectum and then like your sigmoid colon and then your descending colon and then like your spleenic flexure, those all fall under the purview of the hindgot and they are also applied by the inferior misenteric cardry. Basically your mucosa below the pectinic line is actually serviced from a blood supply perspective by the internal ilia cardry, okay? In fact the blood drainage for that like distal to the pectinic line like the lower parts of your rectum, that's actually goes directly to the IVC versus like your hindgots like again like the part above the pectinic line that actually drains into ultimately drains into the into the portal vein. So that's something you don't want to screw over, right? So again the senior cardry supplies the foregot, the superior misenteric cardry supplies the midgot and then the inferior misenteric cardry supplies the hindgot.

So let's talk about the silia cardry and kind of like its branches, those are kind of important So the silia cardry again, it comes off of the thoracic yoder, okay? So it comes off of the thoracic yoder and then it has three major branches, right? The three major branches, there's one known as the left gastric artery, that's the first major branch. The second branch is known as the spleenic artery and then the third branch is known as the common hepatic artery, okay? So I'll say that your silia cardry has three branches, it has the spleenic artery, the left gastric artery, and the common hepatic artery, right?

Now the thing is the spleenic artery ultimately gives rise to another artery known as the spleenic artery actually gives rise to the right, no no no, it gives rise to the left gastroepiploic artery, the left gastroepiploic artery is occasionally known as the left gastro-omental artery, you'll see that if there is a left gastro-omental artery, you'll see in a few seconds that there's also such a thin known as the right gastro-omental artery, the right gastro-omental artery actually comes from an artery known as the gastro-doernal artery, let me back up here for a second, so the big branch of the spleenic artery is the left gastroepiploic artery, now the left gastric artery doesn't really have any significant branches, beyond let's just see left gastric artery is one branch of the spleenic artery, I'll leave it like that, now the thing is the common hepatic artery actually has three branches, right? One branch is what's known as the right gastric artery, okay? So that right gastric artery and as to Moses with the left gastric artery, which is a branch of the actual spleenic artery, so spleenic artery gives off the left gastric artery, and then the common hepatic artery, which is one of the main branches of the spleenic artery, gives off the right gastric artery that are an asthmosis with that left gastric artery, and the anastomosis is actually along the lesser coverage of the stomach, okay?

Now, so I've said the common hepatic artery gives off three major branches, one major branch is the right gastric artery again that an asthmosis with the left gastric artery, which is a branch of the cilia, the second major branch of the common hepatic artery is the hepatic artery proper, okay? And the hepatic artery proper divides further to form the right hepatic artery and the left hepatic artery, okay? So let's trace it down again. Cilia artery gives rise to the common hepatic artery, the common hepatic artery gives rise to the right gastric artery, it gives rise to the hepatic artery proper, and that hepatic artery proper gives rise to the right gastric artery, I mean, sorry, to the right hepatic artery and the left hepatic artery. It so happens that the right hepatic artery gives off the cystic artery, the cystic artery is the blood supply to the to the to the gobladder, right? So again, two big branches I've talked about with the common hepatic artery, hepatic artery proper that gives off the right and left hepatic arteries and then the right gastric artery that anastomosis with the left gastric artery, which is a branch of the cilia, now the third major branch of the common hepatic artery is an artery known as the gastro-bordinal artery, okay? The gastro-bordinal artery. So what is the high yield thing you want to know about the gastro-bordinal artery?

What you want to recognize that the gastro-bordinal artery gives rise to two very high yield arteries that you want to keep at the back of your mind for the USM Ns. So the gastro-bordinal artery or the GDA, okay, gives rise to the right gastropyploid artery, which you can also call the right gastro-omental artery, okay? So that right gastro-omental artery anastomosis with the left gastro-omental artery, which is a branch of the spleenic artery, okay? And that anastomosis is also actually along the greater curvature of the stomach. So right gastro-omental artery from the spleenic artery and anastomosis with the left gastro-omental artery from the gastro-bordinal artery, okay? Along the greater curvature of the stomach, basically that's the blood supply for the greater coverage of the stomach, okay? So right gastro-omental artery is one branch of the gastro-bordinal artery and then the second branch of the gastro-bordinal artery is the anterior superior pancreatic-odinal artery. I'll see that again. It's the anterior superior pancreatic-odinal artery. The anterior superior pancreatic-odinal artery supplies as the term goes. It supplies a part of the duodenum, so it also supplies a part of the pancreas. It so happens that there is actually such a thing as the inferior posterior pancreatic also. Sometimes people call it anterior inferior pancreatic-odinal artery. That comes from the superior mesenteric artery, right? So that's the key region of anastomosis.

So let me kind of summarize three key anastomosis that I've mentioned because again, these anastomosis end up being very, very high-yield for the US Emily Step 1 exam. We have an anastomosis along the lesser curvature of the stomach. That's an anastomosis of the left gastric artery, which is a branch of the cilia-cardory and the right gastric artery, which is a branch of the common hepatic artery, which is a branch of the cilia-cardory. And then along the greater curvature of the stomach, we have an anastomosis between the right gastromental artery, which is a branch of the gastro-dordinal artery, which is a branch of the common hepatic artery, which is a branch of the cilia-cardory. And then that right gastromental artery, anastomosis with the left gastromental artery, which is a branch of the splinic artery. And remember that the splinic artery is a branch of the cilia-cardory. And then the third anastomosis is the anterior superior pancreatic-odinal artery, which is a branch of the gastro-dordinal artery, which is a branch of the common hepatic artery, which is a branch of the cilia-cardory. And again, remember the anterior superior pancreatic-odinal artery, anastomosis with the anterior inferior. Sometimes you see people see posterior inferior. It doesn't matter. Just find the words inferior and you're good to go. So I'll just use anterior inferior. Let me kind of keep my e-string.

So the anterior inferior pancreatic-odinal artery is a branch of the superior mesenteric artery. So that's an region of anastomosis between the SMA and the cilia-cardory. Again, very, very high you to know those things for the purposes of the USMAD step one, exactly. And then since I guess I've kind of talked about the stomach, let me go a little higher and talk about the esophagus. So what are some key high-yo things you want to keep at the back of your mind with your esophagus? Well, some key high-yo things you want to keep at the back of your mind with your esophagus is that the esophagus, right, is you can divide it up in thirds, right? So there's the upper third, middle third, and the lower third. The upper third of the esophagus is made up of purely skeletal muscle. The lower third is made up of purely smooth muscle. And then the middle third is a mixture of skeletal and smooth muscle, okay? So that's a nice way to remember that. So upper third skeletal muscle, lower third smooth muscle, middle third skeletal and smooth muscle. Now the thing is the esophagus has an upper esophageal sphincter at the top and then at the bottom it has a lower esophageal sphincter. The thing is that lower esophageal sphincter relaxes when food is about to weak its way from the esophagus to the stomach, okay?

And the thing is the problem is you can actually have some issues there where let's say for example you don't have like our back splixes remember another name for our back splixes is the myenteric plexus. If you lack our back splixes also known as the myenteric plexus, then your lower esophageal sphincter will not be able to relax. And if it's not able to relax that's something known as ecaligia, okay? That's something known as ecaligia. And ecaligia classically if they ask for the diagnostic step you want to pursue in your exam, at least for the purposes of the year's semilistep one exam you can do a barium swallow, okay? You do that barium swallow and you'll see the classically described bird's big sign. And really the way you treat ecaligia is I mean there are many things you can do you can do like like what is this thing called? You can do like a nomadic dimension of the esophagus although very few people do that because that has a very high risk of esophageal perforation. Another thing you can do is you can also do like an esophageal myectomy. I think some people call it like a ramstead I think it's like a drug like a ramstead myectomy and you use that to get rid of the in like size or muscle and that will you know again relax that lower cell of a just filter, okay? Now some other things you want to keep at the back of your mind with ecaligia and this is one thing that many resources for whatever reason do not cover, right?

But it's very very high to know for the ecaligia semil exams. The thing is the esophagus, right? When a person has ecaligia the aloeus of a just filter feels to relax so the aloeus of a just filter tone is increased that's one but another thing you want to keep at the back of your mind is people that have ecaligia also have problems with esophageal motility. The esophageal motility is not right in ecaligia that's something very high to know. Another thing that's also very high to know is that when a person has ecaligia, you may say oh what are some things that can cause it well. Sometimes when people have ecaligia we don't know the cause but one other thing that can actually cause ecaligia is if a person has chagas disease, okay? Remember chagas disease is caused by a bug known as triphanosomacruzii, okay? Triphanosomacruzii causes a lot of big problems. I've said this I've known them in many podcasts, right? So it can cause ecaligia, eke, e dilithetisophagus, it can cause a my dilithet cardiomyopathy, right? And then another thing you may also observe with that is it can also cause a dilithet bowel, right? It can cause something known as hersapron disease. So those are three high opathologies you want to be able to associate with triphanosomacruzii on inbimic samples. Dilithet GI tract, like dilithet bowel, right? Hersapron disease, dilithetisophagus, ecaligia, and then dilithet heart, dilithet cardiomyopathy from T.cruzii, okay?

So those are all high opathologies when you keep on the back of your mind for exams. And then remember that if a person has chiroderma, right? In fact, there's a kind of chiroderma known as crest chiroderma. You may see a whole divine, what does crest stand for? Well, crest, right? The C's for for caucinosis, right? The R is for renotphenominal, renotphenominal is actually the most common renotphenominal is actually the most common presentation of chiroderma. And then the E's for geodesmotunity, right? So people that have crest chiroderma, they can have like really bad gird because they just have issues with, they just kind of like fibros, the lower isofajil's fincter. So it's like open pathway for acetate to come from the stomach up to the esophagus. So that's why those people can have those problems. And then the S stands for sclerodactin, it's like a fingernail finding and then the T's for tenanjectages. And it's actually very important for the U.S. similarly exams to remember that crest chiroderma is associated with anti-centramir antibodies, okay? Anti-centramir antibodies associated with crest scleroderma. So that's one high u thing to know there. And then some other high u things to know with the esophagus, right? So they may give you a question about a person and then he'll show you some labs and then you tell you that, oh, this person has trouble swallowing. And then he'll show you like the person's tongue and you may see that the person's tongue looks very smooth.

And then they may give you labs that show the person's hemoglobin to be eat with an m with an mcv of like 67. If you notice, right? low hemoglobin obviously the person has an anemia. And if you notice with the mcv of 67, that's a microcytic anemia. So it's likely like some kind of like iron deficiency anemia. If you see iron deficiency anemia in the context of a person having trouble swallowing so dysphysia. And then they tell you that this person, you know, again has like that smooth tongue. They want to think about something known as plumbervincin syndrome. Okay? Plumbervincin syndrome is a trend of iron deficiency anemia and then they have esophageal webs that can cause dysphysia and then they can also have glocitis. Okay? Those are all higher things to know. And then if they give you a question about like an alcoholic, let's see a person that you know drinks like a pint of vodka every day. And I'll try this pint of vodka for like 40 years. And then they tell you that, oh, this person presents with like severe hematemesis and the person is like profoundly volume depleted, very low blood pressure and everything. Then you want to think about like a bleeding issovajel viruses. Remember, sovajel viruses are right from a person having a lot of poor hypertension. So when you have poor hypertension, that will cause like the standard veins and the esophagus.

And if those pressures build up enough, those veins can rupture and those veins rupture, you have a very big problem on your hands where you can have bleeding viruses. And typically those people, many of them die relatively quickly. But if you ask for treatment on your exam, you want to go ahead and perform some kind of endoscopic therapy. And that endoscopic therapy can be one of many things where you can do like banding of the varics. Another thing you can do is you can actually give, you can also do like sclerotherapy, but most people do banding of the varics. So you do a banding of the varics, you can do sclerotherapy. Another thing you can do is something called a tips procedure. So you see, what does a, what does tips stand for? Well, tips stands for trans hepatic. No, yeah, yeah, I think it's like trans hepatic interest, something, porosystemic shock. Basically, it's a shock between the poro vein and the, um, and the hepatic vein, right? So you basically bypass the liver so that you can reduce poro pressures. The only problem is when you bypass the liver, you're bypassing the urea cycle. So those people have a very high risk of hyperamonemia. Remember that hyperamonemia can cause a lot of neurological problems, okay? But that's almost like a last-ditch procedure that you do when a person is not, is usually done by like interventional radiology. It's like a last-ditch procedure you can do when a person is just not doing very well from an esophageal varicis perspective.

And then in terms of pharmacological therapy for esophageal varicis, you can typically give those people like IV octriotide. In fact, IV octriotide is probably like the drug of choice you can use in the acute phase of esophageal varicis. It will cause like splanchony viso-construction and that will decrease poro pressure so that can help. But after that acute phase, sorry, after the acute phase, chronically one thing you can do for esophageal varicis to chronically lower poro pressures, obviously tell the patient to stop drinking. But other things you can do is you can actually give them like a non-selective bit of blocker like proprenololol, olginolol, that will also decrease poro pressures. Another thing you can also do is you can also give them um spirano-lactone. Spirano-lactone, remember, it's an out-dustin receptor antagonist that also has the ability to block um androgen receptors. That's why I can cause nerecomacia as a side effect. But the thing is spirano-lactone also decreases poro pressures by again some unknown mechanism. But those are two big things you want to know. And then I guess if they really wanted to mess with your head on mbim exams, people that have like blinness of ageo-varicis, you should also put them on like a fluorocrylonal lone prophylaxically. Um it's been shown to actually like have some benefits in that population of people that have levied poro pressures giving rise to esophageo-varicis.

And then if they give you a question about a present that vomits significantly and then they start telling you that oh this person becomes like very February, and becomes very hypotensive. And then they tell you that you have like a rice crispy sensation on the skin. If you see that presentation on an mbim exam, uh or they may tell you that oh you see like you you get an image and they tell you that oh on that image they notice like a air tracking along the walls of the order or along the walls of the airway. That's something known as pneumometristinum. If you see that you want to think about uh, perhaps syndrome, okay? And remember the bee in perhaps for the bee in bad. Perhaps syndrome is awful awful awful, right? The mortality is very very high. Things are probably close to 50% or even more if I'm not mistaken, right? So the thing is if you vomit significantly that's sudden increase in esophageo pressures can rupture the esophagus and then you will essentially have a direct communication between the outside world and the esophagus, right? And the thing is your friends at the mbim in the ask you to pick a diagnostic test for perhaps syndrome, um they will try to trick you into picking barium swallow as an answer choice. Do not pick barium swallow. The thing is if you pick barium swallow, barium can cause a very powerful media estimate is so you don't want to use it when you suspect that a person has perhaps syndrome.

The thing you pick is something called gastrography, okay? Gastrography enema. Sometimes instead of putting the word gastrography enema, they may put like a close term known as a water solubo contrast enema, okay? It's the same thing, okay? You can use those to diagnose an esophageo perforation and obviously those people you need to weld them to surgery like yesterday, right? It's a surgical problem is something that has to be fixed with surgery although again like I said the mortality is very high. And then a close causing to perhaps syndrome is something known as the malaria-wise tear, right? So remember basically it's just a pressing just kind of like lacerating the agi junctions. When you last read the gi junctions, those people have like painful hematemesis but it's usually like a very small volume hematemesis. So it's not like lacerating you don't really need to treat just you know the patient will get better with supportive care for the most part, okay? So malaria-wise tear you don't usually need to do anything significant for it. But perhaps syndrome you certainly need to take those patients to you certainly need to take those patients to surgery, right? And then what if they give you a question about a patient you know that has lost like 20 pounds over the last month and then they tell you that this patient has been having like dysphysia to solids, right? And let's say this person has been like you know they've had like a 20 year history of good.

If you see that what are you thinking about? I hope you're thinking about like esophageal cancer, right? I hope you're thinking in fact more along the lines of a sexual esophageal adnucarcinoma, right? Because remember if a person has a long-hearsal prolonged gird, well with gird, you can you're you're essentially exposing your esophagus because normally esophagus is lined by non-charatonized stratified scrimos epithelium. So the thing is if you expose your esophagus to a chronic acid load, well, your esophagus will be like oh crap you know what? Let me try to figure out a way to deal with this problem, right? So you will say you know what since I'm facing a different kind of stress than what I'm used to, I'm going to undergo metaplesia into a type of cell that is better able to handle that acid stress and that better type of cell is simple column epithelium with goblet cells. Sometimes you may see it on NVMA exams refer to as an intestinal metaplesia, okay? So in the good intestinal metaplesia, you form simple column epithelium with goblet cells that will increase your risk ultimately of developing an adnocarcinoma of the esophagus, okay? In fact, the most common cancer of the esophagus in the United States is an esophageal adnocarcinoma, okay? But if you're looking more worldwide, the most common esophageal cancer worldwide is esophageal scrimos cell cancer because again I said that the native esophagus has non-charatonized stratified scrimos epithelium, okay?

But when you undergo that metaplesia, you then have simple column epithelium with goblet cells, aka intestinal metaplesia. And the thing that happens is, you know, when you undergo that intestinal metaplesia, you form something known as baritone esophagus and then baritone esophagus if you have further dysplasia that can ultimately lead to esophageal adnocarcinoma. And I mean esophageal adnocarcinoma has an awful awful awful prognosis. Now, what are some other key things you want to keep in mind with esophageal adnocarcinoma? The thing is, the endemic may give you a question and say, oh, what is the biggest risk factor for esophageal adnocarcinoma? And it can give you, like, option A, gird, it can give you option B, baritone esophagus, resist the temptation to pick gird, pick baritone esophagus as the biggest risk factor for esophageal adnocarcinoma. Because think about it between those two answers because if you think about it gird, does increase your risk for baritone. But the answer choice that has the closest, like, the most direct relationship to esophageal adnocarcinoma is baritone esophagus. Okay? So, naming me exams, one very good testic in strategy is just to pick the answer choice that is most directly related to the diagnosis that you have need in your Q step. And as a rule, because many people are like, oh, divine, how do I remember what risk factor is what for the esophageal cancers? Let me just give you a simple rule.

Baritone esophagus increases your risk of esophageal adnocarcinoma. Every order of esophageal pathology that increases your risk of esophageal cancer will increase your risk of esophageal squamous cell cancer. Okay? We'll increase your risk of esophageal squamous cell cancer, right? So, if, for example, a person consumes li, or a person consumes like, Drainow, or a person has a calisia, or a person has some, like, Plum of Incent Syndrome, those things all increase risk of esophageal squamous cell cancer. Now, one of the high-yield, I guess, series of pathologies you may see with your esophagus on the eSML exam says, let me give you a question about like a 65-year-old guy, you know, they tell you that his wife is complaining that his breath smells really bad in the mornings, and then he'll immediately tell you in the question that, oh, occasionally in the morning, he notices that he regurgitates on digested food, and then they ask for your diagnosis, well, if the ask for your diagnosis, you should be thinking about Zenker's diverticulum, okay? Zenker's diverticulum, remember, Zenker's diverticulum is one of those diverticula that you'll find in the upper third of the esophagus.

There are actually other kinds of diverticula that you'll find in the esophagus, like, in the middle third of the esophagus, there's something known as a traction diverticulum that you'll find, and then in the distal third of the esophagus, just above the gastroes of a geogonction, you have something called an epiphranic, right? Epiphranic, above the phranic, remember, the phranic nerve supplies the diaphragm, right? So, like, right above the diaphragm, you have epiphranic diverticula, right? So, the way I remember, like, oh, you're like, oh, divine, how do I remember which is which? Like, Zenker's in the upper third, traction in the middle third, epiphranic in the lower third. The way to remember this is just remember the company that makes phones like ZTE, right? I mean, I've had a ZTE, it was one of maybe the earliest ones I had when I moved to this country, what ZTE, so Z for Zenker's upper third, T for traction, middle third, epiphranic, lower third, okay? And one key thing to realize is that Zenker's diverticulum is a false diverticulum. The thing is, the thing that helps you delineate a diverticulum as being a true diverticulum, or a false diverticulum is if it includes all the leaders of the GI tract, right? So, if a diverticulum includes like Mucosa, Subucosa, Moschularis, Purupria, then that tells you and like, Serosa at the bottom, then that tells you that it's a true diverticulum. Attractor diverticulum is an example of a true diverticulum.

Zenker's diverticulum is an example of a false diverticulum. It just includes the Mucosa and the Subucosa in those not include the Moschularis, okay? And remember, the Zenker's diverticulum arises because you have weakness as a part of the esophagus known as a Killens triangle. Killens triangle, you have that weakness because you may have like atrophy or like the newdment of the Cricopharyngeal muscles. So, if you have weakness of like your Cricopharyngeal muscles, that can ultimately lead to the person having a Zenker's diverticulum. And when a person has a Zenker's diverticulum, you can actually make the diagnosis by doing a barium swallow, okay? You'll see like the outpouching in the upper third of the esophagus and then that tells you that all this person has a Zenker's. And one very high-yield thing to know in terms of actually two very high-yield things to know with regards to Zenker's. One is treatment. You can treat Zenker's diverticulum by doing something called a diverticulaectomy, okay? You just excise the diverticula. Now, one thing that is contraindicated in a person that has Zenker's diverticulum is to perform an EGD. What does EGD stand for? EG Ds and it's so far go gastro-duoidoscopy. Basically, it's something that's done by GI doctors all the time. I mean, look at the term esophagol gastro-duoidoscopy. It's basically like a scope, like a microscope that you can use to look at the esophagus. You can use to look at the stomach.

That's why there's gastro in the name and then you can use to look at the doodna, okay? That's why it's called esophagol gastro-duoidoscopy, okay? Those are all high-yield things to know there. EGD is contraindicated in people with Zenkers because if you do an EGD, you can prefer it. The person is a esophagus and then you have essentially almost like birhav physiology there. Now, one of the high-yield things to know, the esophagus that you can get on your exam is, you can give you a question about a patient that has like, you know, like a city for kind of 40 and then they tell you that this person has been having an ordino phasia for the past like two weeks. And then they may tell you that, oh, on physical exam, the person has like white membranes on the tongue, right? If you see that then hopefully you should be thinking about candidil esophagitis, right? Candidil esophagitis. Remember, people that have that immunocompromised like HIV patients, they can have esophagitis and they can have esophagitis from one of three causes. They can have esophagitis from candida, right? They can have esophagitis from CMV and they can have esophagitis from HSV. Although, if the probably the most common answer you may see on your MBA exam is candida. So if they give you like a non-specific question and they don't give you any clues like, oh, the person has to throw some of the mouth or whatever, big candida, candida is the most common cause of esophagitis in patients that have HIV, right?

And how do you treat candida esophagitis? Candida esophagitis, where you do like the niestatins vision swallow or you can do like like a clotrimazole or zengis that can help you with that. And then if a person has like HSV esophagitis, right? Obviously, you use esyclovir for that. If the person has esophagitis that's resistant to esyclovir, then you can consider giving foscerny. Remember foscerny is a pyrophosphita and a lot. And then if a person has CMV esophagitis, you can treat that with gansyclovir, right? Remember gansyclovir covers CMV very well. If you don't see gansyclovir as an answer choice, you can go with foscernet, okay? In fact, if a person has like CMV that is resistant to gansyclovir, remember the resistance arises from mutations in a Chinese known as the UL97 Chinese, then you can consider giving those people a foscernet and that should work. There is very little if any resistance to foscernet by HSV and CMV. So those are the big things you want to keep at the back of your mind with esophagitis. Now one thing, occasionally, that your friends at the MBME do, do you know, try to mess with your head with regards to esophagitis? Is, they may tell you that, um, um, they may describe, they may want you to pick the findings you'll find, you'll see them like biopsy or histology. Remember, if a person has candidate-lessophagitis, you'll find hyphae on biopsy specimen, right? On histology.

If a person has CMV, they'll tell you that, oh, this person has intranuclear inclusions. They'll tell you that, oh, this person has like cells that are enlarged and you have like intranucle inclusions and you have like a halo, like a perinuclear halo. If you see that, think about CMV, okay? HSV, HSV also involves intranucle inclusions, but the thing is, HSV does not have that perinuclear halo. People that have like the intranuclear inclusions in HSV push like the chromatin in the nucleus to the side, okay? So you don't have that perinuclear halo in a person that has HSV asophagitis. Contrast that with CMV asophagitis, where again, you'll find the intranuclear inclusions or you have the perinuclear halo. Again, very high you to know those things for purposes of the MBME exam. And then, um, remember earlier, I said that if you consume a lie, that increases your risk of S of a Joe Scrimal Cell Cancer. And I said that it's a Joe Scrimal Cell Cancer is the most common cancer that you find in like worldwide. It's the most common is a Joe Cancer worldwide, but in the US, again, because the US has a high burden of obesity. So the most common is a Joe Cancer in the US. This is a Vajel adnucarcinoma. It's actually high you to know that if they, for example, they give you a question about a person that you know, consumes like lie or drink and then they tell you that, oh, this person is having like like a few weeks later or a few days later, this person is having like dysphagia.

You want to think about structures being the cause of the person's dysphagia, okay? Structures where you can essentially have all these adhesions, like all these like linear fibros bands that fall in the esophagus that can cause dysphagia. Now, another thing that can cause structures in the esophagus is if a person has just prolonged gird and it's not treated, the thing is gird as you burn away your esophagus with all that acid that can also lead to the formation of structures, especially like in the, especially like in the distal esophagus. And if you form those structures that can also cause dysphagia. So if you see a person that has a history of gird having dysphagia, I would really encourage you to think about, I would really encourage you to think about structures being the etiology on that those circumstances. And then let me try to keep this podcast under an hour. I think let me, let me maybe talk about like a few quick pathologies. Yeah, let me talk about a few quick pathologies here. Let me see, is there any other thing I want to say about the esophagus? Well, I'll see, maybe one thing I should say about the esophagus is the esophagus doesn't have a serosa. Remember I said for the GI tract, right? You have like your three big layers, you have your micosa, you have your subbicosa, and then you have your muscularis external. The thing is, and then usually for most other parts of the GI tract, you have a serosa.

Not so for the esophagus, the esophagus does not have a serosa. So because the esophagus lacks a serosa, it is actually very easy for a surgical cancer to be testicized to other contents of the medias tylam. And then remember that the esophagus traverses the diaphragm at the T10 level. Remember, there's this classic nomonic I810x at 12 to help you remember that the IVC, the inferior vein cable traverses the the diaphragm at the T8 level, right? The esophagus traverses the diaphragm at the T10 level. So I eat 10 eggs, so 10 teeth, 10 eggs as a suffigus. Okay? And then at the T12 level, you have the thoracic order. That's where it traverses the diaphragm, you may see? How can things traverse the diaphragm at different thoracic levels? Well, remember, the diaphragm is not a straight structure, it's a dome shaped structure, right? So there are certain parts that are lower or higher than the others. So those are all high of things to keep at the back of your mind on exams. So what else do I want to say? Okay, let me say a few last things and then maybe teach for like five more minutes and then I'll run off the spot. I just want to keep them under an hour so that it's not like excessive for a person to listen to and understand. But basically, the thing I want to see is, let's kind of, I guess, talk about some of the glands that you find, so in the tongue, we have the parodid gland, we have the sublingual glands and then we have the submandibular glands.

So we have the parodid sublingual and the submandibular glands. The thing is the parodid gland for the most part makes like serious secretions, like watery secretions. What are your sublingual and your submandibular glands? Those tend to make more like mixed secretions. So secretions that are both watery and so they are both watery and like mucusy as well, right? So they are like thick and these things obviously help you mix saliva and saliva is important, right? Because saliva contains like alpha amelies, right? And that alpha amelies actually helps you with the beginning, the digestion of carbohydrates, right? So carbohydrate digestion actually starts in the mouth under the action of alpha amelies, okay? That's very high here to know for exams. And remember that saliva, right? Also contains, you know, like other things like defense scents and lysosines that can also have like some antibacterial function. And one thing your friends at the endemic dormant exam is to ask you about the immunoglobulin that you may find in saliva. IGA is the primary immunoglobulin that is found in saliva. And then remember, right? They are certain things you want to keep in mind with regards to like these glands, right? They are certain cancers that can arise in these glands, right? So like for example, the person can have something called like a pyomorphic adenoma. A pyomorphic adenoma is actually the, it's actually a benign tumor.

It's actually the most common, most common benign saliva reglan tumor. Usually it arises in the parodiglants as against like the sublingual or the submandibular gland. Usually it arises in the parodiglants. And I mean, look at the name pyomorphic, right? So when somebody is pyomorphic, it means it almost like takes different shapes, right? Like they are, like they have different things in it, right? So the different things in a pyomorphic adenoma is just you have in like there, you have like epithelium, but you also have like almost like some stem cells, some things people call them like mesenchymal cells, okay? So you tend to find those in pyomorphic adenomas, it's benign. The thing is because it's in the parodiglant, remember that your crinonerv 7, your official nerve, it does not innovate, it cuts through the parodiglant. Remember, the parodiglant if anonymous, thinking is innervated primarily by the glossopharyngeonerv, crinonerv 9. So, check me on that factoid, but I'm fairly starting, that's the case. But the official nerve, right? You remember before you use of his terminal branches, you know, it's not a cause through the parodiglant. So the thing is when a person has a pyomorphic adenoma, they can actually cause bells palsy, okay? They can cause bells palsy or it can cause like phisior nerve palsy because basically if the benign tumor grows enough, it can compress, it can compress the phisior nerve, right? So again, that's something high you have to know, for example.

And then one of the tumor you may find on MBM is something called a mucoepidermoid carcinoma. This is actually the, it's actually the second most common overall, salivary gland tumor, but it's actually the most common malignant. So remember the M in mucoepidermoid for the M in malignant, okay? It's the most common malignant salivary gland tumor, the mucoepidermoid carcinoma, okay? It has, I mean it has like not so bad of a prognosis, but obviously it doesn't have as good of a prognosis as a pyomorphic adenoma. And then you also see something referred to as like a orthoemstumor. Orthoemstumor is just a benign salivary gland tumor, is the probably like the second most common benign salivary gland tumor behind a pyomorphic adenoma. It kind of looks like a germinal center is almost like a lymph node in a sense. And one epidemiological factor, you want to know for purposes of the USM in the exam, says that most times when a person has a tumor in one of any of the salivary glands, if you see a tumor in the sublingual gland, the chance of that tumor being malignant is very very high, right? What if you see a tumor growing the parodic gland, the chance of that tumor being malignant is very, very low. So basically if you, and then your submanipular glands are kind of like in between, right? But basically let me summarize, if you see a tumor in the sublingual gland is likely malignant, if you see a tumor in the parodic gland, it's likely benign.

And then the sublingual gland is kind of a mixture between the two. So those are again all big things to remember. And then remember that people that have chogrin syndrome, right? They can have like dry mouth, because chogrin is like, it's like an autoimmune disease of exocrine glands. So those people can have problems producing like saliva, right? So they'll have like, they can have like dental carries, they can have like poor dental hygiene, because again, they are not making those salivary contents that can help you kill bacteria that you find in the in the mouth, okay? So those are again all big things to keep in mind. So chogrin's and remember chogrin's has an association with antirell and antelah antibodies, right? Remember antirell at the anti-SSB antibodies, and then antila at the anti-SSB antibodies. And it's actually very high you to know for purposes of the USMLA exams, that those antibodies can cross the placenta and damage the conducting system in the feeders and cause like a third degree heart block, like a complete heart block in the feeders. And then since I'm talking about saliva, let me just real quick talk about the tongue. The tongue, your friends at the MV, we love you to know about the tongue in the context of like the cranial nerves, right? So remember the tongue you can divide it by the anterior to thirds and then the posterior one third. The anterior to thirds of the tongue, right?

You want to know the cranial nerves that control teeth sensation, right? So the general teeth sensation, right? So what do I mean by general teeth sensation? I mean things like, oh, are you able to feel like pin prick, pain and all that stuff in the anterior to thirds of the tongue? That's controlled by the third branch of the trigeminal nerve, the mandibular nerve, okay? cranial nerve V3. But the special sensation of teeth is controlled primarily by cranial nerve 7, the official nerve for the anterior to thirds of the tongue. For the posterior third of the tongue, it's your glossopharyngel nerve that controls both the general sensation of teeth and the special sensation of teeth. Although in the very back of the tongue, you have like the vagus nerve controlling some of that function. So again, those are high of the insula and then the motor activity of the tongue is controlled by the hypoglossal nerve. cranial nerve 12, remember all the intrinsic muscles of the tongue are supplied by the hypoglossal nerve cranial nerve 12 neuron with one exception. The one exception is palatoglossus. Palatoglossus, if you remember, turns laws that I've talked about in one of my prior podcasts. Palatoglossus is actually inhibited in, not inhibited, innervated by the vagus nerve cranial nerve 10. And whenever a person has hypoglossal nerve injury, remember the tongue would deviate towards the side of the lesion, right?

A very nice way to remember that is like a person like leaking their wounds, okay? Like a person leaking their wounds. And then remember that occasionally, right, the person may have stones that can obstruct their like the salivary gland ducts, okay? They can have stones that obstruct their salivary gland ducts. That's something called like salulithiasis. I remember like lithiasis means stone, right? So salulithiasis is when you have like again a stone obstructing like your salivary gland ducts. The thing is that can cause severe pain. And behind that obstructing stone like infection can build up and then you can have something called salalidonitis, okay? Like it's an inflammation of your salivary gland ducts, right? It's most commonly caused by like staphoreus. Also strebveridanc can also cause a salalidonitis. And some big things that can increase your risk of having those are like again, having like chugrin syndrome, right? So chugrin syndrome. And if you also like just chronically dehydrated, that can increase your risk of salalidonitis. I would just say S-D-N, just if you see me say S-D-N in salalidonitis, it's just a hard work to print out. So risk factors for S-DN are things like having chugrin syndrome, right? Or being like dehydrated or having like having an undergone intuition, okay? Those things all increase your risk for S-D-N, okay? All the increase your risk for S-D-N. And also mumps can also cause that remember mumps can cause like a paratitis, right?

Although mumps usually causes like paratitis and or kindness, right? Like like really large huge bigger testicles. And then again, I said again chugrin, right? Chugrin, like causes dry mouth because again you're causing destruction of your of your salalid red glands. I remember that dry mouth, the five dollar worth for that is something known as Xero Stomia, okay? Xero Stomia. And the thing is when a person has like dry mouth or a person has like like a stone obstruct in their salalid redland ducts, one thing you can actually do is you can actually give them like gamma like sour candy. And as the chugrin, that gum chugrin, that sour candy that will increase the production of saliva and that can flush that stone through those ducts. So again, kind of big things to know for exams. So I think I'm going to go ahead and stop here. Oh, sorry, one last thing I want to sneak in. When a person has basically your salalid red glands as inner redded both by your sympathetic and passive-ethetic system, the parsympathetic system tends to cause more for water secretion, right? Because water secretion is better for digestion, right? But your sympathetic nervous system tends to make more of a thick secretion. That's why if you're like nervous or anything like that, right? You feel like you see people that are giving talks, they drink a ton of water because they're nervous. So they have like thick salalid red glands secretions, right?

So they're drinking all this water to try to kind of like moisting of their amounts a better. So let me go ahead and stop here. There are some more things I want to talk about. I'll talk about them in the next podcast. And as I do at the end of the podcast, I don't want to want to learn from any exams, right? So step one, step two, CK, step two, CSTEP 3. I do, I also tutor for like pre-clinical medical exams, 30-ish-off exams. And then I do this thing called longitudinal tutoring, where if you're a first-second or 30-medical student, I'll tutor for like your block exams in medical school or your shelf exams. But at the same time, I also tutor for your upcoming USMEL exam. Again, people have done this with they've been like wildly successful. And then I have these things that I call repair courses, where this is more for people that are like in their dedicated periods. If you have like a specific subject weakness, like cardiology is your weakness. Like you take a practice exam, and your cardiology bars up to the left or whatever. I can do a repair course. It usually goes for like two hours or two and a half hours at the most, where we just go over in a Q&A format. We just go over like most, essentially most if not all of the high yield stuff you can see tested on that subject for that giving USMEL exam. And most people have done that with again. That has very effectively raised those errors.

And then I also offer like these booster courses, I call them booster courses for the USMEL exams. It's like 20 hours for step one is 10 hours for step two seconds, step three. Where again, if you feel like you know you at the end of your day get appeared or you want to kind of like put everything together really quickly in a short frame of time. I offer those courses for those exams. And then I also offer like just like comprehensive USMEL courses when I need a group of five people. So if you have a group of five and you have a location, just let me know. Basically send me an email if you have a group of five people and we can kind of arrange like location and the timing and everything. I should probably not be talking about specifics on this podcast. Just either like reach out to me through the website or send me an email, a divine intervention podcast with an S at the end at gym.com. And then I will give you some more details. And then finally, if you're a med student or plant or residency, so like an ERS application or a college student or plant or med school, so like an AMCA application, I offer like coaching for those things. So like reclater, personal statements, application, I didn't more interviews. I go those things. And again, the vast majority of people have worked with they've all much that their first choice.

And then if you're medicine resident and you need to ebi and board the exam or like the medicine, you need to be an exam or your college student and you need to be a student for like Gen CAM, O-CAM, Physics, Bio CAM, Histology, Physiology offer to you for all those states. So have a wonderful rest of your day. I hope you find this podcast to be helpful. Thank you. God bless you.

Parathyroid adenoma/hyperplasia, pituitary adenomas, and pancreatic neuroendocrine tumors (e.g., gastrinoma).

Gastrin-releasing peptide (GRP), released by the vagus nerve.

Mucoepidermoid carcinoma; it is the most common malignant type overall.

1) Lesser curvature (Left Gastric Artery/Right Gastric Artery); 2) Greater curvature (Right Gastro-omental Artery/Left Gastro-omental Artery); 3) Anterior Superior Pancreaticoduodenal Artery/Anterior Inferior Pancreaticoduodenal Artery.

CMV shows intranuclear inclusions with a perinuclear halo; HSV shows intranuclear inclusions but without the perinuclear halo.

Anti-centromere antibodies; C=Calcinosis, R=Renal Phenom, E=Edema, S=Sclerodactyly, T=Telangiectasias.

Hydrogen/Potassium AT Pase pump (H+/K+ AT Pase).

Proton Pump Inhibitors (PP Is), such as Omeprazole, Lansoprazole.

Foregut $\rightarrow$ Celiac Artery; Midgut $\rightarrow$ Superior Mesenteric Artery (SMA); Hindgut $\rightarrow$ Inferior Mesenteric Artery (IMA).

Cranial Nerve VII (Facial Nerve).

Immunoglobulin A (IgA); Risk factors include Sjögren's syndrome, dehydration, or instrumentation.

Chagas disease.

Pyomorphic adenoma; usually arises in the parotid gland.

Hydrogen/Potassium AT Pase pump (H+/K+ AT Pase).

Proton Pump Inhibitors (PP Is), such as Omeprazole, Lansoprazole.

Foregut $\rightarrow$ Celiac Artery; Midgut $\rightarrow$ Superior Mesenteric Artery (SMA); Hindgut $\rightarrow$ Inferior Mesenteric Artery (IMA).

Cranial Nerve VII (Facial Nerve).

Immunoglobulin A (IgA); Risk factors include Sjögren's syndrome, dehydration, or instrumentation.

Chagas disease.

Pyomorphic adenoma; usually arises in the parotid gland.