DIP Episode 294 - NBME Gastroenterology Series 2 (for all USMLEs)

Okay, welcome. My name is Divine. This is episode 294 of the Divine intervention podcasts. In this podcast I'm going to be continuing the MBME Gastroenterology Review series. This is gonna be series two. It's that is series one, yesterday, that was episode 293. So let's just get right to it. So what if you get a question about like a 25-year-old female and you know the theory that she has like floating, a larger stool, she has signs of my absorption, right? And then I'll tell you that her symptoms improve when you withdraw gluten from the diet. What should you be thinking about? Well I really hope you're telling me that this person has celiac disease, right? And I think one thing that may actually help you here is if you notice this person has physical exam findings. They have some kind of abnormality, right? This is not something that you can see about a person that has lactase deficiency. For person has lactase deficiency. Excuse me. What's going on this morning, right? So if a person has lactase deficiency, they will not have any physical exam, they will not have any lab abnormalities. In fact, for some reason people on the have celiac disease on MBME exams, they tend to have like a pretty low weight, right? They tend to have a pretty low weight, right? So this person again obviously has celiac disease, right? And what are some high yield things your friends at the MBME kind of expect you to know about celiac disease?

Well the first one is thinking in terms of what part of the of the small intestine is affected, right? So any celiac disease can pretty much affect the doorknob. They can also mess up the jejuna, right? But it's actually very high yield to know that celiac disease actually spurs the ilium. In general, on MBME exams, right? So I'll say that again, celiac disease usually affects the doorknob and jejuna, but it commonly spurs the ilium on MBME exams, right? So that's a very nice comparison with Crohn's disease, right? Because remember Crohn's disease is also an inflammatory disease of the GI tract. It affects you know, not just the small intestine, also the large intestine and all that stuff, but the thing is a person that has Crohn's Crohn's always on MBM Es will involve the terminal ilium, right? Remember, so because the terminal ilium is involved in Crohn's, they can get a B2 of deficiency, right? And remembering Crohn's because the terminal ilium is involved, they also have increased reabsorption of oxalita, right? So that increases those people's risk of getting oxalita crystals in the urine, right? So like an oxalita, nephrolythiasis. Now, one other thing your friends at the MME can ask you is, what would you likely expect to find on intestinal biopsy, right? So if you take a biopsy and look under the microscope, right? You should find lymphocytes. There is this buzzword they love to test, right?

Where you'll see like, you can see like blonding of the microvilli, you can see intraepithelial lymphocytosis, right? The thing is a lot of the damage is mediated by B cells, okay? A lot of the damage is mediated by B cells, but also T cells as well, right? So because we know that the damage is mediated by B cells and some T cells, well is there a potential malignancy that can happen in a person that has a history of celiac disease? Well, I hope you're telling me that it's going to be like a T cell lymphoma, right? So in fact, it's called EATL, enterica, associated T cell lymphoma. It's relatively common in people that have a history of celiac disease, right? You know, it's almost like some kind of non-hotchins lymphoma, right? So it's very, again, high yield to know these things. This EATL, this, uh, enterica, associated T cell lymphoma, is not something that pops up in many resources, but it's something that's actually very high yield to know specifically for endemic exams. And then again, obviously, if you're trying to do your diagnostic test then for a person that has celiac disease, what are the other antibodies that are associated? Well, don't forget, right? These people will have like IgA antibodies, right?

Against like tissue transgressive terminus, they can have IgA antibodies against gliadine, I mean, they can have a, so IgA antibodies against tissue transgressive terminus, or they can also have antibodies against like gliadine, they can also have like anti endomysial, ENDO, M-Y-S-I-A-L, right? So they'll have anti endomysial antibodies, right? And remember, it actually has some HLE associations, right? So it's a HLE, DQ2, and HLE, DQ8, right? Just things to keep in mind, right? And then what if the tell you that all the person has a rash, right? On around the elbow, right? You know, like rash on extensive surfaces, what should you be thinking about? Well, I hope you're thinking about dermatitis or prediformis, right? Remember, you actually treat that with dapsalm. So you may ask, well, divine dapsalm, what are the uses of dapsalm on endemic exams? Well, first of all, let's maybe just cause the mechanism of action of dapsalm, right? So remember, if bacteria, whatever, are trying to make folic acid, first, this, that with papa, right? That papa is converted by dihydroploid synthetase, right? So dihydrofolate. And then dihydrofoloid reductase will then convert that dihydrofolate to tetrahhydrofolate, so DHF to THF. So the thing is, that dihydroploid synthetase, you can actually give a drug that's a competitive inhibitor of it, right? That's dapsalm in this case.

Dapsalm, and also the sulfonamide, just in general, they are competitive inhibitors of dihydroploid synthetase, so they pretty much compete with papa for binding to dihydroploid synthetase. So that's how those drugs inhibit the synthesis of folic, right? So one important thing for sure, right, is to know is that dapsalm is used in the treatment of dermatitis or peridiformis, but is that really also one of those things you can use to treat new assisties, duravetsi, slash prophylaxis, against it, on embium exams, if there is some kind of weird contraindication to take in trimethoprimal, so from the thoxazone. And then don't forget, you can also use dapsalm to treat leprosy, right? Whenever a person has leprosy, you really have to, you know, usually remember leprosy, a person has like the person having like a neuropathy on like cold, open surfaces of the body, right? Like the tip of the nose, the tip of the ears, and they'll have like a mischaping phase from all these swelling, right? When a person has leprosy, you know, again, caused by microbiome leprosy, we're going to treat those people for 24 months, right? We're going to treat them with a combination of dapsalm, rifampin and clofazimine, right? So dapsalm rifampin and clofazimine, right? dapsalm rifampin and clofazimine. That's how we treat those folks on embiming exams. And then, so again, we can use it for dermatitis or herpathy form, right?

And again, like I've said, on embiming exams, they love to ask, even on step-joseg, step-3, they love to ask what you'll see on my cross copy, right? After you've taken an intestinal biopsy, again, you'll find velosatrophy, right? You'll find intrepithylolimphosphytosis, that's probably like the Bos word, that's a lot more common on tests, right? And I guess for some explanation, as to the pathophys behind celiac disease, well, what's the actual pathophysiology? Well, the thing that happens is that tissue transglutaminase, it actually converts the gluten that you ingest, it can convert it to gliade, right? And then that gliade, and sadly, can be taken up by your antigen-presenting cells, right? Remember, like your macrophages, your dendritic cells, for example, right? And then, especially antigen-presenting cells that have like a DQ2-DQ8 sub-t... That tunics, again, when all the antigen-presenting cells represent the have MAC2 on the surface, right? So if you have an antigen-presenting cells that have MAC2 on the surface, and they have that DQ2-DQ8 sub-type, right? That's almost like a genetic susceptibility there. That will actually lead to T-cells being activated, and then those T-cells will then come, and you know that every T-cells shop somewhere, they don't shop for funsy, right? They're going to come and destroy everything inside, right? So they're going to come and cause destruction.

So, I mean, like it's almost like a somewhat similar process that happens in people that have some of these nephrodics and drums like... like minimal chain disease and focus segmental glomerulus sclerosis. Those things are mainly mediated by T-cells. T-cells are the things that primarily mediate that destruction. So you have that effacement of the porousite foot processes. Okay, now what if they give you a question about a person that you know has just had like a very severe burn of some sort, and then they say, you know, in addition to, you know, maybe antibiotic therapy or referral to a brand center, what's your next best step? I believe it or not, they've started throwing these next best step in management questions on step one, and obviously they are pretty predominant on step two, see, can step three. If you see that, one of the drugs you really want to give to a person that has just suffered a burn of some sort is a proton pump inhibitor, right? Proton pump inhibitor. Because again, remember, whenever a person has a severe burn, never a person has a severe burn, that's what they can begin to develop a peptic ulcer disease, right? That's what's called a curling solcer, right? So you use it as prophylaxis, right? If you give PPI's as prophylaxis, that will actually decrease the likelihood that they will develop like an ulcer as a result of that.

I mean, they can also give you a similar question in a person that has high intracranial pressures from like meningitis or whatever, or a stroke, right? Routine when people have strokes when they come into the ICU like that, typically one of the things that's given to them is a proton pump inhibitor, right? Because remember, when you have increased IC Ps, right? That's going to increase the activity of the vagus nerve. And remember that increased vagal activity, right? It can cause you to release all this gastro-relaising peptide, you'll make more gastrointial, you make a ton of acid, and then you burn them because of the stomach, right? So that can cause that can cause an ulcer. That's a cushing ulcer. Remember, cushing's, you know, kind of has a lot of associations with brain. So that may be a nice way to sort of kind of remember that, right? So again, these PPI's that I've been making a big force about, well, what's the point of these drugs? How do they work? But remember that these drugs, they actually work by inhibiting the hydrogen potassium ETP's pump that we find on the surfaces of parietal cells, right? I mean, the basically inhibits like the gateway to all synthesis of acid in the stomach. So obviously, they'll probably be the most powerful, it'll make sense that they're the most powerful acid-reducing medications. They're the most powerful acid-reducing medications.

And then another thing I'll say about PPI is that's actually how you to know is, remember that these drugs since the mess up with the acid production, they're actually pretty good for treating insolential elicin syndrome, right? So remember, that's what people have when they have a gastronoma, right? And this hydrogen potassium ATP is pump, right? Like if you make a ton of antibodies against it, that's going to be prenecious anemia, right? That's one of the things that happens in a person that has a prenecious anemia, right? So again, these drugs, they work extremely, extremely well. They're the most powerful acid-reducing medications, they all end in Brazil, right? So it's a meprosol, Pantopryzol, and so, Prosol, and meprosol. And we use them for triple therapy, right? For person has like H. Bylory gastritis, remember, triple therapy, right? The pneumonia is cap, 40 years cap, so the C. Forchlorythromycin, the A4-Amoxicillin, and then the P4-PPI. But also, if a person has H. Bylory, right? So you're trying to use quadruple therapy. That's usually something doing triple therapy, it doesn't seem to be caught in it. PPI is also part of that regimen, right? The regimen there, obviously, is like metronides, all. There's bismuth, subsalicylate, so metronides, all bismuth, you know, pretty much peptobism, and then at tetracycline and a PPI, right? So that's what you're using, those are, those circumstances.

And then besides this, cushings also, high ICP, curliance, also, burn injury. Another situation where prison should also be placed on a PPI, like chronicly or naming the exam, says, if for some reason this person has to take steroids, chronically. Whenever a person has to take chronic steroid therapy, that's actually an indication for placing those people on PPI's, on prophylactic PPI's, right? Because steroids can increase a presence risk of a peptic ulcer disease, right? And also, if you're taking steroids, chronicly should also be placed on a bismuth, right? Remember steroids, the inhibit the activity of osteoblasts, right? So you have net osteoclastic activity, so your bones can be com-weaker, right? Osteoporosis right there. So you give bismuth, right? To essentially prevent osteoporosis in a person that's taking a long term clinical steroid therapy. Okay. Now what if they give you a question about a 50-year-old guy, you know, has a BMI of 35, so it's really bad? And then he tells you that he has this chest pain that gets worse when he's lying down. He has this cough that's worse at night. If you see that, what should you be thinking about on an MBM? Well, I really hope that you're thinking about good, right? Gustlers of a general reflux disease, right? And again, many times, your friends at the MBM, instead of putting good as an answer, they'll put all these things that I call pathophysiological answers, right?

So pathophysiological answers, what in the world do I mean? By a pathophysiological answer, is there a putting good as an answer? They'll put the pathophysiology as the answer, right? So remember, when people have a gird, is because they have like failure of the lures of a geosfinger, right? They have failure of the lures of a geosfinger, right? So essentially they have like decreased ton of that lures of a geosfinger. So there's a lot of reflux of acid, which obviously will cause a lot of problems, right? So what are some things that make people get gird? Well, if you're a big-time drinker, right? You have a very, very high risk of gird. If you're a big-time smoker, right? High risk. Basically just think of all the bad things that you can do with your life, right? If you drink a ton of alcohol, if you smoke a ton, if you're obese, right? I'm a caffeine, so I know that we feel bad for healthcare workers. I feel like healthcare workers are probably like the biggest coffee consumers in this country. I mean, the hospital probably collapse with all the coffee shop, but yes, so caffeine, right? Definitely increases the person's risk. And also if a person has hydrohernias, right? For a person who has hydrohernias, those things can definitely raise the person's risk of having a gird, right? So how do you treat a person that has gird? Well, again, try these lifestyle changes. Although the first line actually treatment is a PPI. PPI is always what you go for first, right?

But you know, you can also try a H2 blocker, right? A Histamine receptor blocker. So something like RAN-Neededine, right? I remember Cymededine is one of these H2 receptor blockers that's a little, little bit problematic actually on NBM exams. In fact, your friends have NBMD love to test Cymedidine. They love, love, love, love, love, love, Cymedidine, right? So why do they love Cymedidine? Well, one big thing with Cymedidine is that it's a very powerful inhibitor of Cymedidine P450, right? So it can make drugs that are metabolized by Cymedidine P450 more toxic because those drugs be auto-operated. So that's one thing with Cymedidine. Another thing with Cymedidine is that it actually has a very powerful association with Ganycomastia, right? Has a powerful as a strong Ganycomastia. So they give you a question about a person that has a H-Show gird or recently placed on some kind of medication, right? And then the person is developing boobies, right? If you see that, you want to think about Ganycomastia as a Cymedidine side effect. And then one of the unusual reason the Ganycomastia, Cymedidine, on MBM exams, they can give you a question about like some child and they tell you that this child or may not be a child this young adult. And this person, you know, is probably studied on like Kabarimizapine as a seizure medication for trigeminal neurology or something or maybe the breast injury in South and even the drink alcohol, they develop these neuropsychiatric symptoms.

They have a lot of abdominal pain and the ap has like a weird color. If you see that, I'd really hope you're thinking about I get into myth in Bofaria. The thing is whenever people have these Bofarias, you can actually slowly bring down, you can actually slowly bring down the levels of these Bofaria intermediates by giving us Cymedidine, right? You can lower the levels of these, you know, pothyrins by giving us, by giving us Cymedidine, right? So Cymedidine is kind of useful for those are kind of useful for those are purposes, right? So if a person has acute intermittent Bofaria or pothyracutinia tarda, you can actually help your symptoms, you can again, you can help your symptoms are actually giving Cymedidine, you see divine, how do Cymedidine helping these circumstances? Well, the thing is if you think about the retinine enzyme for the synthesis of HEM or those pothyrins, alas, right? Delta amino levelinic acid synthetics. Remember, it basically combines a glycine and succino coa and remember that uses B6 as a cofactor and you make delta amino levelinic acid. That's the first step of HEM synthesis. You can actually go ahead and give it that enzyme with Cymedidine, Cymedidine is a powerful inhibitor, right? So you can actually help in those circumstances. Remember glucose and HEM and HEM in, right? So glucose and HEM in, HEM in is spelled as HEMIN also in HEM data also in HEM enzyme as well, right? So, okay, right? So let's call back from this Cymedidine a bit, right?

So again, we said to trigger, you can use a PPI which we've talked about already. It means a H2 blocker, right? Remember, PPI is can actually also increase the presence risk of aspiration pneumonia, right? I mean, like that really low pH of your stomach, that pH of two is a big, big, big, big, big deterrent for, you know, lots of bacteria, right? You don't have very well a pH of two, right? So, you know, if you're killing the production of acid, it's going to cause a problem, right? It's going to cause a problem because those bacteria can then, you know, have things given, have a big party and then they can find your way up your suffigals, get into the lungs and cause an aspiration pneumonia. So, just something to keep at the back of your mind on the exams. And then remember, again, some lifestyle approaches to treating good, right? Again, tell these patients, lose weight, tell them to stop eating these inciting foods, you know, not be obese, don't smoke, don't drink alcohol, spicy foods kind of cut down on those, right? And that usually helps. But then let's say they're trying to get you to pick some kind of surgical procedure for a good. I remember you can do this procedure called the Nissan Fund Obligation, right? The Nissan Fund Obligation, right? So, again, just good, in general, how do you manage this stuff, right?

So, if a person comes in with a good like symptoms, you don't have to do any diagnostic testing, just go ahead and give them a PPI, try for six weeks, right? If that doesn't work, you can actually bump the dose of the PPI, give them like the maximum possible dose of a PPI. But then let's say you try all those things and it doesn't work, then, you then have to go to an EGD, right? And it's so far go, gastro-doatornoscopy, right? And it's so far go, gastro-doatornoscopy, an EGD, that's a basically like a colonoscopy, but instead of the colon, you're looking at the esophagus, the stomach, and the doirno, right? So, an EGD will help you look at this, or a gym, your closer, just to make sure there's nothing weird going on. Although, there are some people that you actually have to kind of skip that process, and that's if they present with a good, and they have alarm symptoms, right? So, let's say they have good, and they have weight loss, and that's not awesome, right? You're going to jump straight to an EGD, or they can give you a question about a person that has a good, and they already age of 50, for a person who has a good, and they already age of 50, but if had good for like many years, usually they'll be like a person that has had good for like 10 years or more, right?

Those people you don't bother doing the PPI, just jump straight to the EGD, because we want to make sure that you don't have anything weird going on, so let's say you've done the EGD, and you notice that, that's weird, this EGD is normal, then what should you be worried about? Or should you say, oh, you know what, because this EGD is normal, the person doesn't have good, no, no, right? Normal EGD does not roll off of diagnosis of good, right? So, in that case, you then proceed to 24 hours, so the JLP is monitoring, right? That's like the gold standard diagnostic test for good, right? That's the gold standard diagnostic test for, diagnostic test for good, right? So, remember again, obviously good can have some SQL I, right? People can have like, baritone, softagos from good, I remember baritone, softagos is a metaplesia, right? So, it's a metaplesia from the stratified, swimus non-characterized epithelium, you'll find in the esophagus, right? It's a metaplesia from that to intestinal epithelium, so one in the world, I mean by intestinal epithelium, I just pretty much mean a person having colomemone epithelium that is non-seleeded with goblet cells, right? Because remember, you do metaplesia when you are trying to deal with a different kind of stress, right?

So, normally the lower esophagus is not supposed to be dealing with acid, but once it starts having to deal with acid, you'll be like, okay, let's look more like kind of epithelium that's better suited to dealing with this acid problem, right? So, again, you have that metaplesia to intestinal epithelium, right? And typically when a person has baritone, softagos, when you do an EGD, like, you know, operating theoscopy, you'll see like pink or red like esophageum eucosa, right? And again, the thing you'll find on histology, non-seleeded colomemone epithelial cells, right? That have like interspersed goblet cells, and obviously that's going to increase a presence risk alpha adenocarcinoma, right? Remember, adenocarcinoma is tend to come from a glandular epithelium, right? So, it increases the presence risk of esophageal adenocarcinoma. Basically, the only risk factor on imbim exam is for esophageal adenocarcinoma is gourd. Every other thing that is overgose is exposed to smoking, drinking a ton of alcohol, having a calija, yada, yada, yada. Those things will increase the risk of esophageal scuimo cell carcinoma. That's very high up to no esophageal scuimo cell carcinoma. So, again, I kind of want to keep these podcast short. So, I'm going to go ahead and pause here, actually also have a meeting in about six minutes. So, thank you for listening today.

Again, if you want to sign up for the step one course coming up in April or the step 2ck slash step 3 course coming up at the end of this month, just go ahead and shoot me an email through the website. Their limited space is available, as long as they're still space, I'll be happy to give you details on pricing and having registered. And then I also offer one on one titerane for step one step 2ck step 2c step 2c step 2cs, which is now, I guess, a defunct exam. Although some school still offers step 2cs like exam, right? So, about step one step 2ck step 3 preclinical medical exams, 30-ish-off exams. If you're a medicine resident, I tutor for the medicine-entrinating exam and the medicine boards. So, if you need teaching in any of those areas, tutoring, just reach out to me again. I've worked with thousands of students at this point. And again, I've worked with people that have failed you as similar exams. Also, you know, if you also have like just a tricky application, right? They're trying to say to yourself for success with DRAS or your medical applicant. Again, just reach out to me. I do a lot of consulting in that regard. I mean, I've been on an admissions committee of a top two med school in the country. So, again, I have a lot of experience with this. I have lots of people that have USMD failures on the application and everything that have ultimately been successful. So, just reach out to me through the website.

Shoot me an email and I'll be glad to give you some more, some more direction on that. And please subscribe to the website again, Dividing Intervention Podcast.com. Whatever I mean, can a new podcast you get an email notification. And then I also have a You Tube channel Dividing Intervention USMD podcasts and videos. That's where I put my videos. So, again, please subscribe to that. And then obviously, I have these podcasts on Google podcasts on Apple podcasts on Spotify. Those apps keep the most recent 150 episodes. If you want to order the episodes from episode one, you have to go to the website again, Dividing Intervention Podcast with an S.com. So, thank you for listening. I'll see you in the next podcast. God bless you. Thank you.

The duodenum (or proximal small intestine).

Celiac patients may present with signs of malabsorption and/or low body weight; lactase deficiency typically has no specific physical exam or lab abnormalities.

Crohn's disease.

PP Is (Proton Pump Inhibitors).

Obesity, smoking, excessive alcohol consumption, or hiatal hernia.

Dapsone; it inhibits folic acid synthesis by targeting dihydrofolate reductase (or similar pathways).

Anti-tissue transglutaminase IgA (tTG IgA), anti-endomysial antibodies, and anti-gliadin antibodies.

Enterica Associated T Cell Lymphoma (EATL).

Increased ICP increases vagal activity, leading to excessive gastric acid release and the risk of developing a Cushing's ulcer.

It inhibits folic acid synthesis by acting as a competitive inhibitor of dihydrofolate reductase.

Barrett's esophagus; this is the precursor to esophageal adenocarcinoma.

Inhibition of CYP450 enzymes (making other drugs toxic) and causing gynecomastia.

Anti-tissue transglutaminase IgA (tTG IgA), anti-endomysial antibodies, and anti-gliadin antibodies.

Enterica Associated T Cell Lymphoma (EATL).

Increased ICP increases vagal activity, leading to excessive gastric acid release and the risk of developing a Cushing's ulcer.

It inhibits folic acid synthesis by acting as a competitive inhibitor of dihydrofolate reductase.

Barrett's esophagus; this is the precursor to esophageal adenocarcinoma.

Inhibition of CYP450 enzymes (making other drugs toxic) and causing gynecomastia.