DIP Ep 575: USMLE Step 2/3 Rapid Review Series 118

Strongly encourage you to go back and take a look. Go back and take a look. Um, go on my website, divine intervention podcast.com, and then look at exam topics list. On the exam topics list, I do actually talk about Um, the you know, it's like, hey, rapid review series one is this, series two is that, you know. All right, so let's jump right into it. So what if they give you a question?

About a patient, they tell you that this patient, you know, their hands, uh the the skin around their hands and their fingers looks very tight, around their forearm, you know, looks very tight. And you're told that this person has been having dysphagia for the past one month, right? And that the person's symptoms have not been well controlled with over-the-counter therapy. And then they then ask what's your most appropriate next best step in money.

So I would really hope that on your exams, you're probably thinking of getting an EGD, getting an esophagal gastrodoodenoscopy. So this person probably has scleroderma, right? This person probably has scleroderma. Right. And we know that scleroderma can cause a lot of problems with the esophagus. You know, many of you probably know about crest scleroderma. So what does the crest stand for? Well the C stands for calcinosis.

The R stands for Renault Phenomenon, the E stands for esovagio dysmortility, the S stands for Sclerodactyl, and then the T stands for telingjectes. Now, the thing is, the MBMEs, again, they know that we live in an onky generation, right? They literally know that, hey, all of you have memorized.

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Well if you think about it, people that have scleroderma, right, they've literally fibrosed like their esophagus, they've fibrosed many parts of their GIG. So that fibrosis, right, can actually cause incompetence of the lower esophageal sphincter. Okay. That fibrosis can cause incompetence of the lower esophageal sphincter. And those people, these people can have significant girth.

But let me ask you this this significant GERD, what can it lead to? What kind of big long term problem can it lead to that can also cause dysphagia? It can, you know, obviously you can have a sulfagiodis motility that makes it hard for you to swallow. But one weird thing that you may see on your exams, believe it or not, is that these people may develop esophageal structures. Okay? They may absolutely positively develop what? Esophageal structures.

This is actually something that many people do not keep in mind for their test. Whenever you have chronic GERD, that can lead to the development of adhesions and structures in your esophagus. And when you have those adhesions, when you have those structures, it can make it hard for food to pass through. So your our friends at the MBMEs, they can literally give you a scleroderma question.

And they intentionally omit information that relates to esophageal dysmotility or relates to GERD. And the right answer will end up being um the person having uh esophageal stretch. So it's just something you want to keep at the back of your mind on exams. In fact, they can give you a question about a person that has scleroderma and this person is losing weight and this person is having dysphagia to solid.

Right? You know, uh if you see that again, you wanna get that EGD because these people can absolutely get a Sovagiladinocarcinoma. Again, see, let me tell you something. In fact, I was saying this to people in the 20 hour class that was started yesterday. I said that. The USMLEs these days is not like they've suddenly stopped testing the classic pathologies that they have always tested. No, they've not stopped. That's one thing people need to get into their brains. They have not stopped.

But one thing that they've started doing these days as almost like I I feel like it's almost like a counter against this pervasive anky use and people just memorizing things without understanding. Is that they create questions these days where it's the same classic pathologies they test, but they test it in an unusual population. Right? Like for example, it's like giving pneumocystis girovetsi to a person that does not have HIV.

Everybody knows the association. Interstitial pneumonia, HIV patient, pneumocystis giroveti, all of you know that. But how about giving pneumocystis girovetsi to people that are on chronic steroids? How about giving pneumorcy drovetsi to people that are on chemotherapy? How about giving pneumocystes Giroveti to post transplant patients that are on immunosuppression? These are all things they can do to you on an exam, right? So don't think that Barrett's esophagus.

And esophageal adenocarcinoma will just be restricted to people that consume alcohol, people that are unhealthy and obese. Although alcoholism probably raises your risk more for esophagel squino cell can. Right. So j j just be careful that anything that causes incompetence of the lowest of a Jill Sphinx.

Right. So say for example, if you have um scleroderma because you're fibrosed your you know your your esophagus, that can cause you to have barrels esophagus, that can cause you to have esophageal cancer. You saw how I just discussed a dysphagia question in a person with bar in with scleroderma, and it was due to strictures, right? So you want to be careful about that on your exams. Please be careful about that on your exams.

Another thing that can also cause incompetence of the lowest of a jail sphincter. Since we're talking about it, let's make the integration. Although many times these people are not going to proceed all the way to Barrett. all the way to a severe cancer because it's a temporary thing. It's pregnancy, right? So they can give you a question about a pregnant woman. They'll say that this lady, you know, her last menstrual period was like ten weeks ago.

And that this patient has noticed uh you know s you know uh like this uh sow sensation in her in her upper throat. Uh that is worsened by laying down and it improves when she sits up. It improves over the course of the day. Right? But it's worse at night. Right. And they'll say that uh, you know, omeprze was administered which significantly improved her symptoms.

And then they ask you, uh, what is the most likely on the line mechanism behind this patient's presentation? Pick the answer that says word. Lower suffagel sphincter hypotonia, right? Or pick the answer that says incompetence of the lower suffages sphincter. So you may wonder, divine, what in the world are you talking about? How can a person have incompetence of the lowest of a gel sphincter? How can they have hypotonia of the lowest of a gel sphincter and be pregnant?

Well the thing is when you're pregnant, there's this amazing thing called the placenta, right? Now one of the things that is produced in high quantity by the placenta is progesterone. Many people do not give progesterone credit for this, but progesterone is a very powerful smooth muscle relaxant. I'm gonna say that again. Progesterone is a very, very powerful smooth muscle relaxant. So because progesterone is a powerful smooth muscle relaxant.

It can actually relax your lower esophageal sphincter and you can have a ton of reflux that can cause significant GERD. If any of you are listening to this podcast and you've ever been pregnant, you probably know that G, once pregnancy comes, Amazing GERD just shows up. And it's pretty remarkable after you deliver your baby, you notice that within like a few days, a few hours, that gird just completely resolves. Why? Because the placenta is out. If the placenta is out, let me tell you this.

Where's that source of progestine? It's gone. That's why you notice many women that are pregnant are placed on PPI therapy, are placed on PPI therapy. Again, keep those integrations in mind. Right? Progesterone explains so many things you see in pregnancy, even like the reduction in blood pressure you see in pregnancy. Right. Think about it. If you're smooth muscle relaxant, you're gonna decrease the systemic vascular resistance.

If you decrease the systemic vascular resistance, that's gonna lower your diastolic blood pressure, it's gonna lower your blood pressures, right? Or think about it in pregnancy, you know, you notice that man, most times when you go for your prenatal visit, And again, all these things are USME questions, by the way You know, you're going for your prenatal visits and you notice that hmm.

Uh they're always collecting a urine sample because you have a high UTI risk during pregnancy. Well why is why why is that the case? Well the reason that's the case is because in pregnancy, in pregnancy, in pregnancy, remember, what is one thing that happens? One thing that happens is that uh You d you know your your ureters your ureters are lined with smooth muscle. If you re if you relax the smooth muscle that lines your ureters.

That is going to cause you to have ureteryl dilation. If you have ureteryl dilation, that's going to cause urinary stasis. And if you have that urinary stasis, guess what can happen? That can increase your risk of developing UTIs, right? Just think of like stationary fluid that's a great nidus for bacteria to build.

Right. And what's going to be the most common cause of UTIs? I would hope you're saying divine is going to be E. coli. It's going to be E. coli, right? So make sure you know these things for your test. All right. Now, what if they give you a question about a patient and they tell you that this patient

um has appointed a durable power of attorney. But this patient, you know, yes, they've appointed a durable power of attorney, but the patient is still uh I guess I don't really know how to frame this as a question. I guess it's a fact I'm just gonna tell you. Right? Uh but the th this person still has capacity.

And who is gonna make decisions for the patient? Is it gonna be the patient or the DPOA, the durable power of attorney? I would hope you're saying that divine, the person that's gonna make decisions for this patient is gonna be the patient themselves. This is one thing that many people screw up on the US MLE exam. The fact that you have a durable power of attorney does not mean that you cannot make decisions for yourself.

I'm gonna say that again. The fact that you have a durable power of attorney does not mean you cannot make decisions for yourself. You absolutely positively can still make decisions for yourself. What is the role of a durable power of attorney?

The role of a doable power of attorney is to help you make decisions in the event that you become incapacitated. In the event that you become what? Incapacitated. In the event that you become incapacitated. But as long as you are still lucid, as long as you can still make Decision? You can absolutely positively

still make your make your decisions, right? You you'd even if the DPOA is in the picture, it doesn't mean anything. Again, your DPOA only comes into full view when you're in a situation where you're incapacitated. You've lost the ability to make decisions for yourself. All right. Now, what if they give you a question?

About a patient and they tell you that this is a you know a 14-year-old male and that for the past five days he has been having bloody bowel movement. Right? You're told this person has been having bloody bow movements. This person has uh

You know, having bloody bowel movements has been having like nosebleeds. Um, they tell you that this child has a chemosis of the skin. And then they give you labs and you notice that the child's platelet count is twelve thousand and the creatine is like three point. Right, the creatinine is like 3.5. And then they say what is the most likely underlying cause of this patient's presentation.

And then they put an answer that says Salmonella, they put an answer that says Shigella, they put an answer that says uh enterotoxygenic E. coli. They put an answer that says uh uh giardia lamblea and then they put an answer that says entamiba histoletica what answer should you pick i would really hope you're picking the answer that says shigela i would really really hope you're picking the answer that says shigela

So let's talk about this, right? So what does this child have? I would hope you're seeing divine. It appears that this child has hemolytic uremic syndrome. I'm gonna say that again. This child has what? Hemolytic uremic syndrome. Now, I know some of you may be like, Devine, the answer you're picking makes no sense. Why are we not picking the E. coli answer? Well, this is where paying attention to your exam question is very helpful.

What E. coli did I mention? I mentioned enterotoxygenic E. coli. Right? Remember, that's one of the most common causes of travelers' diarrhea, right? Enterotoxygenic E. coli. I did not say E. coli O157H7. E.0157H7 is the one that causes, is the one that causes, is the one that causes HUS. Not E-Tech. E-Tech does not cause H2S. But if you notice, I was very coy in putting an equalized species as the answer.

Because in the heat of an exam, when people are not focusing, when people are not concentrating, they can by sleight of hand pick E. coli as an answer instead of picking Shigella. Make sure you're picking the right E. coli species. E-Tech does not cause HUS on the exam. E-Tech does not cause hemolytic uremic syndrome. The thing that causes hemolytic uremic syndrome is enterohemorrhagic E. coli. Ehec right? E. coli O one five seven H seven. That is the most common cause of HUS.

But since we did not see that specific E. coli species in this question, you need to go for the next best thing, which is Shigella, right? And what tells us in this question that this person has uh Hemolytic uremic syndrome. Well, we know this person has HUS because the person has bloody diarrhea, right? The person has uh thrombocytopenia and its antecedents. You see I said that the platelet count I think I said twelve thousand.

And then you also see antecedents of low platelets, right? The person has like nosebleeds, right? So like bleeding because they don't have good primary hemostasis. The person has um Echemos C TKI prepared on the skin. The thing is sometimes with these questions, instead of giving you the low platelet count, because the low platelet count kind of gives things away, they can give you antecedents of low platelets instead, like what?

They can give you things like echemoses. They can give you things like pTchii. They can give you things like purpura on the skin. So just be mindful of that. And you see this person has acute renal failure as well, right? We'll see the person's creatinine is elevated.

So, what are some follow-up questions you may see with this? Well, if you think about it, they can ask you what is the most likely finding on a blood smear, on a peripheral blood sample in this patient? I would really hope you're saying that oh divine, I'm gonna pick the answer that says shistocytes, right? Schistocytes. Remember, another name you may see for schistocytes on your exams are fragmented erythrocytes. Okay, fragmented erythrocytes.

typically you're gonna see schistocytes on a blood smear When a person has something causing a maha, what do I mean by maha? Maha means microangiopathic hemolytic anemia. Microangiopathic hemolytic anemia. Microangiopathic hemolytic anemia.

So typically these people, right, they they they can have all these things, you know, some sometimes they can have these von Willibrand factor, you know, multimers that are literally sharing the red blood cells in their in their bloodstream, right? That's what creates those schistos. And I would really hope that you know the other causes of schistocytosis on your exams, right? DIC, right? You can see this in DIC. You can see this in a person that has a uh

Uh so a person that has DIC, a person that has TTP, thrombotic thrombocytopenic prepora, right, that can cause schistocytes on your exams as as well. Right. And then they can ask you, what is the most likely mechanism behind this patient's bloody bowel movement? Well, I hope you're picking the answer that talks about invasion of the intestinal mucosa. Invasion of the intestinal mucosa.

The thing is, whenever you see a bug that causes bloody diarrhea, it usually causes that problem by invading the intestinal mucosa, right? Invading the intestinal mucosa, right? So, like for example, if you think about it, Shigella. Shigella invades uh what it does is that it's picked up by your immune system cells that we find around like the terminal ileum. It's picked up by those cells.

But the thing is, when it's picked up by those cells, it destroys those immune system cells. Right? It destroys those immune system cells. And when you destroy those immune system cells, guess what's gonna happen? The thing is, as it destroys, it then spreads into the other epithelial cells that line your GI. Right. And it's going to cause those cells to die. And as those cells die and they slough off, you're going to have bloody diarrhea.

Don't mess with Shigela. Shigela does not Shigela, you know, for all the Golden State Warriors fans out there, uh, strength in numbers is not a model, is not a theme with Shigella. What Shigella does is it doesn't Shigella is like a special operations uh operative, right? Like special forces or operative. Well, it just needs like 10 organisms and you're in deep trouble, right? You're literally in deep trouble.

And the thing is, since again our friends at the USMLEs love to go after basic sciences these days, first things first. What are the immune system cells we find, or what's like the big component of the immune system that you'll find around the terminal ileum? I would really hope you're seeing divine we have those pyres patches.

those pyres, patches, please. Do not ignore these basic science things. Do not think that, oh, I am done with the US semile step one examination. I do not have to worry about these things anymore. No. You could not be more mistaken on your exams. Again, since step one became past fail, and especially since last year. Our friends at the MBMs have become very good at shunting a lot of basic sciences to the USMLE step two CK and Step Three exam.

Right. So again, don't forget your pyre spotches that we find in the where in the terminal ileum. Right. In the terminal ileum. Right. And remember the classic Shigella that they love to go after on the exams is Shigella Sony. Shigela Sonyi. S-O-N-N-E-I. Shigela Sonyi. Right. So keep that thing in mind. Right. And this child that has H U S. How are we going to treat this child that has H U S?

Well, you're gonna treat this child with supportive care. Okay, supportive care. They will try to trick you on your exams into treating the Shigella by giving antibiotics. That could not be a worse decision that you could take for this child. You know why? The problem with that is that it's the toxin, the sugar toxin, that is causing the problem. So if you give more anti if you give antibiotic, you're gonna kill more bugs. If you kill more bog, you release more toxin.

If you release more toxin, you will explode the child's kidneys. You will absolutely destroy this child. So don't do that, right? That's not a smart thing to do. Okay, please. That is not a smart thing to do on your exams. I'm gonna say that again. That is not a smart thing to do on your exams, right? That's not a smart thing to do on your exams. Many people ignore how powerful bacterial toxins can be on the on the in real life, but also on the USMLE exam.

Right. In fact, since I'm talking about toxins, let's make some toxin integrations. Right? Let's make some toxin integrations that our friends at the MBMEs love to throw on. Number one, right? We we've kind of talked about the sugar toxin, right? Um, well, what's another toxin you may see on your exams? Well, think about a person having. Uh toxic shock syndrome, right?

Toxic shock syndrome usually is going to be caused by toxins, right? It's caused by toxins. It's caused by the release of exotoxins, right? Those exotoxins are released and those things cause you significant pain, significant trouble. This is why when a person has toxic shock syndrome, one of the things you want to try to give them on your exams is clindamycin.

is clindamycin. Again, I don't know why I'm going off on this tangent of toxins, but toxins are very, very high yield to know for step two CK and step three. Again, they're not only relevant for step one. Right. But those toxins, right, they cause a lot of damage. Those exotoxins. Exotoxins. Exotoxins. Remember, we tend to find exotoxins with what? With gram-positive organisms.

uh with gram-positive organisms, right? So those exotoxins cause problems. That's why if you're treating a person that has toxic shock syndrome, you want to use something that includes clindamycin, right? Clindamycin is a 50S inhibitor. It's a protein synthesis inhibitor.

Because it's a protein synthesis inhibitor and a toxin is a protein, it will reduce the production of those toxins and that's going to help out the patient. Okay, what's another high yield toxin thing to keep at the back of your mind for exams? Another high yield toxin integration. Well, think of a person. Think of a person that you know, let's say that they have like redness and severe tenderness around their knee.

And then you're told that man over a two, three hour period, they now start having bullsh changes in the skin. And the redness has spread to the person's um uh foot. Uh that person probably has necrotizing fasciitis, neck fascia. Again, many times neck fash is caused by uh by organisms that elaborate a lot of toxins. This is why part of the treatment regimen for necrotizing fasciitis is clindamycin. Again, 50S inhibitor, protein synthesis inhibitor.

What's another toxin thing they can toss on step two and step three? Well think of a person that has watery diarrhea, right, after they've been treated for community acquired pneumonia in the hospital. Well why would those people have watery diarrhea? Well they have C diff colitis. C diff colitis. Well, remember C. diff. How does C diff get you in trouble? It gets you in trouble by uh using toxins, right? In fact, one of the ways we diagnose C diff.

Is by looking for the toxin in the stool. Obviously, if a person has CDF infection, you're gonna treat them with oral vencomycin or oral fidaxomycin. Again, our friends at the MBMEs, they're not stupid. They know that all of you that have the job description medical student know about Vencomycest. But you know that many people, or at least an appreciable number of people, do not know about fidaxomycin. So please consider fidaxomycin on your exam.

Right? Or what if they give you a question about a patient and they tell you that this patient, you know, is a sex worker, and this sex worker patient. has this painless lesion on the you know, on the v vaginal mucosa, right? And the patient is placed on, you know, oral antibiotic therapy or IV antibiotic. Okay, let's say IV antibiotic therapy. And then you're told that this patient, uh, four hours after therapy was initiated, the patient begins to have like a a a rh.

Right? The presin b begins to have like reddening of the skin, becomes hypotensive. But what are you thinking about? I hope you're thinking about treponema pallidum. You're thinking about syphilis and the jarish hexheimer reaction. The jarish hexheimer reaction, right? So you're treating a person that has syphilis, you're giving a cell wall inhibitor, right? Penicillin. Remember, penicillin is the treatment of choice.

for syphilis and as you release those uh as you use a cell wall inhibitor the cell is literally exploding as the cell explodes what do you think is going to be happening to all those stuff that it has within it you know, cellulite intracellular environment. It releases it into the blood stream.

Again, kind of like a toxin, those things that are inside, like the cell soap of an organism, can trigger very powerful inflammation and that can cause the person to have problems, right? So keep that in mind for your exam.

Right. What's another toxin they can test on your exam? Well, what if they give you a question about a person that's an immigrant from a foreign country, right? Immigrant and they tell you that the person's vaccination history is unknown.

And that this person for the last you know four days, the person has been having like sore throat and the person has been having like odinophasia, right? And they tell you that the person is drooling. And I can almost promise you on your and you know they'll they will give you some laugh. And they will even give you like a throat exam, right? And you'll notice like big, big, big time swelling of the person's like firings and things like that.

I can almost promise you on your exam, do you know one answer they're gonna give you? They're gonna give you epiglottitis, right? They're gonna give you epiglottitis. And they know that many people will rush headfirst to picking that answer. Resist the temptation to pick that answer. Look at the context that I'm giving here. Again, context really matters on the US MLEs. I'm giving context of an immigrant.

I'm giving context of like wow you see this swelling of the pharynx and things like that. What is this? This person has diphtheria. This person absolutely has what? Diphtheria. Remember, diphtheria makes a toxin. That toxin, uh, in fact, we call it the ABXotoxin. And how does this toxin work? This toxin works. By ribosylating elongation factor two. Okay, it causes ribosylation of elongation factor two. When you ribosylate elongation factor two, it's gonna stop working.

Well where do you remember elog elongation factor two from? You probably remember elongation factor two. from the process of translation, right? Of mRNA into a protein. Again, maybe like, wow divine, you're drawing on so many things that I've learned from step one. Again, see. C, why do you think I'm going through the trouble of going through all these toxins and the mechanism of action of these toxins?

I'm not going through them because I like to hear myself speaking. Again, see, you don't even have to believe what I'm saying. Just ask people that have taken steps too recently. Or people that have taken step three recently, you're gonna see that they ask these basic science questions where they ask about the mechanism of action of toxins. In fact, I'm telling you this, that's actually a very, very high-ield knowledge to know for step two, and especially for step three.

Step three is one of those exams. So don't get me wrong, step two has a lot of basic science these days. But step three has more basic science than you're even expecting, right? Step three is almost like a step one exam and a step two exam rolled into one with CCS cases thrown in for good measure.

And a lot more biostats than you're used to, right? So please be careful about this. I know you may be like Divine, who cares about this stuff? Well, you're gonna care about it when you see it on your test. Actually do the studying and make sure you know these things, right? So remember uh the diphtheria toxin, it's an ABXO toxin. And what does it do? It causes ribosylation of elongation factor two.

When you ribosilite elongation factor two, you're going to shut down the synthesis of proteins because translation, right, does not work as well as it should. You're not going to be able to go from mRNA all the way to protein. Is there another toxin that does uh Is is uh are there other toxins that cause ADP ribosylation? Absolutely there are.

right? There are absolutely other toxins that can cause this ADP ribocy, right? So w we've talked about this in the context of Uh we've talked about this in the context of the Of the diphtheria toxin. But what are some other toxins that cause this same thing? What are some other toxins that cause this same thing that you need to know for your exams? Right? What are some other toxins that cause this same thing that you need to know for your exams? Well don't forget Sudomona.

Pseudomonas!Pseudomonas has an A-toxin That causes ADP ribosylation of elongation factor 2. Okay. Pseudomonas also has a toxin that causes ADP ribosylation of elongation factor 2. Again, please make sure you know this. Make sure you know this. Right, elongation is a step in translation. If you don't know this stuff again.

Wish you all the best as you're prepping for your exams. Okay, what's another toxin uh that you should know for your tests, right? Think about the cholera toxin, right? Remember cholera has a toxin. What does that c cholera toxin do? Well the cholera toxin it causes you to secrete lots and lots and lots of chloride iron. Into the lumen of your GI tract. It causes you to secrete lots and lots of chloride ions into the lumen of your GI tract.

As you secrete all those chloride ions, water is gonna follow. And as water follows, you're gonna have a secretary diarrhea. You're gonna have a secretary diarrhea. Please do not lose sight of this on your test. Let me actually tell you this. The cholera toxin basically is or it activates adenylate cyclase, right? So as you activate adenylate cyclase, you're gonna make a ton of cyclic AMP, and that's gonna cause you to release a lot of chloride ions into the lumen of your GI.

All right. So I think I've kinda hit toxins in uh in uh i i in a lot of the depth that I that I wanna hit. At least these are a lot of the classic ones they love to go after on exams, right? Let let's say a few more things and then we'll kinda wrap this up, right? So what if they give you a question about a patient?

And they tell you that this patient has osteoarthritis, right? But that this patient also has a history of peptic ulcer disease, right? So they say that, you know, what is the most appropriate pharmacotherapy for this patient? Right. I would really hope that you're picking an answer that talks about like selecoc. Right. You you you want to use a COX-2 inhibitor because this person that has a history of peptic ulcer disease.

You don't want to give them like a regular NSAT because if you give them a regular NSA, that can absolutely cause them to have uh you know exacerbation of their peptic ulceral disease, they can bleed, right? Because remember, how does an irregular NSAT work? A regular NSAID works by inhibiting COX one and COX two, right? It's a reversible inhibitor of COX one and Cox two. Remember, aspirin is an irreversible inhibitor of

Cycloxygen is one and and two, right? But if you you and and the thing is COX one works in the GI tract, right? Cox one works in the GI tract. Now you may be like divine. Why is that such a big deal? Well the problem is if you inhibit COX1 in the GI tract, you're gonna make less in the way of prostagland.

And if you make less in the way of prestaglandins, then you're going to make a lot of acid in your GI tract, especially in your stomach. And as you make more acid, right, that's gonna mess up your stomach and that's gonna cause you to have peptic osteo disease. Right. So that's why if we can avoid something that targets COX1, then we can help these people that have peptic ulcer disease but still relieve their pain.

Still help them with inflammation like in the setting of osteoarthritis, right? So COX2 is some you you you Is something that's not found in the GI tract, right? So if you want to get like an N set like effect, but Not target COX1. Use a COX2 inhibitor like Sele Coxib. Okay. Use a COX2 inhibitor like Sele Coxib. Again, COX2 inhibitors, they have very minimal gastrointestinal side effects. Alright.

So I think I'm gonna go ahead and stop here. Uh again, this is a rapid review podcast. Again, as I do, at the end of every podcast, again, I do offer a bunch of classes for the USMLE exams. I have a ton of classes in the month of March. Um starting with the step one class is in the first week of March.

I mean it's a 25 hour class if you're if you're prepping for step one or you're studying for step two and step three and you have a poor basic science foundation, let's say you failed step one or you had a long dedicated period for step one or you've just forgotten a lot of things from step one. You'll really appreciate the twenty five hours step one clock.

Uh and then uh later in March I have like an MBME test taking class, I have a biostats class, I have a social sciences, ethics, QI, and healthcare systems. hospital medicine class. That's a five hour class. Those those three classes I just mentioned are for step one to step three. And then I have a last minute review and a 20 hour step two step three review. Uh those classes are for step two and step three specifically. And then in the month of June,

First two weeks of June, I have a 50 hour step two, step three class. I've actually made a podcast where I talk about these classes in detail. If you're interested in more information, just shoot me an email and can give you some more information. And then I also offer one or one tutoring for all the USMLE, all the complex complex exams.

And I have these podcasts on Apple, Google, Spotify. I have a YouTube channel you can check out. That's where I post the videos that I make. And then uh don't forget that I also help with Eras applications, mock interviews, personal statements and things of that nature. Um, and then I have another website called divine intervention lifelessons.com. Divine intervention life lessons dot com. Every week I post like two or three podcasts. Many of you know I'm a Christian.

Uh so from a biblical perspective I address a life lesson. Biblical perspective. Uh it's called again Divine Intervention Life Lessons dot com. There's actually an Apple podcast associated with that called the Divine Intervention Life Lessons Podcast. Divine Intervention Life Lessons Podcast. Again, tons of people listen to these podcasts and find it to be very, very helpful.

Thank you for listening to me today. I will see you in episode 576. God willing. Have a wonderful rest of your day. God bless you and bye for now. Thank you.