DIP Episode 575 - USMLE Step 2/3 Rapid Review Series 118

All right welcome to episode 575 of the Divine Intervention Podcasts. In today's podcast we're going to be Pantina Rapid Review Series for the US Emily Step 2 CK and Step 3 exams. This is going to be series 118, series 118. Again if you want to know the specific episode numbers for these things, strongly encourage you to go back and take a look, go back and take a look. Go on my website, divineinterventionpodcast.com and then look at exam topics list. On the exam topics list I do actually talk about the, you know, it's like hey Rapid Review Series 1 is this, series 2 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, 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 therapies. And then they then ask what's your most appropriate next best step in management. So I would really hope that on your exams, you're probably thinking of getting an EGD, getting an S.O.F.R.G.O. gastro, do it anoscopy. 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 sea stands for calcium doses. The R stands for renotes phenomenon. The E stands for esophageal dysmortality. The S stands for sclerodactyl and then the T stands for telegenic tissues. Now the thing is the MBA me's, again, they know that we live in an Anki generation, right? They literally know that, hey, all of you have memorized. Scleroderma, scleroderma, scleroderma, you know the crest, crest, crest, crest. It's an an Anki, it's in many Anki decks out there. So what is the easiest way to see if people really understand what's going on? Is to just bring in an esophageal problem in a somewhat different light from what you're used to. So for example, what could this be like? Well, if you think about it, people that have scleroderma, right, they've literally fibros like their esophagus, they've fibros many parts of the agitract. So that fibrosis, right, can actually cause incompetence of the lower esophageal's finger. That fibrosis can cause incompetence of the lower esophageal's finger. Those people can have significant gird. But let me ask you this, this significant gird, what can it lead to? What kind of big long-term problem can it lead to that can also cause this phasia? It can, you know, obviously you can have esophageal dysmortality 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 tests. Whenever you have chronic gird, 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 friends at the MBM is they can literally give you a scleroderma question. And they intentionally will meet information that relates to esophageal dysmortality or relates to gird. And the right answer will end up being the person having esophageal structures. 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, the haschleroderma. And this person is losing weight and this person is having this phasia to solid, right? You know, if you see that again, you want to get that EGD. Because these people can absolutely get a esophageal adenocursinoma. Again, see, let me tell you something. In fact, I was seeing this to people in the 20-hour class that was started yesterday. I said that the USML is 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 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 with the same classic pathologies they test, but they tested it in an unusual population. Right? Like for example, it's like giving no more sisters to a person that does not have HIV. Everybody knows the association, interstitial pneumonia, HIV patient, no more sisters are a wetsi. All of you know that. But how about giving no more sisters to wetsi to people that are on chronic steroids? How about giving no more sisters to wetsi to people that are on chemotherapy? How about giving no more sisters to wetsi 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 baritone suffragous and a so-for-gyll adenocursinoma will just be restricted to people that consume alcohol, people that are unhealthy and obese. Although alcoholism probably raises your risk more for a so-for-gyll skin cells cancer. Right? So just be careful that anything that causes incompetence of the lower so-for-gyll's finger. Right? So say for example, if you have scleroderma because you have fibroast, you know, you're suffragous, that can cause you to have baritone suffragous, that can cause you to have a so-for-gyll cancer.

You saw how I just discussed a dysphysia question in a person with baritone 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 lower so-for-gyll's finger, 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 baritone, all the way to a so-for-gyll cancer because it's a temporary thing, it's pregnancy. Right? They can give you a question about a pregnant woman. They'll say that this lady, you know, her last menstrual period was like 10 weeks ago, and that this patient has noticed, you know, like this sore sensation in her, in her upper throat, that is worsened by laying down, and it improves when she sits up, it improves over the course of the day. Right? It's worse at night. Right? And they'll say that, you know, Omeprazo was administered, which significantly improved her symptoms. And then they ask you, what is the most likely on the line mechanism behind this patient's presentation? Pick the answer that says, what? Lower so-for-gyll's finger hypotonia, right? Or pick the answer that says, incompetence of the lower so-for-gyll's finger. So you may wonder, divine, what in the world are you talking about? How can a person have incompetence of the lower so-for-gyll's finger?

How can they have hypotonia of the lower so-for-gyll's finger and be pregnant? Well, the thing is, when you're pregnant, there's this amazing thing called a 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 going to 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 so-for-gyll's finger. And you can have a ton of reflux that can cause significant growth. If any of you are listening to this podcast that you've ever been pregnant, you probably know that G1's pregnancy comes. Amazing growth just shows up. And it's pretty remarkable, after you deliver your baby, you notice that within like a few days or few hours, that growth just completely resolves. Why? Because the placenta is out. If the placenta is out, let me tell you this. Where is that source of progesterone? It's gone. That's why you notice many women that are pregnant are placed on PPI therapy, at least on PPI therapy. Again, keep those integrations in mind. Progesterone explains so many things you see in pregnancy. Even like the reduction in blood pressure you see in pregnancy. Think about it. If your smooth muscle relaxant, you're going to decrease the systemic vascular resistance.

If you decrease the systemic vascular resistance, that's going to lower your darstolic blood pressure. It's going to lower your blood pressure. You think about it in pregnancy. You notice that, man, most times when you go for your prenatal visit. And again, all these things are USMD questions, by the way. You know, you go for your prenatal visit. And you notice that, hmm, they're always collecting a urine sample, because you have a high UTI risk during pregnancy. Well, 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, you know, your uriders, your uriders are lined with smooth muscle. If you relax the smooth muscle that lines your uriders, that is going to cause you to have your arterial dilation. If you have your arterial dilation, that's going to cause urinary stasis. And if you have the urinary stasis, guess what can happen? That can increase your risk of developing UT Is, right? Just think of like stationary fluid. That's a great need for bacteria to build up, right? And what's going to be the most common cause of UT Is? I hope your 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, um, I guess I don't really know how to frame this as a question. I guess it's a fact I'm just going to tell you, right? But this person still has a capacity. And who is going to make decisions for the patient? Is he going to be the patient or the DPO, the durable power of attorney? I hope you're saying that divine, the person that's going to make decisions for this patient is going to be the patient themselves. This is one thing that many people screw up on the US Emily exams. The fact that you have a durable power of attorney does not mean that you cannot make decisions for yourself. I'm going to 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 durable power of attorney is to help you make decisions in the event that you become in capacity, in the event that you become what in capacity, in the event that you become incapacitated. But as long as you're still lucid, as long as you can still make decisions, you can absolutely positively still make your decisions. Even if the DPO is in the picture, it doesn't mean anything. Again, your DPO 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 14-year-old male and that for the past five days, he has been having bloody bowel movements. Right? Your total dispersion has been having bloody bowel movements. This person has, you know, having bloody bowel movements has been having like nose bleeds. They tell you that this child has a key emotional of the skin and then they give you labs and you notice that the child's pleated leg count is 12,000 and the creatinine is like 3.5. The creatinine is like 3.5. But in this say, what is the most likely underlying cause of this patient's presentation? And then they put an answer that says Samonella, they put an answer that says Shigella, they put an answer that says Enterotoxigenic Ecoli, they put an answer that says G-ardial Ambleia and then they put an answer that says Entamiba Histolirica. What answer should you pick? I would really hope you're picking the answer that says Shigella. I would really, really hope you're picking the answer that says Shigella. 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 hemoletic Euremic Syndrome. I'm going to say that again, this child has what? Hemoletic Euremic Syndrome. Now I know some of you may be like divine. The answer you're picking makes no sense. Why are we not picking the Ecoli answer?

Well, this is where pain attention to your exam question is very helpful. What Ecoli did I mention? I mentioned Enterotoxigenic Ecoli, right? Remember, that's one of the most common causes of travelers diarrhea, right? Enterotoxigenic Ecoli. I did not say Ecoli 0157 H7. Ecoli 0157 H7 is the one that causes. Is the one that causes. Is the one that causes H2 S. Not E-Tech. E-Tech does not cause H2 S. But if you notice, I was very coy in putting an Ecoli species as the answer. Because in the heat of an exam, when people are not focusing, when people are not concentrating, they can buy a slice of hand, pick Ecoli as an answer. It's not picking Shigella. Make sure you're picking the right Ecoli species. E-Tech does not cause H2 S on the exam. E-Tech does not cause hemoletic Euremic Syndrome. The thing that causes hemoletic Euremic Syndrome is Entero-Hemoragic Ecoli. E-Tech Ecoli 0157 H7. That is the most common cause of H2 S. But since we did not see that specific Ecoli species in this question, you need to go for the next best thing which is Shigella. And what tells us in this question that this person has hemoletic Euremic Syndrome? Well, we know this person has H2 S because the person has a bloody area. The person has a thrombocytopenia and its antecedent. You see, I've said that the bleak leg count, I think I said 12,000. And then you also see antecedents of low bleaklets. The person has like nose bleeds, right? So like bleeding because they don't have good primary hemostasis.

The person has echimosis, PTK, I prefer on the skin. The thing is sometimes with these questions, instead of giving you the low bleak leg count, because the low bleak count kind of gives things away. They can give you antecedents of low bleaklets instead like what? They can give you things like echimosis, they can give you things like PTKI, they can give you things like proper on the skin. So just be mindful of that. And you see this person has acute renal failure as well. We 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'll really hope you're saying that, ooh, divine, I'm going to pick the answer that says shistocytes, right? Shistocytes. Another name you may see for shistocytes on your exams are fragmented erythrocytes, okay? Fragmented erythrocytes. Typically you're going to see shistocytes on a blood smear when a person has something causing a maha. What do I mean by maha? Maha means micro-anjopathic hemolytic anemia. Micro-anjopathic hemolytic anemia. Micro-anjopathic hemolytic anemia. So typically these people, right? They can have all these things. Sometimes they can have these vulnerable factor, you know, mortimers that are literally sharing the red blood cells in their bloodstream, right? That's what creates those shistocytes.

And I would really hope that you know the other causes of shistocytes dosis on your exams, right? DIC, right? You can see this in DIC. You can see this in a person that has a... So a person that has DIC, a person that has TTP, thrombotic thrombocytopenic preparer, right? And then they can ask you, what is the most likely mechanism behind the species bloody bowel movements? Well, I hope you're picking the answer that talks about invasion of the intestinomyocosa. Inversion of the intestinomyocosa. The thing is, whenever you see a bug that causes bloody diarrhea, it usually causes that problem by invading the intestinomyocosa, right? Invading the intestinomyocosa, right? So like for example, if you think about it, shigella, shigella invades what it does is that it's picked up by your immune system cells that we find around like the terminal helium. 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 going to happen? The thing is, as it destroys, it then spreads into the other epithelial cells that line your GI tract, right? And it's going to cause those cells to die. And as those cells die on this slough off, you're going to have bloody diarrhea. Don't mess with shigella. Shigella does not, shigella, you know, for all the Godin state warriors fans out there.

Strength in numbers is not a model, it's not a theme with shigella. What shigella does is, it doesn't, shigella is like a special operations operative, right? Like special forces operative. It just needs like ten organisms and you're in deep trouble, right? You're literally in deep trouble. And the thing is, since again, our friends at the USML Es 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 helium? I would really hope you're saying 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 USMLE 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 MB Ms have become very good at chanting a lot of basic sciences to the USMLE step two CK and step three exams, right? So again, don't forget your pyres, patches that we find in the where in the terminal helium, right? In the terminal helium, right? And remember, the classic shigella that they love to go after on the exams is shigella soniai, shigella soniai, SOW and I, shigella soniai, right? So keep that thing in mind, right? And this child that has HUS, how are we going to treat this child that has HUS?

Well, you're going to treat this child with supportive care, okay? They will try to trick you on your exams into treating the shigella by giving antibiotics. That could not be a worst decision that you could take for this child. You know why? The problem with that is that it's the toxin, the shigella toxin that is causing the problem. So if you give more, and if you give antibiotic, you're going to kill more bug. If you kill more bug, 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 going to 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. If any people ignore how powerful bacterial toxins can be on the, on the, in real life, but also on the US Emily exams, right? In fact, since I'm talking about toxins, let's make some toxin integrations, right? Let's make some toxin integrations that are friends that the MBM is love to throw on exams. Number one, right? We've kind of talked about the shigella toxin, right? Well, what's another toxin you may see on your exams? Well, think about a person having a toxic shock syndrome, right? Toxic shock syndrome. Toxic shock syndrome usually is going to be caused by toxins, right? It's caused by toxins. It's caused by the release of exo-toxins, right?

Those exo-toxins 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. It's clindamycin. Again, I don't know I'm going off on this tangent of toxins, but toxins are very, very high you to know for step two, see can't step three. Again, they are not only relevant for step one, right? But those toxins, right? They cause a lot of damage. Those exo-toxins, exo-toxins, exo-toxins. Remember, we tend to find exo-toxins with what? With gram-positive organisms, with gram-positive organisms, right? So those exo-toxins 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. So 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 knees. And then you're told that man, over a two, three hour period, these not-staff having bull-osting in the skin. And the redness has spread to the person's foot.

That person probably has necrotizing fasciitis, necfash. Again, many times, necfash is caused 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 that you 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. Why would those people have watery diarrhea? Well, they have c-deaf, colitis, c-deaf colitis. Well, remember, c-deaf, how does c-deaf get you in trouble? It gets you in trouble by using toxin, right? In fact, one of the ways we diagnose c-deaf is by looking for the toxin in the stool. Obviously, if a person has c-deaf infection, you're going to treat them with oral vancomycin or oral phidaxomycin. Again, our friends at the MDM Es, they're not stupid. They know that all of you that have the job description medical student, not about anything, but they know that many people, at least an appreciable number of people, do not know about phidaxomycin. So please consider phidaxomycin on your exams, right? Or what if they give you a question about a patient? And they tell you that this patient is a sex worker. And this sex worker patient has this painless lesion on the vaginomyocosa, right? And the patient is placed on oral antibiotic therapy or IV antibiotic, okay, let's say IV antibiotic therapy.

And then you're told that this patient, four hours after therapy was initiated, the patient begins to have like a rash, right? The person begins to have like redden of the skin, becomes hypotensive. Well, what are you thinking about? I hope you're thinking about trapponema 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, as you use a cell wall inhibitor, the cell is literally exploded. As the cell explodes, what do you think is going to be happening to all those stuff that it has within its, you know, cellulite, intracellular environment? It releases it into the bloodstream. Again, kind of like a toxin, those things that are inside, like the cell soup of an organism can trigger very powerful inflammation and that can cause the person to have problems, right? So keep that in mind for you exams, right? What's another toxin that can test on you 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 ordinophasia, right?

And they tell you that the person is drooling and I can almost promission you egg and, you know, they will give you some laps 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 promission you exam. Do you know one answer they're going to give you? They're going to give you a pig lotitis, right? They're going to give you a pig lotitis. And they know that many people rush head first to pick in that answer, resist the temptation to pick that answer. Look at the context that I'm giving here. Again, context really matters on the USMELIS. I'm giving context of an immigrant. I'm giving context of like, wow, you see this swelling of the firings and things like that. What is this? This person has deuteria. This person absolutely has what? Deuteria. Remember, deuteria makes a toxin. That toxin, in fact, we call it the AB-exo toxin. And how does this toxin work? This toxin works by ribosilating elongation factor 2. Okay? It causes ribosilation of elongation factor 2. When you ribosilate elongation factor 2 is going to stop working. Well, we do remember elongation factor 2 from. You probably remember elongation factor 2 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, see, see.

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 step 2 recently or people that have taken step 3 recently. You're going to see that they ask these basic science questions. Why do you ask about the mechanism of action of toxins? In fact, I'm telling you this. That's actually a very, very high-yield knowledge to know for step 2. And especially for step 3. Step 3 is one of those exams. So don't get me wrong. Step 2 has a lot of basic science these days. But step 3 has more basic science than you're even expecting, right? Step 3 is almost like a step one exam and a step 2 exam, rooting to one, with CCSKC's Thruin for good measure and a lot more bio-stats 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 going to care about it when you see it on your test. You do the studying and make sure you know these things, right? So remember, the deferotoxin, it's an AB Xotoxin. And what does it do? It causes ribosylation of elongation factor 2. When you ribosylate elongation factor 2, 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... What are the toxins that cause ADP ribosylation? Absolutely, there are. There are absolutely other toxins that can cause this ADP ribosylation, right? So we've talked about this in the context of the deferior toxin. But what are some other toxins that cause the same thing? What are some other toxins that cause the same thing that you need to know for your exams? Well, don't forget 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, we show the best as your prepping for your exams. Okay, what's another toxin that is the most important thing to do? They should know for your tests, right? Think about the cholera toxin, right? Remember cholera has a toxin? What does that cholera toxin do? Well, the cholera toxin causes you to secret lots and lots and lots of chloride ions into the lumen of your GI tract. It causes you to secret lots and lots of chloride ions into the lumen of your GI tract. As you secret all those chloride ions, water is going to follow. And as water follows, you're going to have a secretory direct. You're going to have a secretory direct. Please do not lose sight of this on your test. Let me actually tell you this.

The cholera toxin basically is or it activates adenylite cyclists, right? So as you activate adenylite cyclists, you're going to make a ton of cyclic AMP. And that's going to cause you to release a lot of chloride ions into the lumen of your GI tract. All right. So I think of kind of hit toxins in a lot of the depth that I want to hit. At least these are a lot of the classic ones you love to go after on exams, right? Let's see a few more things and then we'll kind of 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 cello coxib, right? You want to use a cox-twin inhibitor because this person that has a history of peptic ulcer disease, you don't want to give them like a regular insect because if you give them a regular insect, that can absolutely cause them to have, you know, exacerbation of their peptic ulcer disease, they can bleed. Right? Because remember, how does an irregular insect work? A regular insect works by inhibiting cox-1 and cox-2, right? It's a reversible inhibitor of cox-1 and cox-3. Remember, aspirin is an irreversible inhibitor of cycloxygen is 1 and 2, right? But if you, and the thing is cox-1 works in the GI tract, right?

Cox-1 works in the GI tract. Time may be like divine. Why is that such a big deal? Well, the problem is, if you inhibit cox-1 in the GI tract, you're going to make less in the way of prestiglandins. And if you make less in the way of prestiglandins, 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 going to mess up your stomach and that's going to cause you to have peptic ulcer disease. Right? So that's why if we can avoid something that targets cox-1, 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 cox-2 is something that's not found in the GI tract, right? So if you want to get like an NSAID-like effect, but not target cox-1, use a cox-2 inhibitor like CEL-E cox-sip, okay? Use a cox-2 inhibitor like CEL-E cox-sip. Again, cox-2 inhibitors, they have very minimal gastrointestinal side effects. All right, so I think I'm going to go ahead and stop here. 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 USMEL exams. I have a ton of classes in the month of March, starting with the step one classes in the first week of March. I mean, it's a 25-hour class.

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 see, field step one, or you had a long dedicated peer for step one, or you've just forgotten a lot of things from step one, you would really appreciate the 25-hour step one class. And then, later in March, I have an MBA me-test-taking class, I have a bio-stats class, I have a social sciences, ethics, QI, and healthcare systems class, hospital medicine class. That's a five-hour class. Those three classes I just mentioned are for step one, two, step three. And then I have a last-minute review and a 20-hour step two step three review. 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 to you to read for all the USMLE, all the complex exams. And I have this podcast on Apple, Google, Spotify, I have a You Tube channel, you can check out. That's where I post the videos that I make. And then, don't forget that I also help with your applications, mock interviews, personal statements, and things of that nature. And then I have another website called divineinterventionlifelessons.com, divineinterventionlifelessons.com.

Every week I post like two or three podcasts, many of you know I'm a Christian. So from a Biblical perspective, address a life lesson, Biblical perspective. It's called, again, divineinterventionlifelessons.com. There is actually an Apple podcast, so shoot it with that, call the divineintervention lifelessons podcast, divineintervention lifelessons podcast again. Tons of people listen to these podcasts and find it to be very, very helpful. So 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.

Progesterone.

The patient themselves. The DPO only acts when the patient is incapacitated.

Cholera toxin.

Clindamycin (a 50 S inhibitor).

E. coli; Progesterone-induced smooth muscle relaxation leads to urinary stasis/urinary atresia dilation.

Jarisch-Herxheimer reaction, due to the rapid lysis of spirochete cells releasing antigens and toxins into the bloodstream.

Invasion of the intestinal mucosa (terminal ileum) followed by destruction/sloughing of epithelial cells.

Diphtheria toxin and Pseudomonas A toxin.

COX-2 selective inhibitor (e.g., Celecoxib), to spare protective prostaglandins by avoiding COX-1 inhibition in the GI tract.

Schistocytes (fragmented erythrocytes).

Enterotoxigenic E. coli (ETEC) does not cause HUS; Shiga toxin-producing E. coli O157:H7 is the primary cause.

Oral Vancomycin or Oral Fidaxomicin.

Invasion of the intestinal mucosa (terminal ileum) followed by destruction/sloughing of epithelial cells.

Diphtheria toxin and Pseudomonas A toxin.

COX-2 selective inhibitor (e.g., Celecoxib), to spare protective prostaglandins by avoiding COX-1 inhibition in the GI tract.

Schistocytes (fragmented erythrocytes).

Enterotoxigenic E. coli (ETEC) does not cause HUS; Shiga toxin-producing E. coli O157:H7 is the primary cause.

Oral Vancomycin or Oral Fidaxomicin.