DIP Episode 427 - USMLE Step 2/3 Rapid Review Series 88

Okay, welcome. My name is divine. This is episode 427 of the Divine Intervention Podcast. To this podcast, I'm going to be communicating the Rapid Review series for the USMELIS that just eKXM. This is going to be series 88. Let's jump right into it. So, what if they give you a question about a patient? They tell you that this patient for the last six weeks has been on FAMODIDIN. And this patient has like a long history of GERD and the FAMODIDIN is not controlling their symptoms. And then they tell you that the person has started having malpene with swallowing. And then they ask, what is your next best step in management? What should you do on an MBA mix? Well, obviously, one reasonable answer they will offer to you is to switch to some kind of PPI. And then I'm down to see me see is, let's go ahead and get an EGD and basically, so if I go gastro-droid andoscopy, right? That's operandoscopy. I'm really hoping this circumstance will say in all divine. I think I'm going to go down EGD. I'm going to do operandoscopy. So, the thing is knowing the indications for EGD is pretty high up for exams. You know, first thing's first. For person has GERD, you know, typically if you try and I'm to say that it doesn't work, a smart place to say, let's go for a PPI. Well, there are certain things that can really scare you. They'll make you say, I don't know, I think I'm going to go ahead and do an EGD. And what are some of those things?

Well, the first one is if the person has alarm symptoms, the person has GERD and alarm symptoms, you need to take them for an EGD, right? And what are some of these alarm symptoms? The obvious one is weight loss. If a person is losing weight, they're kind of worried about cancer. So, in those circumstances, it would make sense to get an EGD. And then if a person has dysphysia, that's also an alarm symptom. If a person has difficulty swallowing, that's an alarm symptom. If they have a dynophysia, painful swallowing, that's an alarm symptom. You notice any signs or antecedents of bleeding in the person that has GERD, that's an alarm symptom. Or you see a person that has GERD, you notice that, this person's hemoglobin is low, they have anemia, that's an alarm symptom, right? Or if you just see them having very significant symptoms that are just very disproportionate to just having a classic diagnosis of guardian variety GERD, those are alarm symptoms. You should go up and down to the end of the day. And then you notice that this person is still having symptoms. Again, it's not the number of weeks that matters. It's more knowing that they've been on PPI for a long time. It's not doing jack for their GERD symptoms. It's not doing jack for their symptoms. It's not doing jack for their symptoms. It's not doing jack for their GERD symptoms. In those circumstances, you need to absolutely consider getting an upper endoscopy.

And then, if for example, a person has a history of baritone syphagus, and you notice that, well, this person's symptoms are worsening. That's definitely an indication to get an EGD to get an upper endoscopy. That's actually pretty high to know for, for example. And one thing I will just say, they should maybe keep in mind because every now and then, people see this and they're like, oh, what should I think about with baritone in terms of screening? The thing is, when a person has a history of baritone syphagus, right? If, for example, they tell you that, oh, they have a history of baritone and they have no dysplasia. That's like the term you show your exam. They have a history of baritone syphagus and they have no dysplasia. Those people still need screening EG Ds, surveillance EG Ds. We should do it no more than every three to five years. That's the smart play on NV Me exams. Now, if they have baritone syphagus with dysplasia, pick a number of years on your NV Me exams that's less than three years. That's really what you should be doing. Obviously, if you have dysplasia, they're going to get more frequent surveillance. Pick something that is less than three years on your exam. And then, another thing I think I should also mention in terms of EGD that may be helpful is that if you see a man that is over age 50 and he has had chronic gird and then he has some other bad risk factors. Let me explain. So you see a man, he's over age 50.

He has a history of chronic gird and he has bad risk factors. Let's say he's been a smoker, right? Or he's very obese, right? Or, you know, the person has very high BMI stuff like that. Those people should get EG Ds. When a person presents with chronic gird and it's a man over age 50, right? Chronic gird. So they've had the gird for a long period of time. They've had it for years. They'll make it very obvious in the question. In those circumstances, getting an EGD is not a bad idea at all. That's actually pretty high you to know for, for example. And then, what if they give you a question about a 25-year-old male? They tell you that for the past four weeks, he has been having fevers, he has like generalisely infotainopathy. And then, you know, they tell you that on fiscal exam, he's pale, he looks emusheted, his ESR CRP is very elevated, he has like really bad foreign genitis. And then, they tell you that his HIV viral load is like 30,000, some crazy amount of HIV. And then they ask, what is your next best step in management? Well, I would hope that the very first thing you're thinking about is, oh, divine, we're going to place this person on highly active antiretroviral therapy, highly active antiretroviral therapy. Now, here's the thing with highly active antiretroviral therapy, because the thing is, the MBM Es know that, you know, you probably figure out how to pronounce HIV. Okay. So, they'll give you the HIV viral load, right?

The MBM Es, they love writing some of these questions these days where the stuff you're thinking as you're reading the question, they're just giving you more and more of it. And they're like, oh, gee, what's the question that's coming? Right? So, this person has a HIV, right? So when a person's on a HIV, he has HIV, they need to be placed on highly active antiretroviral therapy. But I think I want to talk about highly active antiretroviral therapy. It's going to high youtuber. It's very high youtuber know that heart, I'm going to call it heart, instead of saying highly active antiretroviral therapy. But heart is something that you need to understand on a somewhat deeper level or more recent exams. Let me put it that way. I'm going to live it at that. But heart typically involves three drugs, not two drugs, three drugs. It should be a three-drog regimen, very high youtuber know that. And that three-drog regimen usually includes a backbone of two drugs plus one more drug. So what in the world is this backbone? Well, this backbone are the N-R-T-I's, the N-R-T-I's. The N-R-T-I's are the nucleoside reverse transcriptase inhibitors. I'll say that again. The nucleoside reverse transcriptase inhibitors, the N-R-T-I's. So you have two N-R-T-I's plus one drug from another class. Remember the N-R-T-I's, they are drugs like Zydovidin, for example. Zydovidin, Intracidabin, Tenoffovir, Abakavir.

Don't forget Abakavir as the very notorious drug, pretty notorious for cause of a pretty prominent hypersensitivity reaction. That's something that's kind of high youtuber know for example. Remember Zydovidin, they love to test it from the context of, it's one of those drugs that friends at the MB Ms love to give to newborns as HIV perphylaxis if their moms have HIV. Although remember that Zydovidin can cause a very powerful a lactic acidosis, this one of these things kind of sounds loyal doesn't say in it, but it's actually super high up for example. Zydovidin especially, but really the N-R-T-I's as a class can cause this problem, but they can cause a very powerful lactic acidosis, kind of like metformin. Although the mechanism there is a little different here. So the mechanism here is that they actually inhibits the synthesis of mitochondrial DNA. Well if you inhibit that, because remember they are literally DN As, nucleosyri first-transcriptes inhibitor, essentially inhibits that DNA RNA business. So since you're inhibiting the DNA RNA business, it will make sense that an organelle that contains DNA, DNA especially like the like your mitochondria could be potentially affected by these drugs. So it may be like divine, well who cares if I inhibit mitochondrial DNA synthesis? Well let me explain why you should care. Many of your enzymes and stuff that you need in your mitochondria and things of that nature, where do you think they come from?

So if you cannot make mitochondrial DNA or if you inhibit the synthesis, many of your mitochondrial pathways will not work as well. So for example like your electron transport chain, your TCA cycle, which we call the CREP cycle, it doesn't work. So it's going to be super dependent on glycolysis, when you're super dependent on glycolysis. I don't know, well you'll get to pyruvate and then that pyruvate will be converted to lactate because if you don't convert the pyruvate to lactate, you will not be making any D-H. You won't be making enough any D-H to keep the glycerybar height of three-force feed dehydrogeny step going. That's more for step one but basically you're going to keep building up a ton of lactic acid, right? You can get a myopathy, right? Because your muscles they need a ton of energy. But since your mitochondrial DNA doesn't work again, energy production is kind of impaired. So you have a really bad myopathy. In fact, it's a ragged ragged myopathy. That's pretty high yield to know because many people, they just like, ooh, okay, well, the mitochondrial disorders, I hear it from mom, you know, like me last, and Murf or a leber hereditary optic neuropathy. Yes, those things all cause that ragged ragged fibromyopathy. But it is fluoridhyl. Pay attention to me.

This is fluoridhyl to known exams that the N-R-T-I's, especially Zidovidin, they can cause a ragged red fibromyopathy with lactic acidosis because again, they have the ability to inhibit mitochondrial DNA production. Again, you see me spending like two-three minutes on this stuff. I'm not spending two-three minutes on this stuff because I like to hear myself. Spending two-three minutes on this stuff because it's very, very high yield. That's literally what I'm going to say about that. So we said the high active antiretroviral therapy, right? It's a three-drug regimen, two-drug backbone, which is usually an N-R-T-I, like Zidovidin, a back of ear, remember the hypersensitivity there, tenofoviere and traceta bean. And then, in addition to the two N-R-T-I's, you need one drop from another class. So what could those other drugs be? Well, you would have a fusion inhibitor, right? So you can have something like maravirok and fulver-tide. I mean, there are some saline differences between these drugs, but they're kind of not super high yield for step-to-step solution. I'm going to skip those, but maravirok and fulver-tide, those are your fusion inhibitors. In general, like a drug like maravirok, for example, right? He combines two CCR-5. And if you bind to CCR-5, then each IV will not be able to bind to yourself in the first place. And, again, maybe I should speak to that CCR-5 business, because, again, I'm trying to make integrations here. That's why it's a rapid review series.

But CCR-5 is one of the critical receptors that HIV loves to bind to on the surfaces of cells to kind of get into them. Now, the thing you need to know about CCR-5 is, so people have a mutated CCR-5. When you have that CCR-5 mutation, then you may have some level of HIV resistance. Or, remember, HIV, besides CCR-5, can also use like CXCR-4 to get into a cell. So, if you have a mutated CCR-5, you'll be resistant to HIV infection, because HIV literally cannot bind. Or, if you have HIV, you have a very slowly progressive infection. Because, again, the binding of the HIV virus is just very inefficient in those circumstances. So, don't forget your fusion inhibitors. They can be the third part of the backbone in heart therapy, right? And they're presenting drops there. I think it's like Maravyr or Maravyrarchy spelled M-A-R-R-A-V-I-R-O-C Maravyrarch. And then Enfouvertyte is spelled. I believe ENFU-R-V-I-R-T-I-D-E. I think I have a spelling right on that. Enfouvertyte. Enfouvertyte. And then, what's another thing that can be the third drop backbone in heart therapy? It can be an N-N-R-T-I, right? An N-N-R-T-I. So, these are going to be drops like Nevirapine or Favirins. At least, those are the first generation N-N-R-T-I's. They're beginning to make N-N-R-T-I's a little better. There are some second generation ones, but those ones are super loyal for the exam. Think more about Nevirapine and Enfouvertyte on your exam. I mean, sorry. Nevirapine and Favirins. Nevirapine and Favirins.

Now, the one good thing I want to know about if not a good thing, I guess. The one bad thing I want to know about Favirins is that it can cost suicidal ideation. That's super high yield to know. Because you may be like divine, but the thing I've heard is Vivid Dreams. Don't get me wrong. It can cost Vivid Dreams. It can absolutely cost Vivid Dreams. But the N-N-R-T-I-D is the know that anyone that has the job description medical student has probably memorized that. If Favirins causes Vivid Dreams, if Favirins causes Vivid Dreams, okay, yes, fine. So, the thing is, if Favirins, yes, causes Vivid Dreams, but it causes more problems than that. It causes a wide range of neuropsych symptoms. So, the way our friends at the N-B-E-M is can make an otherwise easy question, a little more difficult. It's just to put that, the person has a history of major depressive disorder, complicated by suicidal ideation, and then the person is about to start highly active and tired of IRAR therapy. And then you'll see which of the following drops is contraindicated. Pick that N-N-R-T-I-Ansure and don't look back, especially if Favirins. It's associated with suicidal ideation. It's really prescribed these days to be honest with you. And then what is another third drug that can make up the backboard? Well, you can use an integrase inhibitor and integrase inhibitor. And with the integrase inhibitors, they all end in Gravier, right? Like, Ralph Tegravier, Duluth Tegravier, LV Tegravier.

These drugs, they actually the HIV drugs that probably have the cleanest side effect profile. And I guess for those that are listening to this rapid review series, you're essentially getting a good dose of HIV from ecology. The HIV drugs are weirdly some of the highest CO drugs to know for the USMD exams, you know, for like four stages, steps two, especially those against the three, who's the three they love their pharmacology. So you should probably know this stuff that I'm talking about. So, so the integrase inhibitors, they have the essentially the cleanest, they're very well tolerated, cleanest side effect profile of most HIV drugs. Again, they all end in Gravier. They don't really have any significant side effects that are worth this question. And then the next group of drugs that can be again a third addition to your HIV cocktail in highly active antiretroviral therapy are the proteins inhibitors, right? The proteins inhibitors. But remember, after HIV mixes protein, it mixes like this big polypeptide, the polypeptide is kind of useless. So the polypeptide has to be split off into like smaller bits. So the way you split it off into smaller bits is with proteins, pretty obvious, right? So that pro those proteins inhibitors, many of them in the navier, so like retornovere, in the navier. And these drugs are kind of important to know why because they can cause a ton of problems. Right?

I mean, first things first to know if these proteins inhibitors is that they can inhibit cyrochromp 450. And that would not be good, right? Because that's going to raise the levels of a toxic drug that is normally metabolized by your cyrochromp 450 system. And then these drugs can also cause lipodistrophy. They can cause like a weird redistribution of fat in the body. They can cause a weird redistribution of fat in the body. And then they can also cause you to have problems like M Is. These things can cause accelerated atherosclerosis. They can cause M Is. In fact, many times in the present that is pretty well controlled with HIV, we're worried more about some of the metabolic disease problems that they get from these medications that they're taking. So again, if they give you a question about a person that has HIV and they have a history of MI or they have a history of like angina, he's probably not the smart and he's saying, which of the following drugs are contraindicated. It would make a lot of sense to not put them on a release inhibitor because that's kind of like a fast track ticket to to my cardio infarction, which is probably not a, probably not a not a good thing. Again, pretty, pretty high yield to know the stuff on exams. And again, for those that again, if you like the way explained things, consider attending the review courses I offer, I offer a step two and a step three review course. In fact, I have one taking place next week.

Monday, Tuesday, Friday and Saturday, so the 21st, 22nd, 25th and 26th. And then I also have a test ticket strategy course taking place this Saturday, this Friday from 5 to 7 30 pm mountain standard time. And then finally, I have a biostatistics bootcamp taking place later this month on the 20th. So if you're interested in any of these classes, just shoot me an email through the website and I can give you some more information. So let's continue. So why is it that I guess some of these questions, they are more like fuck these questions. Why is it that or why do we have, so say for example, if a person needs that knows with hypertension, you know, obviously we try to bring their blood pressures down. Why do we have higher blood pressure thresholds in people that are older? Well, the reason in there is as you get older, your vessels become less compliant. Your vascula compliance actually goes down as you get older. So why is this important? Well, the reason that's important is if your vessels are not very compliant, they cannot disdain and collapse efficiently in response to changes in blood pressure. So people that are older in general tend to have higher blood pressures because again, because think about it as a person gets older, they've laid down a lot of collagen in things, right, including their blood vessels. So those people in general can have decreased the vascula compliance. That's pretty important to know.

And I guess it's also high yield to know here that they have other things that can decrease your vascula compliance. They can actually make that decrease because the thing is that decreased compliance is almost like happens in most old people. But if you see really bad blood pressure in a much younger person, they've had an accelerated decrease in their vascula compliance because again, they have some metabolic thing going on like diabetes, like high blood pressure, like nstational disease. All these things cause an accelerated decline in a person's vascula compliance. In fact, if you think about it, diabetics especially if I'm throwing in a PED integration here, diabetics sometimes when they have PED symptoms, you try to measure their ankle-breakial index. It's falsely like normal. In fact, it can be like a super-normal ankle-breakial index. That's what's called Moncoberg calcifixlerosis. The reason they have that super high EBI is because their blood vessels have been calcified, especially in the lower extremities. So when you check the blood pressures there and you measure relatively relative to the break-up pressures, you're like, wow, this is high. How does this person have ABI symptoms? I mean, how does this person have a PED symptoms? Well, the reason they have those symptoms is because they've calcified their vessels. So those falsely normal readings you're getting the lower extremities they are false.

They're not good reads because again, they've calcified their vessels. That calcification of the vessel is one of the major contributors to a rapid decline in vascula compliance in a person that is diabetic. In a person that is diabetic. And I guess with this whole theme, I guess I should probably shred our up-ups since this is more than 20 minutes already. But with this whole theme of a person having decreased vascula compliance as the age because of all the collagen business that's going on. I guess another smart thing we can talk about is EE Gridients. If you really think about it, the person gets older. The EE Gridients actually goes up. Again, some of it is, again, as you get older, you lead out collagen in places in many parts of your body. You can lead that down in your long-power income. So that can make the feasibility a lot more difficult. And if your diffusibility is a lot more difficult, then the spread between your ovula oxygen tension, that's your PBG-02, and your pulmonary capillary oxygen tension, that's your PED-02, the spread will get bigger because the oxygen cannot diffuse efficiently. That's a fully something that's pretty high-youtu-no for the purposes of exams. I'm going to go ahead and pause here as I do at the end of every podcast. But please, I guess I want to say something here, please, for those of you that listen to this podcast, the stuff you heard me mention about a lot of these HIV drugs, they're pretty important things to know.

Do not blow the stuff off. I'm telling you, you can have some very drastic consequences for your exam score. And also the stuff about the EGD, if you notice those were like the two big topics, kind of focused on today. Again, for whatever exam, let's really focus on these things, because again, they are very, very important to know. So I do offer one or one tutoring for all the USML exams, step one to three, complex one to three. I just don't tutor to OMM. And then finally, I have, again, my review courses have a 20-hour, step two, step three review course. I have an MBME Testicking Strategy course, I have a Biostatistics Bootcamp, and also I have a 25-hour step one course that's actually going to be taking place in January of next year. And then I help with ER As applications and mock interviews, I've done this for years, worked in lots of people that are even now attendants. Again, if you need help in any of those things, just shoot me an email. And then I have these podcasts on the major podcast apps, Apple, Google, Spotify, at least the most recent 150. Then I have a You Tube channel called Divine Intervention USML podcast and videos. That's where I post the videos that I make. And then finally, I do also have a new website called Divine Intervention Life Lessence.com. That's where I post a bunch of life lessons. I post about two every week. Many people have found them to be super, super helpful. Just go to Divine Intervention Life Lessence.com and you'll find those podcasts.

People said that, oh wow, Divine, I love the life lessons you put at the end of your podcast. So I made a separate website. I'll just put that stuff on there. I'll use the Bible to just bring you an 10 to 15 million lesson on a common problem that people face. And there's also an associated podcast with this on the Apple Podcast platform as well. Just look for the Divine Intervention Life Lessons podcast. So thank you for listening to me today. I will see you in episode 428. Have a wonderful day. God bless you. Bye for now. Thank you.

Weight loss, dysphagia (difficulty swallowing), odynophagia (painful swallowing), signs of bleeding, anemia, or symptoms disproportionate to classic GERD diagnosis.

Three drugs (a three-drug regimen).

Two NRT Is plus one drug from another class (e.g., fusion inhibitor or NNRTI).

Zidovudine, Tenofovir, and Abacavir (the class as a whole is at risk).

Suicidal ideation.

Integrase Inhibitors (all end in -gravir, e.g., Dolutegravir).

Increased deposition of collagen in the vessel walls.

Surveillance EGD every 3-5 years.

Abacavir (an NRTI).

Inhibition of mitochondrial DNA synthesis/replication.

Upper endoscopy (EGD) must be performed due to failure of medical therapy.

Decreased pulmonary capillary diffusion capacity, often due to decreased vascular compliance/elastin.

Protease Inhibitors (due to risk of accelerated atherosclerosis).

Monckeberg calcific arteriosclerosis.

Surveillance EGD every 3-5 years.

Abacavir (an NRTI).

Inhibition of mitochondrial DNA synthesis/replication.

Upper endoscopy (EGD) must be performed due to failure of medical therapy.

Decreased pulmonary capillary diffusion capacity, often due to decreased vascular compliance/elastin.

Protease Inhibitors (due to risk of accelerated atherosclerosis).

Monckeberg calcific arteriosclerosis.