DIP Episode 614 - USMLE Step 2/3 Rapid Review Series 126 (Basic Sciences)

All right, welcome to episode 614 of the Divine Intervention Podcasts. In today's podcast, I'm going to be addressing the USMLSTEP2 CKANDSTEP3 rapid review. This is going to be series 126 series 126. And this podcast, I'm really going to try to focus on some of the basic sciences that we're seeing a lot these days on step 2, CKNSTEP3. Let's begin. So what if they give you a question about a patient, they tell you that she's a 61-year-old female, and that she has a history of, you know, grave disease. And she was brought to the emergency room because she was found unresponsive by her husband. And on presentation, her blood pressure was like 200 over 120. Her heart rate was 300 beats per minute. And we're told that the patient was given an intravenous infusion of a drug. And which led to a rapid, you know, decrease in her blood pressure and in her heart rate. And then they ask you which of the following is the most likely mechanism behind resolution or control of the patient's symptoms. I would really hope that you're picking the answer that talks about a peripheral inhibition of a 5 prime diodenies, a 5 prime diodenies. So what's going on with this question? Well, this person came in with a thyroid storm, right? This person came in with a thyroid storm. And you may wonder, divine, why did this? How do you know this person came in with thyroid storm?

Well, typically, the way is going to present on the exams is you're going to see a person with some kind of thyroid history, although sometimes they will not supply it. But it will be a person with some kind of hyperthyroidism history. And you'll notice that they have this really bad acute worsening of their symptoms, where their heart rate just goes sky high. They even have a fib, right? Because remember, the most common arrhythmia in people that are hyperthyroid is atrophy relation. But their heart rate will be extremely high. Their blood pressure will be extremely high. They'll be very unstable, right? And many times their TSH will be like completely undetectable, right? That's going to be thyroid storm. Or they may not give you that thyroid history, but it will give you like these very crazy hemodynamics. And the person will have an undetectable TSH. Again, that's thyroid storm. When a person has thyroid storm, the first thing you're giving them is an IV beta blocker, right? The beta blocker is going to decrease T4 to T3 conversion in the periphery, right? T4 to T3 conversion in the periphery, right? Because remember, T3 is the metabolic, is like the very reactive form of thyroid hormone, right? It's like the one that wrecks things, right? It gets the job done. So you want to reduce production of that T3. You want to reduce production of that T3, right? That's done by a 5 prime diode in this, right?

Sometimes on the USML Es, you may see it referred to as a 5 prime mono diode in this. Okay, 5 prime mono diode in this, right? So we give IV beta blockers, right? Especially those ones that are lipids soluble because they can really like in that periphery, it's shut down T4 to T3 conversion. Okay? So please don't forget the first line treatment, the first line treatment for thyroid storm is an IV beta blocker, a lipids soluble beta blocker, right? Very high yield to know the stuff for your exams, please. Make sure it's something that you know and you understand, right? And then the second line thing we do is to give PTO, propyl thyrioracyl. Because propyl thyrioracyl is an antithyroid drug, it inhibits thyr peroxidase. But one other thing it does is it also has this ability to inhibit that peripheral T4 to T3 conversion, okay? So please, the mechanism behind resolution of their symptoms is the inhibition of T4 to T3 conversion by that 5 prime, that peripheral, that peripheral is very important, that peripheral 5 prime diode in this. Which sometimes on your exams can be called a mono diode in this. And then why does the person have tachycardia? Because this can be another basic science integration, they throw you exams, right? The reason this person has tachycardia is that thyroid hormone increases the insertion of beta one receptors on the surfaces of your cardiomyocytes, okay?

Thyroid hormone causes you to insert more beta one receptors on the surfaces of your cardiac myocytes. So because it causes you to insert more beta one receptors, right? It's going to make your heart more responsive to cardiacholamine, that's how they get all this a-fab and all these crazy high heart rates, right? Because they are now more responsive to cardiacholamine, okay? That's why they tend to have all these hyperadrenergic symptoms. And that's why typically for these people, right, for these folks want to go ahead and give them, want to go ahead and give them, uh, uh, uh, IV beta blockers, right? Now, one other thing you may actually see as an ROB's question on your US Emily exams is they may actually ask you, again, it's, I promise, it's basic science related. What happens to the pulse pressure in an individual that is hyperthyroid, or in an individual that is in thyroid storm, right? Like for example, on, on your exams, you can absolutely get a question about a person thyroid storm and they'll cover it into an RO question, right? They can, like one of the hours may be peripheral, uh, T3 production. They'll put hours that show increased or decreased or on changing. And then they'll put another column that talks about, uh, beta one receptor activity on the heart, right? And then another one they can absolutely put is systolic blood pressure, another one they can absolutely put his pulse pressure, right?

Because the thing is these are just very easy ways to see if a person has any level of understanding. Doesn't matter how many on key decks you do in prepping for your exams, there's not many on key decks is going to help you answer questions like that. It's just the truth, right? So what happens to the pulse pressure when a person is hyperthyroid? The pulse pressure is going to rise. It's going to rise. Put what's the mechanism? Why is that? Well, remember that pulse pressure is the difference between your systolic blood pressure and your systolic blood pressure, right? When a person is hyperthyroid, the systolic blood pressure rises a lot. Why have already explained? You're putting more beta one receptors on the surface of your cardiac myos, on the surfaces of your cardiac myosites, they become more responsive to cardiac color means. So cardiac color means can stimulate those beta one receptors that's going to increase your heart rate, that's going to increase your stroke volume, that's going to increase your cardiac contractility. So your cardiac output is going to rise. If your cardiac output rises, your systolic blood pressure will rise, right? Think about it if your systolic blood pressure is rising, then what's going to happen to the difference between your systolic and your stolic blood pressure? That difference is going to rise. So your pulse pressure is going to increase, okay? Your pulse pressure is going to increase.

Very important to keep that at the back of your mind, for example. All right. Now, what if they give you a question about a patient and they tell you that this patient is 31 year old female and that she's coming to the physician because she has noticed a lot of just like blue and red spots around her arms, right? And then you're told that, oh, this patient has a history of some skin disease. You know, the USMEL is the, like to be intentionally vague with stuff like this skin disease and that she has been using something that's like a cream that she found over the counter, right? And then they will show you like a picture of this person's arm, right? And then they ask you which of the following is the underlying mechanism, right? For the most likely theology of this patient's physical examination, find it. Well, I would really hope that you're picking the answer that talks about the loss of collagen, okay? Pick the answer that talks about what? The loss of collagen. So what's going on here? Well, the thing that's going on here is that this person has been using topical steroids. This person has been using topical steroids. People use topical steroids for many things, right? The use topical steroids for like audit carrier. Use topical steroids for, what is it called? For exama, right? A topic dermatitis. These topical steroids for many different things, right?

Now the thing is, there's a reason why you're encouraged not to keep using steroids, steroids, steroids, steroids, steroids, right? For a long period of time. Because the thing is steroids can cause you to lose collagen. Well, what's the mechanism behind that? Well, the mechanism behind that is that steroids, they are very powerful fibroblasts in inhibitors. And fibroblasts are producers of collagen. Fibroblast or what? They are producers of collagen. They are producers of collagen. So if you inhibit fibroblasts, then you will stop making collagen. If you stop making collagen, then you're going to get in trouble. Your skin is going to get thin, right? The subcutaneous vessels are going to be closer to the skin surface, right? They're going to have loss of that cushion that they have. So guess what? Those vessels will easily rupture. And if they rupture, you're going to have like echimoses on your skin. You're going to have echimoses on your skin. You're going to have all these telangetages on your skin, right? That's very high yield to know your exams. And that's why as the person gets older, guess what? Their skin, things. Because they have, you know, decreased fibroblast activity, loss of collagen and they get in trouble. They get in trouble. The thing is collagen as a concept is actually really high yield to know for your exams, right? And the reason is like the alt is one of the ultimate multi-systems processes and disorders concepts to know for your test.

Because there are just so many things that you can test on your exams that revolve around collagen, right? You already know where I'm going here. You know that divine is about to go on a boatload of integrations. Again, the thing is, if you think that these basic sciences are only for step one, well, I guess I can't convince you otherwise until you see it on your test, right? Well, let's hit a few integrations here with collagen, right? The first one I think I want to talk about is, you know, they give you a question about a person that has like a person that has mitrovov prolapse, right? A histrov mitrovov prolapse. So they can tell you that this person is presenting with like a sodium onset severe headache, right? And they tell you that, oh, on examining the patient, you hear like a holosis stomach murmur at the apex, right? This person probably has earless, down low syndrome, right? Earless, down low syndrome. Remember, what's the deal with earless, down low? It's an orizomo dominant disorder, right? It's a mutation in type three and type five collagen, right? Type three and type five collagen, right? So people that have this mutation, they tend to have issues with, you know, type three, type five collagen, right? So they're going to have like hyperextensible skin, hyperextent, you know, you know, very, very relaxed joints. So they're going to have a lot of different types of collagen. So they're going to have a lot of different types of collagen, right?

So they're going to have a lot of different types of collagen, right? So they're going to have a lot of different types of collagen, right? So they're going to have a lot of different types of collagen, right? So people that have this mutation, they tend to have issues with, you know, type three, type five collagen, right? So they're going to have like hyperextensible skin, hyperextent, you know, you know, very, very relaxed joints, right? Very, very relaxed joints. They can have issues with, their tissues are very fragile, right? So these people, you know, if they saw a stenial wound, like a skin wound, man, it's going to take like a long time to heal, right? A long time to heal, right? They can have pelvic organ prolapse, right? They can have mitral valve prolapse. That's that holosis stomach memory you're hearing at the apex, right? Because that's the mitral area, right? And why does this person have a headache? Well, because they have a rupture of an aneurysm in the circle of willis, right? Or they can even tell you that the person presents with sodium onset severe chest pain. That's because of the erotic dissection, right? Or rupture of an erotic aneurysm, right? These are all things we find in people that have a headache. And to be honest, with your friends at the NBM Es, they're not going to say, which of the following types of collagen are deficient or impaired in this person? That's ridiculous, right? Because that's in every onky deck, known to mankind.

Type three and type five collagen. No, that's ridiculous. No, that's not what they're going to do on your exams, right? No, they're going to put something that is like a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, a bloodline, that's not what they're going to do on your exams, right? No, they're going to put something that is like kind of peripherally related to collagen, right? You can see, like, for example, like impaired collagen, you know, metabolism, impaired collagen synthesis, right? Or you can just put some kind of enzyme answer. And that's kind of related to collagen, that's not working, right? Like, you know, there's this enzyme called a pro collagen peptidase, pro collagen peptidase, that enzyme really does not work, right? That enzyme really does not work. It's one of the enzymes you use in cleaving certain parts of collagen, right? Ultimately, if you're trying to synthesize it, right? So the thing is, if it's not working pro collagen peptidase, right? Look at the name peptidase, something that cleaves peptides, right? Then you're going to get in a lot of trouble, right? You're literally going to get in a lot of trouble with proper functioning of your collagen, right? That's why you get many of the signs and symptoms that we see in people that have, in people that have errors, than those. Okay, now what are the other collagen integrations to know for your exams?

Well, what if they give you a question about a boy? And this boy, you know, they tell you that, oh, when you look in his eyes, you know, he's been having like decreased visual acuity, he has like, you know, issues with, they tell you see like, opacification of the lens, and you're told that, oh, this boy uses hearing aids, and he's on ACE inhibitors, you know, because he's had like a mild renal failure, right? This is clearly a person that has outpourred syndrome, right? Outpourred syndrome, remember, it's an exling dominant disorder, it's an exling dominant disorder, where, you know, they have an issue with type 4 collagen, the alpha 5 chain. Okay, the alpha 5 chain of type 4 collagen is not good, right? So those people are going to have eye problems, they're going to have like cataracts, right? Vision issues, they're going to have hearing problems, right? So they will have like a hearing loss, and then many times they're going to have an ephratic syndrome as well, right? That's a type 4 collagen, alpha 5 chain issue. In fact, the gene that's messed up in outpourred syndrome is the COL4 A5 gene, the COL4 A5 gene, alpha 5 chain type 4 collagen, right? Why do you think I keep saying this alpha 5 chain type 4 collagen? Well, the thing is, I want you to be able to contrast this with alpha 3 chain of type 4 collagen. The alpha 3 chain of type 4 collagen is the antigen that you make antibodies against in a person that has good posture syndrome, right?

Good posture syndrome, anti-glomerular basement membrane disease, right? When people have good posture syndrome, right? Remember, it's a type 2 hypersensitivity reaction. You're making autoantibodies against the alpha 3 chain of type 4 collagen. You can already begin to see how friends at the NBM is, they can put up a, alpha 3 chain type 4 collagen, of Cyan B, alpha 5 chain type 4 collagen, or whatever, just to mess with your head, right? So, again, remember, good pastures, right? Good pastures is alpha 3 chain type 4 collagen, you make autoantibodies against it, right? Output syndrome is alpha 5 chain type 4 collagen that screwed up, right? So, let's go to good pastures, right? So, good pastures remember they're going to have like a lot of lower respiratory tract issues. They're going to have hemoptysis, right? And in addition to that, they're also going to have nephritic syndrome. They're going to have a rapidly progressive glomerular arthritis. Remember, that's a pretty deadly disorder. So, you're going to give those people steroids on cyclophosphamide, steroids on cyclophosphamide, right? And then, don't forget, another collagen thing to be aware of is osteogenesis in perfecta. Osteogenesis in perfecta, right? It's an issue with type 1 collagen, an issue with type 1 collagen. When you have type 1 collagen issues, you're going to have issues with your bone. You're going to have issues with what with your bone, right?

Type 1 collagen is found very extensively in bone and cartilage, in bone and cartilage. So, this will be going to struggle with a lot of those things, right? So, make sure you keep all these things at the back of your mind for your exams, right? Or you can even give you a question about like an immigrant, like a child that was adopted from a foreign country. And then, they tell you that, oh, this child has been having a, the experience I've noticed that is been having a lot of like, bleeding in the mouth when they try to brush his teeth, right? And then, they show you pictures of the child's skin. And you see a lot of like pTKI, you see a lot of achymosis, what's going on here? This is what? Skurvy. This child has what? Vitamin C deficiency, right? Vitamin C deficiency. Remember, on your exams, they can ask you which of the following processes, right? Or what's the most likely theology of this person's symptoms, right? Again, I want you to pick the answer. If they want to be kind, let me tell you what the kind answer will be that it could supply, and what the difficult answer could be that it could supply. The kind answer is impaired collagen synthesis, right? Or they can say impaired collagen metabolism. That would be nice. But what are our friends that the MBM is love to do from time to time? Well, they can put an answer that talks about impaired hydroxylation of protein residues, or impaired hydroxylation of amino acid residues, right?

Because remember, vitamin C helps in the process of hydroxylation of protein and lysine residues in collagen, right? The hydroxylation of protein and lysine residues in collagen. Basically, like when you hydroxylate protein and lysine, it makes collagen stronger. You don't want to make like weak collagen, right? You want like strong collagen. You want to have strong collagen. Then you need to hydroxylate those protein and lysine residues, right? Those protein and lysine residues, right? So the thing is vitamin C is a co-factor for that process, okay? Vitamin C is literally a co-factor for that process. If vitamin C is not working well, then you're going to get in a lot of trouble, right? That's why this child has like gingival bleeding. They have like these echinocys on the skin and things like that, right? And I guess since we're talking about many of these extracellular matrix proteins that are important, as we begin to slowly wrap up this rapid review, what are some other extracellular matrix proteins that you want to be aware of? That they just love to test a lot on step two and step three. Well, don't forget things like elastin, right? Don't forget things like elastin. Elastin, you know, it makes up a lot of the parenchum of your lungs. It kind of keeps everything together, right? It kind of keeps everything together. But the thing is if you have a lot of inflammation in your lungs, because you smoke, right? Amacrophages are releasing a lot of proteases.

Those proteases are going to drop your lung parenchema. They are literally going to like eat up the elastin of your lungs. And as that happens, your lungs lose the ability to snap back. They become very compliant. You may be thinking that yeah, the vine seems to be describing him for Zima. That's exactly what I'm describing, right? So you lose that elastin because of protease activity, right? Because of protease activity, you know, excess protease activity, right? So literally they can actually make a COPD question on your exams and ask about the mechanism behind the person's increased compliance. And the right answer will be extensive protease activity or increased protease activity, right? Although if you was in a person that has a foreign antitripsing deficiency, it will be decreased antiprotase activity, decreased antiprotase activity. Because the thing is, how foreign antitripsing deficiency, right? How foreign antitripsing is an antiprotase? It basically neutralizes the proteases that drop your lungs, right? That drop your lung parenchema, right? So the mechanism behind the increased compliance in a person that has COPD, a person that has an aroma, is from increased protease activity. It's released by all these macrophages that come to clean up all that junk that's in your lungs from you like smoking like a crazy person, right? So that's something I want to keep at the back of your mind for exams. And I guess things we're still talking about a lasting.

Remember a lasting has a scaffolding, right? Elastin has a scaffolding, right? What's that scaffolding for a lasting? That scaffolding for a lasting is febrieling. And febrieling can be messed up in a person that has morphine syndrome, morphine. Right? Morphine is an autosomal dominant disorder where you have a mutation in febrieling, right? Where you have a mutation in febrieling, right? Especially febrieling one, right? Febrieling one is like a scaffold for a lasting. It's a scaffold for a lasting. And we find febrieling one in like the lens of your eye, right? Like in the periostia of your bones, in the middle of your yoder, right? Remember the the middle of your yoder is like the muscle layer, right? That's why people that have morphines, they can have like dilation of the yoder, they can have rupture of the yoder, they can have a yoder, can heurisms, right? They can have that ectopia lentis, right? With lenses that dislocated upward and outward, right? They can have mitrovov prolapse, they can have rupture of aneurysms in the circle of willis, right? They can have many of these things, they can have many of these things, right? So please, these things are actually pretty high yield to know for your exams, right? These things are pretty high yield to know for your for your exams. So I think we should go ahead and stop here. Kind of getting the sense that I've talked about a lot of basic signs. So let's stop here.

Again, if you're interested in 101 tutoring, I do offer 101 tutoring for all the USMLE and Comlex exams. Starting next week, Tuesday, I do have a bunch of classes that I'm teaching. For step one, all the way to step three, you know, have a test-taking class next Tuesday for 20,5 hours. I have a bio-stats class on Wednesday, that's for four hours. I have a social sciences and ethics review, that's for five hours, that's next Thursday. And then, and those first three classes are for step one to three. And then on Friday, I have a last mini step two step three review. That's for three hours. And then the week after that, I have a 20 hour step two step three review. And then in the month of September, I have a 25 hour step one review. So if you're interested in any of these classes, many people have taken these classes and done extremely well. Like I kid you not. I've literally got in emails this week from people that took my classes, like very recently, like, as recently as like a month, two months ago. And they got like, mid to 70s on their exams. They got high to 60s on their exams. And they're like, wow, divine. I never had these scores on any of my practice tests. Man, your classes really helped. These classes, they're updated very frequently to be on par with the USML Es. They are well worth your while, they're over Zoom. So shoot me an email, I can give you some more information. And then I have these podcasts on all the major apps, Apple, Google Spotify.

And then I also have a You Tube channel that you can check out, Divine Intervention, USMLE Podcasts and videos. And then I have another website titled, Divine Intervention Lifelessens.com. Divine Intervention Lifelessens.com. Every week, I post like one or two podcasts from a biblical perspective, I address a life lesson. There's actually an Apple podcast for that, the Divine Intervention Life Lessons podcast. And if you also need help with your ER As applications, personal statements, more interviews, letters of recommendation, I do edits for all these things. I've worked with many people over the years that I residence and even attendings now. So again, if that's something I'm interested in, just shoot me an email, I can give you some more information. So thank you for listening to me today. I will see you God willing episode 615. Have a wonderful day. God bless you and bye for now. Thank you.

IV beta blocker, preferably a lipid-soluble agent.

They decrease T4 to T3 conversion in the periphery via inhibition of 5'-deiodinase.

Thyroid hormone increases $\beta_1$ receptors on cardiomyocytes, increasing cardiac output and thus raising systolic blood pressure disproportionately to diastolic pressure.

Goodpasture targets autoantibodies against the $\alpha 3$ chain of Type IV collagen; Alport involves a defect in the $\alpha 5$ chain of Type IV collagen.

Vitamin C is required for the hydroxylation of proline and lysine residues, which stabilizes the collagen triple helix.

Fibrillin-1.

Peripheral inhibition of T4 to T3 conversion by 5'-deiodinase (or 5'-monoiodase).

Increased pulse pressure due to increased cardiac output and heightened $\beta_1$ receptor activity.

Ehlers-Danlos Syndrome (EDS).

The $\alpha 3$ chain of Type IV collagen.

Vitamin C (Ascorbic Acid).

Increased protease activity from inflammatory cells (macrophages) degrading elastin.

Peripheral inhibition of T4 to T3 conversion by 5'-deiodinase (or 5'-monoiodase).

Increased pulse pressure due to increased cardiac output and heightened $\beta_1$ receptor activity.

Ehlers-Danlos Syndrome (EDS).

The $\alpha 3$ chain of Type IV collagen.

Vitamin C (Ascorbic Acid).

Increased protease activity from inflammatory cells (macrophages) degrading elastin.