DIP Episode 279 - The NBME and Prostaglandins

Okay, welcome. My name is Divine. This is episode 279 of the Divine Intervention Podcast. In this podcast I'll be continuing the rapid review series for the USMELY Step 1 exam. This is going to be series 12. And for this I'm going to be just for most of our talking about Prestiglandins. Prestiglandins are unfortunately kind of a high-yield thing to know for the USMELY Step 1 exam. There are many of them. There's like a ton. But I just want to go over the classic ways they attest it. Go over the pathway. Make sure it's something that you really understand. So this should be a short and sweet podcast. So let's jump right into it. I guess maybe I shouldn't call this a rapid review series. I'll just call this the Prestiglandins podcast for Step 1 or the USMELY or whatever. Okay, so let's just jump right into it. So what if they give you? So maybe let's talk about the pathway. I think maybe that may be the smart thing to do for us. Right. So I know that Prestiglandins don't just drop from the sky, right? They don't just come from thinner. So what's the deal with these Prestiglandins? Well, we know that membrane phospholipids, you ultimately need to convert them to arachidonic acid. Right. So this is done by an enzyme known as phospholipase E2. Right. And that phospholipase E2 then is inhibited by cortical steroids. So that's ultimately how steroids work as a minus suppressants, right? The crush phospholipase E2.

So you're not able to convert those membrane phospholipids to arachidonic acid. And then as a side note here, I think I would want you to remember that phospholipase E2 has a receptor that it acts on. Okay. And when you develop antibodies against that receptor, that's actually associated with people having membranous nephropathy. That's one of those weird associations that are floridly high-autono for step one, for sure. Right. When a person has other antibodies against the phospholipase E2 receptor, that's associated with membrane phospholipathy. That's something that you routinely test on the USMDXAP, especially step one and also step to ZK as well. So again, membrane phospholipids, phospholipase E2 helps you make arachidonic acid. And in that arachidonic acid can go down the lucotrain pathway under the action of lipoxygenase, right? So lipoxygenase helps you convert the arachidonic acid to lucotrain. And then if you're looking on the other end of the spectrum, cycloxygenase can help you convert the arachidonic acid to first the gland ends, right? And obviously we know that cycloxygenase can be inhibited, right? So you can be inhibited by NSAI Ds. Although remember that aspirin is an irreversible inhibitor of the cycloxygenase enzyme. And then other NSAI Ds are reversible inhibitors of the cycloxygenase enzyme. And then if we're looking at things from the lucotrain perspective, there's also a drug that inhibits lipoxygenase, right?

In this case, lipoxygenase will be inhibited by Zyloton. Zyloton is a lucotrain antagonist, right? That works specifically by inhibiting lipoxygenase. So just something to commit to memory there. Now, the next thing I would say is that lucotrain, right? Remember, lucotrain is a very important on NBME exams. Probably like the biggest one is lucotrain B4. Remember, it's a big-time chemotactic factor for neutrophilts, right? It's a chemotactic factor for neutrophilts. So if, for example, a person has like a lucotrain deficiency, right? Or they have like lipoxygenase dysfunction, but I think that's going to happen is they're not going to be able to attract neutrophils to the side of acute inflammation, right? So lucotrain, right? When they're produced, they can act on receptors. The big receptor I want to know for your exam is the CYSLT1 receptor, right? That's just another fancy name for the lucotrain receptor. That receptor is blocked by those lucast drugs, right? So drugs like one to lucast or Zafri lucast. So key to know about those things, right? And then again, we've talked about the cytoloxygenase pathway. And then one thing I want to talk about before I jump into the Prosteglandins is talking about aspirin-induced asthma, right? So aspirin-induced asthma. So remember, these days it's now known as aspirin exacerbated respiratory disease.

The thing with aspirin-exasperatory disease is that when you give a person aspirin, it would make sense that you should have less flux through the cycloxygenase pathway and more flux through the lipoxygenase pathway. If you have more flux through the lipoxygenase pathway, the thing that's going to happen is you're going to produce a ton of lucotrains and lucotrains, they have very powerful bronchoconstrictors, right? So they can potentially exacerbate a person's respiratory disease, especially if a person has a hypersponsivir way, like a person that has asthma. And then again, before I jump to the Prosteglandins, I promise I'm going to jump to them, but it's also helpful on MIM exams to know the function of thromboxin-e2, right? Remember, thromboxin-e2 really causes thrombosis, right? It really causes thrombosis. In fact, this is one of the reasons why, actually, this is the primary mechanism behind aspirin, being an antiplotelate agent, right? By inhibiting cyclooxygenase, you're not going to make thromboxin-e2. If you don't make thromboxin-e2, the pressing will be fine, right? They're not going to, they're basically not going to promote that aggregation step of primary humorous stasis, so they're ultimately going to be good, right? And again, I've talked about lucotrain-B4, right? Has a specialized function as being a chemotactic factor for neutrophils. Another classic one you may also see is lucotrain-D4, occasionally that pops up on immune exams, right?

Lucotrain-D4, what does it do? Basically, it does a lot of bronchoconstruction, right? So again, it's not not the nicest thing for a person that may have reactive area of disease. Basically, just think of it as the constriction lucotrain, right? Because it's bronchoconstruction, it causes viso-construction, right? And then it can also increase vascular permeability, because you may wonder, like, divine, why is it that many of these people autoimmune diseases tend to have hypertension? It's pretty easy. If a person has a lot of immune disease, they have a lot of inflammation going on all the time in their bodies. Well, many of these inflammatory agents are very powerful viso-constructors, right? And if you do that, that's going to raise your systemic vascular resistance, it's going to put the patient in some trouble, and they're going to have hypertension, right? So now let's go to the prostaglandins, right? So what if they give you a question about a lady, and they tell you that membranes have ruptured like, I don't know, like, 24 hours ago, right? Which has not started having contractions yet, right? Again, that person has premature ruptured membranes, because in general, right, when you ruptured membranes, you should be having contractions at the same time, right? So you can try to induce those contractions with a bunch of drugs, right? You can obviously use like oxytocin, for example.

That's probably the most common agent that is used, but one agent you can use for sure is a prostaglandin E2 analog, right? A prostaglandin E2 analog, a dino prostone, right? You can use dino prostone. Although dino prostone's job for the most part is to help you, like, ripen the cervix, but in some areas, it can sort of help you induce labor. So that's a PGE to analog, right? And one other thing that's high to know about dino prostone is that you can actually use it technically to keep the doctor's arteriosus open. The thing is, there's a lot of cross, cross functioning between these prostaglandins, because typically, on ambient exams, the first line thing you should go with in terms of keeping the doctor's arteriosus open is actually the prostaglandin E1 analog, a prostadil. And an easy way to remember that is PGE1 for first line, right? So a prostadil is a prostaglandin E1 analog. That's something used to keep the doctor's arteriosus open on ambient exams, right? So going back to the prostaglandin E2 analog, again, dino prostone. Again, you can keep the doctor's open, you can use it to induce labor. And it's also one of those things that induces fever and pain, right? Induces the sensation of pain, right? Again, that's why when you're on that inflammatory state, like you have an infection or something, you know, you can have my algeas and all that bad stuff going on, right?

And then I'll prostadil again, I said it's a PGE1 analog, is something that is classically used to keep the doctor's open on ambient exams, right? So what are those classic situations that you give your ambient exams where you'd have to keep the doctor's arteriosus open? The classic presentation will be a newborn. Newborn was fine at birth, right? And then within a few hours to days of the newborn being born, the newborn has like a stature and burning, right? The theory that this newborn becomes superhypoxic and they are trying to give this newborn supplemental oxygen bodies O2 sets are not rising, or if they are buried. Whenever you see stuff like that, right? You want to think about the child having some kind of sanitary congenital heart defect that is being on masked by the closure of the doctors, right? Because see, for example, if a child has transposition of the grade vessels, walk with me here for a second. In transposition of the grade vessels, the right e-trem drains into the right ventricle, that's normal, but then the right ventricle drains into the yoder, that is not normal, right? So the right ventricle is draining into the yoder, and the yoder sends blood around the body and brings them back to the right e-trem and then back to the left e-trem and then into the yoder. So you see that you essentially are circulating the oxygen-ethid blood.

On the flip side, the left e-trem is draining into the left ventricle, the left e-trem is draining into the pulmonary artery. The pulmonary artery sends blood to the lungs, gets it oxygenated, gets into the pulmonary vein, and then back to the left e-trem, and then left e-trem, left e-trem, left ventricle pulmonary capillary gain. So you have like two separate systems. One system is circulating oxygen-ethid blood, that's the left side of the heart. The other system is circulating the oxygen-ethid blood, that's the right side of the heart. So the thing is, if you have two completely separate systems, the child will not get born in the first place, the child will die, right? Because you can't live circulating the oxygen-ethid blood, right? So the thing that ultimately happens is if a person has a doctor, like a doctor's arteriosus, which is something that many, you know, you have in uterus, that doctor's arteriosus allows mixing between the blood in the yoder and the pulmonary arteries, right? So you know, the child is still in some relative form of hypoxia, but it's better than it could be with two completely separate systems. But so it's almost like that Sanodic congenital heart defect the child has, is masked by the presence of a conduit, like the doctor's arteriosus, that is letting blood between the left and the right side of the heart mix. But what does the doctor's usually do? The doctor's closes.

So once the doctor starts closing, it's almost like you're going to do two separate systems. The child is not going to survive that, and then the child can pass away pretty much, right? So your first step in management, whenever you see those things, they will try to trick you on the example into a beaten, don't do that. You're pretty much wasting your time. That hyperoxia actually kind of works in the like speed of the child's demise, right? So because when you have hyperoxia, right? Or when you have like just a ton of oxygen around, a ton of oxygen around actually causes like a rich lex viso construction in most blood vessels. Remember the lungs are kind of different when there's hypoxia, actually let me take a step back. So in the lungs where there is hypoxia, the pulmonary vessels constrict so that you can redirect a lot to other parts of the lungs that have adequate oxygenation, right? But in the body, if you think about it, right? When there is hypoxia in a part of the body, the body tries to dilute the vessels leading to those areas so that you can send more, send more blood there. But when there is a ton of oxygen around, and the body is like, you know, we got it from here, we have enough oxygen, so it's going to constrict. That constriction can be mediated by things like neurobenefrag. Right?

So when you're giving that child supplemental oxygen or trying to bid that child and give high flu like a ton of oxygen straight into the airway, I'm already helping that child because that's causing like viso constriction. And because remember the doctors at the rehearsals is literally a blood vessel, right? So you're literally closing up with that blood vessel so more. So you're worsening your physically speeding up the child's demise. So in those circumstances, the best thing to do or it is to give a person a glending e1 out of log like out prostitutes, right? So I think the big thing to point out here is and maybe like as a pro tip for the future, maybe consider this to be like your life lesson from this. Whenever you're making decisions, try to understand the why. Don't just do things because you want to do things, right? Many people fall into trouble in life because they feel that as long as I'm active doing something, it's the right thing to do. Now, the fact that you're doing something doesn't necessarily mean you're doing something profitable, doesn't necessarily mean you're doing something that has much of an impact, right? So don't keep running this rat race in life where like you're doing all these activities. You see people, especially some med students, you see them there like in the popping of tomacoffee, studying from 8 a.m. to like 9 p.m. every day, but you don't have good grades to show for it.

Do some, again, I'm not trying to judge you, but just do some kind of self examination. What am I doing around with my life? What am I doing around with my study process? Because if you're putting in that much time, you should be getting better results. So maybe just do something that's very important is just doing some self examination. Do some self examination. That will show you like, maybe I should change my ways, change some things I'm doing so that so that I can do better. But let me get off that tangent. So again, when the president's hypoxia, given oxygen is not always the right thing to do. I guess is what I'm trying to say here. But again, as I say in this podcast, this podcast is not meant for clinical decision-making. It's meant for testing purposes only. When you see that child's case, give the child out prostitutes. That's a PG1 analog. That's going to keep the doctors at your ears open until you can then proceed to surgery. Another classic PG1 analog emission example is misoprosto. Remember, you can use labor, but the thing that they love to test on NBM Es with misoprosto is how if a person has peptic osteo-disease from taking NZ, but they really do need to take those NZ because they have like some really bad inflammatory thing, joint problem, blah, blah, blah. You can give those people misoprosto. Misoprosto will essentially protect the lining of the stomach. So how does he do that?

Well, remember, misoprosto, the inner prostitute, the glandin analog actually cuts down on the secretion of gastric acid. So it's almost like it has this mucosoprotective effect. So whenever a person has to take an NZ, but they're having like gastric complications of taking that NZ, like a gastric ulcer, you can basically give them misoprosto prophylaxically at the same time so that they don't get those problems. And then what if they give you a question about a patient that has like scleroderm or something like that? And the patient, let's say the person has like, you know, has like the renotes phenomenon and all that stuff. For the last six months, the person has been having like trunness or breath, exercising tolerance has allowed P2 heart sound. Obviously that person has pulmonary vascula hypertension, right? So when a person has pulmonary hypertension, we want to try to give them something that can dilute the pulmonary vessels.

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Phospholipase $\text{A}_2$.

Corticosteroids (Glucocorticoids).

It is a major chemotactic factor for neutrophils.

Zileuton (a leukotriene antagonist).

A prostaglandin $\text{E}_1$ analog ($\text{PGE}_1$ analog, e.g., Alprostadil).

Antibodies against the phospholipase $\text{A}_2$ receptor.

Phospholipase $\text{A}_2$.

The leukotriene (LOX) pathway.

Cysteinyl Leukotrienes ($\text{LTC}_4$, $\text{LTD}_4$).

It reduces gastric acid secretion, providing mucoprotection against NSAI Ds.

A $\text{PGE}_1$ analog (e.g., Alprostadil).

Membranous Nephropathy.

Phospholipase $\text{A}_2$.

The leukotriene (LOX) pathway.

Cysteinyl Leukotrienes ($\text{LTC}_4$, $\text{LTD}_4$).

It reduces gastric acid secretion, providing mucoprotection against NSAI Ds.

A $\text{PGE}_1$ analog (e.g., Alprostadil).

Membranous Nephropathy.