DIP Episode 392 - Pulmonary Pathophysiology Series 1

Okay, welcome. My name is Divine. This is episode 392 of the Divine Intervention Podcasts. In today's podcast I'm going to be talking about some PONORI pathofysiology. I'm really the goal of today's podcast and really many of my podcasts right. I just to address things that I know that people struggle with. So for me today I just want to explain some things because PONORI physiology is probably one of the hardest kinds of physiology. So I want to address some key areas in this podcast that I know people tend to struggle with. And as we go through the PONORI physiology, I'm also going to spend some time talking about some cardiac physiology. So this is more of a reasoning podcast but it will help you understand a lot of things that you observe physiologically. So what if they give you a question about newborn, the tale that this newborn is profoundly hypoxic, he is super tecapnic and he was born at 29-weeks gestition. What's happening with that child? Well you don't have to overthink it but we know that this child has new needle respiratory distress syndrome in our DS. New needle respiratory distress syndrome. So what causes NRDS? Well NRDS is caused by a deficiency of surfactant. So maybe like okay well why is surfactant important? Well let's backtrack a little bit into discussing how your VULI work. So the thing is your VULI expand with inhalation. I mean just literally think about it some is like you're blowing up a balloon. You inhale your VULI expand.

So it makes sense that as you exhale your VULI deflate. Now the thing is complete collapse because if you kind of think about it let's assume you have a balloon right? If you deflate the balloon just a little bit you don't deflate it all the way till it's flat and if you want to blob the balloon again it's our all easier. So the thing is if you have complete collapse of your VULI during exhalation right that's you know collapse of your VULI that's what color like this is. If you have complete collapse of your VULI during exhalation it makes it much harder for you to expand that out of your line again and that increases your work of breathing. It makes your gas exchange super difficult again. If you have a balloon that has been inflated and you deflate it just partially if you want to re-inflate it it doesn't require as much work as if you've completely deflated that balloon if you've completed deflated that balloon they need to really really blow for that balloon to the extent. So again if you have complete collapse of your VULI during exhalation it increases your work of breathing because you have to work harder to extend those out of your line and it makes gas exchange difficult. This is why at a lectasis is dangerous because it increases your work of breathing and it makes gas exchange really difficult and this also explains part of the reason why one of the ways we treat the hypoxia associated with ARGS is to increase peep.

Pretty much what peep helps you accomplish is that it distends your VULI it keeps it partially distended so that you don't have to put in as much work to open up your longer VULI that's where peep comes in right that's why it's called positive end-expertory pressure. Again I'm gonna hopefully try to make some integrations as we go along here. Now the thing is to understand the pressures that keep their VULI open one thing you really need to get them apart is something known as the law of Laplace. Something known as the law of Laplace. So what is the law of Laplace? Well on one side of the equation we have the pressure needed to keep the VULI open. It is equal to 2 multiplied by your surface tension divided by the radius. So basically I'll save the equation again right the pressure required to keep your VULI open is equal to 2 multiplied by your surface tension divided by the radius. So that tells you that the pressure needed to keep your VULI open is directly proportional to the surface tension but it is inversely proportional to the radius of that Avuelus. So if you have a small radius Avuelus you're gonna require more pressure to keep that Avuel I open. If you have more surface tension you're gonna require more pressure to keep that Avuel I open. So if you think about it I mean again if we're trying to respirate you want to keep your Avuel I open.

So you can begin to see that decreasing radius that happens with acceleration makes this process of inflating Avuel I very difficult because again remember literally when you exhale Avuel I collapse and yes you know you want to blow that seal too but you also don't want to work too hard to breathe that is not something that is very good for persons continued livelihood. So to balance things out since the body knows that wow okay as I collapse as as I exhale Avuel I collapse that raises the pressure needed to keep the Avuel I open. Your body has a counterbalancing mechanism. Now what is this counterbalancing mechanism? This counterbalancing mechanism is surfactant. This counterbalancing mechanism is surfactant. So the body uses surfactant to decrease surface tension. Now one so two point I want to emphasize here is that for conceptual purposes it's pretty high to understand that is not necessarily the amount of surfactant on board that matters. It's that concentration. There are many things the body likes to you likes to regulate by way of concentration. I'll say that again your body likes to regulate many things by way of concentration. This is a principle you can apply to hematology but I want to focus on pulmonary and cardiac physiology for this specific podcast. So your body I'll say that again your body likes to regulate many things by taking into consideration the concentration of those things. So it's not the amount of surfactant in each Avuel I that matters.

It's the concentration of the surfactant in each Avuel I that matters. So what is concentration? We know that concentration is the amount of something per surface per unit area. So the amount of surfactant per unit area please a bigger role in the way the Avuel I are kept open. You're gonna see why that's important as we as we go along. So let's say for example you're comparing to Avuel I. So you're comparing a large Avuelis, you're comparing a small Avuelis. It should then become apparent from the Law of Law plus right? That again the smaller one, the one with a smaller radius is going to have the bigger demand for descending pressure to keep that Avuelis open. It's going to have that bigger demand because it has a smaller radius so the pressure you're required to keep it open is much higher. But if you think about it if you have the same, so you have a smaller Avuelis, a larger Avuelis, but think about it. We know that the smaller Avuelis has a smaller radius, more pressure to keep it distended. But let's look at this counter-balancing mechanism. If you have the same amount of surfactant in both Avuel I, literally the same amount of surfactant in both Avuel I. There is much less surface tension because of this concentration effect that I just mentioned a few minutes ago. Because if you think about it, if you have, let's say five grams of surfactant in a small Avueli and five grams of surfactant in the big Avuelis, the smaller Avuelis has more grams of surfactant per unit area.

Okay, let's say, let me use up for a number. So let's say there is, I'm not saying there's five grams of surfactant in every Avuelis, but you get the point. So let's say the small Avuelis is one meter and the big Avuelis is five meters and they have five grams of surfactant in each one. For the small one, if you look at the concentration of surfactant there, it's five grams per meter. But for the big Avuelis, if there are five grams of surfactant in that five meter space, five divided by five is one. You have one gram per meter of surfactant. You have a lower concentration of surfactant. And I said, it's not the amount of surfactant that matters. It's the concentration of surfactant that matters in those circumstances. Okay, is the concentration of surfactant that matters in those circumstances. So the thing is smaller Avueli tend to have a greater concentration of surfactant, giving the same amount of surfactant compared with a larger Avuelis. So smaller Avueli tend to have a greater concentration of surfactant. So again, that same amount of surfactant in a smaller area will have a much greater concentration. And since there's a greater concentration of surfactant, you're going to have less surface tension in that Avuelis because there's just more concentration of surfactant. So the thing is, as those smaller Avueli get even smaller, the concentration effects get even larger because the surfactant molecules are brought closer together.

The closer you bring those surfactant molecules together, the more the better they are at lowering your surface tension. Right? So again, that's why having a deficiency of surfactant puts you in a very tight spot because if you think about it as a child, as a newborn born prematurely, if you don't have an surfactant, that counterbalancing mechanism against the decrease in radius that happens with your Avueli on exhalation becomes a huge massive problem. And the thing is, it takes a really long time for you to begin to produce an offshore factor for, you know, so you need to wait till right around 35 weeks or thereabouts. Right? So infants that are born prematurely, they're going to run into problems with breathing and they're going to have, again, many of the findings that you see in a person that has new neural respiratory distress syndrome. I mean, pretty much many of these kids, you know, they're going to have low-long volumes. They're going to need oxygen therapy for a long time. But we know that that oxygen therapy, oxygen, is good, but oxygen can also make free radicals, can cause all these problems. It can cause like a rethnopathy of prematurity, it can cause a bronchopominary dysplasia, it can cause interventricular hemorrhage, because if you think about it, in this case, they have NRD as the hypoxic. So they're going to start proliferating a lot of blood vessels just to increase oxygen supply to their brain.

But those blood vessels could be pretty flimsy and they can rupture and that can cause a brain bleed. That's an interventricular hemorrhage right there. So again, that's just something you want to keep in mind as you as you study for for exams. So it's kind of high you to know that if a child has been born, if a woman goes into labor at least than 34 weeks, that woman needs to get Bethemethasone. Usually you get two doses to promote fetal longer maturity, to promote fetal longer maturity. And then you should also remember for an evening exam purposes as an added point here that if you're going to labor at least than 32 weeks, that mom deserves magnesium for neuroprotection. Basically you're trying to decrease the child's risk of developing a cerebral palsy. That's something you want to keep in mind for purposes of NBME exams. Now, I don't know like I know I said that. I don't want to I said, oh, you know, your body likes to work in concentrations. Your body really, really likes to work in concentrations. If you really understand this concentration phenomenon, it can help you rationalize a bit of pathophysiology in the body. So I think one thing I should do I said I won't talk about it for hematology, but I don't know like I just can't hold myself back. So let's talk about it. So many people wonder why does iron deficiency cause a micro-city canemia? Like really this podcast, the goal of this podcast is to just get your thinking straight.

I'm telling you this, when you have understanding of things, then your memorization becomes significantly limited. You have to memorize a ton of stuff because people always memorize, oh iron deficiency anemia causes micro-city canemia. Hmm, what do you think that is? Okay, let's explain. Now, many people think that, oh, your body regulates the size of a red cell just based on the amount of hemoglobin you have. That's not necessarily true. Your body actually likes to regulate the size of a red cell based on the concentration of hemoglobin in that cell. Think about it. If a person has iron deficiency, they're not obviously going to have an anemia because the way we define anemia is low hemoglobin. But if you really think about it, if you really really deep, dark deep and thought about it, when you have an iron deficiency, you're essentially going to have a hem deficiency because remember, hem is made of iron plus protoprofaring. So protoprofaring is not your problem in iron deficiency anemia. But iron is your problem in iron deficiency anemia. So if iron is not around, there is no partner for protoprofaring to bind with to form him. There is no partner for protoprofaring to bind with to form him. And if protoprofaring doesn't have a partner, your hem is going to be low. And we know that him plus globin forms hemoglobin. So if your hem is low, there is no partner for globin to bind with. So your hemoglobin is going to be low.

Now your body loves to keep a defined concentration of hemoglobin in its red cells. So if you think about it, if your hemoglobin is low, again, remember concentration is mass over volume, mass over volume. So if you're looking at the top of that mass over volume construct ratio, when you have iron deficiency anemia, for reasons I've explained, the mass of your hemoglobin goes down. The mass of your hemoglobin goes down. So if the mass of your hemoglobin goes down, well, if you're looking at that factor alone, the body is like, wow, the mass is going down. So we know that concentration is mass over volume, as mass is going down, concentration is going down. So your body is going to be like, wow, how can I keep a normal concentration of hemoglobin? Well, your body is going to be like, you know what? Let me tank the volume of the volume of this red cell. If I can bring the volume of the red cell down, because remember, volume and concentration, I inversely related. If I can bring the volume of the red cell down, then I can raise the concentration or normalize the concentration of that hemoglobin. So if you bring down the volume of your red blood cell, surprise, surprise, surprise, surprise, your red blood cells are going to be microcetic. That's why iron deficiency leads to a microcetic anemia. Again, if you think about things pathophysiologically like this, makes things so much easier to remember.

If you really think about it, you never have to memorize that point again, because the understanding is just there in your mind. The understanding is just there in your mind. Okay. And before we go to the next concept, just again as a form of a reminder, I do offer two courses that are coming up pretty soon for Stecjusicase Step 3. Obviously, they also apply to complex level 2 or 3. One is the NV Me Testicking Strategy course. It's going to be taking place on the 3rd of June from 5 to 7 30 pm, Pacific Standard Time. Many people have taken that course. They found it to be supremely helpful as they studied for their exams. I've had many people have their UROC Cuban percentages increased significantly, or I've had a lot of people that they're like, wow, divine. My scores went up like 30 points after taking your course. Again, I don't offer any score guarantees because there are many factors that play into how well a person does on exams. But there is many, many people that have taken these the test taking course and don't extremely well on the exams. And then I have a 20 hour review course. It's going to be taking place from the 6th to the 11th of June. We're going to be skipping the 8th. That's the Wednesday. But on Monday, Tuesday, Thursday, Friday and Saturday will be meeting from 5 to 9 pm, Pacific Standard Time, Viozo. And then I also have a 75 hour Step 2 CK, Slash Step 3 School. Obviously, it also applies to complex level 2 or 3.

And that is going to be taking place in the first two weeks of July. That'll be version 2. Version 1 was a resounding success. You're going to learn things on a deep level in much depth as comprehensively as is humanly possible. That course, that school has is called a disc school. It has much limited attendance. So if you're interested in any of these schools or courses, they'll take place via Zoom. Just strip me an email through the website and I'll give you some more information on cost and registration. So either course, you know, 20 hour courses really good. I've had many people take it. They've done extremely well. 75 hour course, really, really good. Again, something you're going to find to be incredibly helpful. Test the hands strategy scores, incredibly helpful. So if you're interested in any of those things, just strip me an email through the website. Now, what's the next thing we want to talk about? So what if they give you a question about 35-year-old guy? He tells you that over the last four years, he has been chronically short of breath. And they give you some labs in the question. You notice that while his FIV1 is 35% of predicted for his age, his FVC is 65% of predicted for his age. Then you're like, one drink, huh? 35 years old. And then they tell you that this person has smoked two packs per day of cigarettes for the last 15 years. If you see this, what should you be thinking about? I really hope you're saying, oh, divine.

This person has a four-one antitripsing deficiency. Remember, many times when you see an old person's disease in a young person, the first things you really should start thinking about is there's probably some genetic thing going on here that's causing this issue. So what is the deal with alpha-1 antitripsing deficiency? The thing is, when people have alpha-1 antitripsing deficiency, they... maybe let me give some backstory. The first thing is, make sure you know your motor inheritance, right? It's inherited in a Rosomov-Cordominant fashion. The thing is, when you have alpha-1 antitripsing deficiency, you make alpha-1 antitripsing, but the alpha-1 antitripsing you make is defective. The alpha-1 antitripsing you make is defective. It has improper folded. It's not properly folded. So because it's not properly folded, it's going to first accumulate where it's made. That's in the liver. So it's going to cause liver damage. So many times, these people are going to have elevated LF Ts. But the thing is, the alpha-1 antitripsing that's made in the liver is supposed to get shipped to the lungs. Well, if you're not really making good alpha-1 antitripsing, it's going to hang out in the liver. It's not going to go to the lungs. And in the lungs, it serves as an anti-protease. So what's an anti-protease? An anti-protease is something that protects your lungs, your lung parankoma against the proteases. So what are these proteases?

Proteases many times are things that are released by macrophages in your lungs. You know, macrophages, they come to clean up dust, smoke particles, and everything from your lungs. But macrophages are one of those food. They do a good job. But they leave a nasty after effect in their wake. They leave these proteases around. And those proteases, the thing they do is they chop your lung parankoma. Well, usually that's not a problem because you have anti-proteases like alpha-1 antitripsing coming to your rescue. The jump in and the protects you against these proteases and everything is right with your lungs. But if you don't have an alpha-1 antitripsing, these proteases are going to have a field day. They're going to drop your lung parankoma. And if you drop a person's lung parankoma, guess what? You're killing the surface area in that person's lungs. You are. You're literally killing the surface area in that person's lungs. If you kill the surface area in that person's lungs, then there is not enough surface for diffusion to happen. Remember, the feasibility depends heavily. In fact, it's directly related to the surface area available for that gas to diffuse. So if you have protease activity, if true of your lung parankoma, you have a decreased surface area for diffusion, then you're going to have hypoxia because you don't have enough surface to exchange oxygen between what is inside your of your life and your pulmonary capillaries.

That is actually the mechanism behind hypoxia. And a person that has alpha-1 antitripsing deficiency or the person that smokes. Now, one thing that's helpful to know with alpha-1 antitripsing deficiency is you're going to have a pretty good life expectancy if you just don't smoke. Is that smoking that really speeds things up for these people? Because cigarette smoke increases protease activity in your lungs. Again, why would that be the case? Well, think about it. If you smoke more, you're going to put more smoke particles in your lungs. So, macrophages that clean up, sometimes they call these macrophages, dust cells. The macrophages that clean up those smoke particles, they're going to just hang out in your lungs more because it's almost like, wow, they are constantly needed. It's almost like you're keeping them on a 24-hour shift. Instead of maybe on a five-hour shift because you know, you don't smoke. Maybe you know, they're just cleaning up the stuff that you get from living in a big city. So, if you smoke, smoke, smoke, smoke, smoke. You're going to have, you're going to become very symptomatic from an awful one-antitripsy deficiency perspective. So, that's something to keep in mind on on exams, right? So, again, people that have a full-antitripsy deficiency, they can easily ask you a question on the test, which of the following actions or activities will reduce this person's risk of bad outcomes or improve mortality is just don't smoke.

If these people don't smoke, they're going to have much better outcomes than a person that smokes. So, that's something that's, again, pretty high up to make sure you know and understand on exams. Now, one thing I forgot to mention with the first being that I talked about with regards to a person having, you know, neonatal respiratory distress syndrome. Remember, the prevalence of neonatal respiratory distress syndrome is actually increased in an infant of a diabetic mom. So, sometimes our friends at the NBM is can give you questions. About a person that is born a term, what do you have many signs and symptoms? Many antecedents associated with neonatal respiratory distress syndrome. Well, what's the cause? The cause is the hyper insulinemia. The cause is the hyper insulinemia. So, let me explain. If you think about it, if you're a child, you're in the field, you're in the womb, and mom has diabetes. Well, mom's blood glucose is high. Well, whatever mom's blood reflects, it's pretty much what the fetus, fetal blood is going to reflect because all that glucose is going to diffuse from mom to the baby. So, in the baby, the baby's, the baby's blood will have all this sugar. So, the baby's pancreatic beta-ilett cells will be like, wow, there's a lot of sugar here. Well, we need to make insulin to deal with this sugary problem. So, the baby is going to be like, you know, okay, let's, let's make more insulin.

Well, to make more insulin, you need to have hyperplegia of your pancreatic beta-ilett cell. So, it's a genetic process. They're going to undergo hyperplegia. They're going to stop pumping out a ton of insulin. Well, here's the problem with having that ton. Again, insulin is not bad. When you have too much of it, it becomes a problem because those elevated levels of insulin interfere with surfactant synthesis. So, if you're not making an off-surfactant, you may be a term child, we're just not making an off-surfactant to be fine. So, you can have the antecedents of the inner respiratory distress syndrome. And just as a sidebar, this hyperinsulinemia, you may think nothing of it, but it can cause a lot of problems for these kids. Lots and lots of problems. Because again, remember the hyperplegia that made it possible for your beta-ilett cells to make all this extra insulin. It's a genetic process. So, if you want to reverse it, it's not something that is going to reverse quickly. No, it's a genetic process. It took a while to happen. So, it's going to take a while to go away. So, after these kids are born, they can have hypoglycemia. Why? Because the insulin, even if the source of the high glucose, they've been disconnected from that source of high glucose, because they've been born. They still have hyperinsulinemia. That hyperinsulinemia can tank the child's glucose. If it tanks the child's glucose, that can cause hypoglycemic seizures.

So, believe it or not, sometimes the treatment in an infant of a diabetic mom that's having seizures can include glucose therapy. Remember, insulin also loves to drive ions into cells, especially like potassium and calcium. It can drive that calcium into the cells, and that can cause hypoglycemic seizures. Or you can even get ekegi abnormalities, because remember things like hypoglycemia, hypoglymia. Those things have the ability to prolong the cutie interval. Again, these are all things you want to make sure you keep in mind, for example. These are all integrations you want to be able to make. You want to have on your fingertips for NVME exam purposes. Now, last veneath, I think, I will discuss. What if they give you a question about a patient and they tell you that this patient, basically I will give a veneath, and then I will discuss the physiology and make integrations around that veneath. That's my goal. But I want to keep this podcast for like 30 minutes. So, what if they give you a question about a 75-year-old guy? And in the past year, he has had three episodes of pneumonia, low-bar pneumonia, and there's always been in the right lower lobe. If you see something like that, what should you think about? This person likely has lung cancer. Now, why is it in the right lower lobe? Well, remember, sometimes some lung cancerists can cause an obstruction, right? And then you just have pneumonia that settles. Because of that obstruction, you have impaired clearance of stuff.

You'll settle in a dependent region of the lungs, like your right lower lobe. And again, many times, if you even aspirate things, so for example, say for example, a person has a neuromuscular disease. Let's say they have LS, immiotrophic lateral sclerosis, or they have myestinia graves, or they've just had a stroke, right? And they can't protect their earway. Those people, they tend to aspirate. If you see an aspiration pneumonia, think of the right lower lobes. Why is that? The reason that it's that way is because you're right means them bronchus. Yes, it drains into the right lung, but it drains at a more vertical angle. And it's wider. It's wider than the left means them bronchus. So, it's almost like a straight shot for whatever you aspirate. So, you just go down that pathway. So, that's just something you want to keep at the back of your mind, for example. So, you can even give your question about a child that was playing. And then, you know, five minutes later, you know, this is a child is hypoxic and barely responsive. Well, the child has just, you know, aspirated or foreign, but he probably put a coin or something in their mouth. That's why if you're a parent, I just make sure you watch your kids, especially like your kids that can just put stuff in their mouth. So, that's why that's the mechanism.

That's the pathophys behind most aspirational monias or aspirated foreign bodies ending up in the in the lower loop of the lungs, especially the the right lower loops of the lungs. So, again, that's something you want to make sure you keep in mind for for exams. So, I think I'm going to go ahead and stop here. As I do at the end of every podcast, I do for one or one two or any exams. Step one, step two, two CK step three, pre-clinical, medical exams, 30-ish-off exams. I also offer help with ERAS applications and mock interviews. I've worked with, I've been on an admissions committee before. I've worked with tons of people that are residents all over the country. And I've been very successful in my much process with many people. So, if you need help with personal statements, recliders, editing your applications, including the supplemental application for select specialties, I'm able to help with that. I've worked with many people that have much that very competitive disciplines all over the country. So, if interested in any of these things, just ship me an email through the website and I'll give you some more information. If you're interested in any of the review courses I offer, like the 75-hour disk school or the 20-hour review course or the MB Me testing strategy course, just ship me an email through the website and I can give you some more information. The courses are all held over Zoom.

And then I have a You Tube channel called Divine Intervention, USML.ly podcast and videos. That's where I post the videos that I make, which I do from time to time. And then I have all these podcasts that I make on Apple podcasts, on Google podcasts, and on Spotify. So, at least the most recent 150. If you want everything from episode one, all the way to episode 392, just go ahead, go on the website, divineinterventionpodcast.com. I have all the podcasts listed on there. You can even download them on the website. And then if you actually have a Word Press account and you subscribe to my podcast, you'll get an email notification whenever I make a new podcast. And then finally, many of you know that I've got a lot of positive feedback on the life lessons. Actually, I'm going to discuss a life lesson here in a bit. But many people have given me, I've got countless emails on the positive feedback on the little life lessons I put at the end of my podcasts. So I decided to start a new website. I call it divineinterventionlifelessens.com. And it's a website where I post podcasts like basically two every week that I address from just from a biblical perspective, they're about 10 minutes longer or less. So, a problem that relates to humanity, but I use a biblical perspective to discuss it. So, if you go on the website, divineinterventionlifelessens.com, you can find out those podcasts. I believe I've made about 82 of them. Again, I think you'd find them to be profoundly helpful.

Again, I use a biblical perspective to discuss common life problems faced by people. And I even have the podcast on Apple Podcasts. It's called the divine intervention life lessons podcast. So, what's my life lesson for today? My life lesson for today is that you always think about the future. Many people go about their lives and literally all they think about is the present. Oh, you know, I'm just going to enjoy the moment. I'm going to enjoy the moment. Don't get me wrong. I'm not saying you should not enjoy the moment, but you kind of think about the future. The future matters. And the thing is, the future is a function of the way you've lived your life in the present. For example, as a medical student, you say, oh, you've got into medical school, your first year student, hmm, I just want to enjoy the moment. I want to enjoy the moment. If you keep enjoying every single moment, and you don't sit down and study for your USMEL exams, you're going to fail. You're going to fail. Your life is your future. You don't want to think about. It's going to be a very difficult future. So, I'm just encouraging you today. Take smart decisions in the present time so that your future will be bright. Why mess around and delete that with your present and then destroy your future. You secure your future by taking smart decisions in the present. You look at it from a financial perspective. You don't see for retirement, but you just like do whatever you want now. Blow your money now.

You see many physicians are in great debt. They have 500 homes. I'm just over obviously exaggerating, right? But they have a lot of things they don't need. They don't plan for retirement. So, just kind of keep that in mind. And just your actions. Just your actions. The fact that you're alive today means you can start taking good decisions. Your actions control your future. Your actions in the present be control your future. The way you leave your life today, they are all seeds. Literally, your actions in the present are seeds for your future. So, just make sure that in the present you're showing the right seeds. So that when the harvest comes down the line, you're getting a good harvest. How do you live in? How do you treat people now? Do you treat people like trash in the present? I don't know what kind of future you're looking for. How do you leave your life? Are you a person that just does evil or whatever? Again, remember there is such a thing as a deal of reckoning. The deal of reckoning may not be in the present, but it's very surely going to be waiting for you in the future. So, what I'm just encouraging you to do with this life lesson is do the right thing in the present. Leave a good life in the present. Leave an honorable life in the present. Do the right thing now. Do the right thing now. As you do the right thing now, you'll see your future will be bright. Don't do, don't be waiting to do the right thing in the future because the future is not guaranteed.

You can be alive right now. And I mean, there were literally people last nights that were alive. And right now this morning they're gone. They're normal. So, what kind of decisions are you making right now? What kinds of decisions are you making right now? Meet the right decisions now. Don't say, oh, you know, start making the right decisions from tomorrow. No, you can start making those right decisions now. Here when a part of the Bible says, now is the time of salvation. Not tomorrow, not in the future. Start making the right decisions now because again, the future is not guaranteed. You literally cannot guarantee the next hour. You could be alive right now and be dead the next hour. So, why don't you start making the right decisions now? So, your future will be bright. So, thank you for listening to me. I will see you in the next podcast. I'm fairly certain that the next podcast is going to be a continuation of this Pomonaire Pathofisiology series. So, thank you for listening to me. God bless you. Have a wonderful day. Thank you.

It keeps alveoli partially distended, preventing complete collapse (atelectasis) and thereby decreasing the work of breathing.

Pressure ($P$) is directly proportional to Surface Tension ($T$) and inversely proportional to Radius ($r$), represented by $P = 2 T/r$.

Surfactant, which decreases surface tension.

Proteases released by macrophages degrade lung parenchyma, leading to reduced alveolar surface area and impaired gas exchange.

The right main bronchus drains at a wider and more vertical angle compared to the left, acting as a straighter path for aspirated material.

Hyperglycemia $\rightarrow$ hyperinsulinemia (due to increased beta-cell activity) $\rightarrow$ interference with surfactant synthesis and risk of subsequent hypoglycemia/seizures.

Surfactant deficiency.

By producing surfactant, which decreases surface tension ($T$).

Increasing PEEP (Positive End-Expiratory Pressure).

Smoking cessation.

The body attempts to maintain normal concentration of hemoglobin (mass/volume) by reducing cell volume (microcytosis), not just mass.

Betamethasone (if labor $\ge 34$ weeks for lung maturity); Magnesium sulfate (if labor $\ge 32$ weeks for neuroprotection).

Surfactant deficiency.

By producing surfactant, which decreases surface tension ($T$).

Increasing PEEP (Positive End-Expiratory Pressure).

Smoking cessation.

The body attempts to maintain normal concentration of hemoglobin (mass/volume) by reducing cell volume (microcytosis), not just mass.

Betamethasone (if labor $\ge 34$ weeks for lung maturity); Magnesium sulfate (if labor $\ge 32$ weeks for neuroprotection).