DIP Episode 397 - Pulmonary Pathophysiology Series 3

Okay, welcome. My name is Devine. This is episode 397 of the Divine Intervention Podcasts. And into this podcast we're going to be continuing the Pomeranary Path of Physiology series. We started it, I think, right around episode 393 or there about, or 392. It's gonna be a series we're hopefully by the end of it. You feel very comfortable with manipulating a lot of the Pomeranary concepts that are classically tested on the exam. The goal ultimately with this Pomeranary Path of Physiology series is to get people to really understand poem because I know poem is something that people might at least struggle with just in terms of understanding. Pomeranology has probably some of the hardest pathology, physiology, and pathophysiology to understand. So if you methodically work through this series, which I will continue by the grace of God, then you should be very good with Pomeranology going forward. The thing is if you have a deep understanding of things, then you kind of understand how everything relates to each other. You don't have to go down the route of just insane amounts of memorization. And as a reminder, if you're taking the USMELY Step 2, CKO Step 3 or complex level 2 or 3 exams, I have one of two courses that will be helpful to you. Actually, one of three courses that will be helpful to you. The first is more for Step 2 and Step 3. It's the MBME Testicking Strategy course. I'm actually going to be hosting that tomorrow on Zoom from 5 to 7 30 PM Pacific Standard Time.

I was going to be over Zoom on the 24th, which is tomorrow. And then if you're taking Step 2 or 3 or complex level 2 or 3, I have a 20 hour review course that's going to be starting next week Monday. It's going to be running all the way till Saturday. It's going to be for four hours each day. We're going to be skipping Wednesday. It's going to be from 5 to 9 PM Pacific Standard Time. And then if you know that you strongly bio-statistics, which I know there is a lot of people that struggle bio-statistics, then you may want to attend my bio-statistics review, it's going to be taking place on the 21st of July from 5 to 9 PM Pacific Standard Time. Again, I strongly suspect that is a course that you're going to be fine to be supremely helpful for your exam. I believe it's from 5 to 9 PM Pacific, but I know for sure for sure it's on the 21st of July. Okay, so let's jump into asthma. So again, we know that asthma is a kind of type 1 hypersensitivity reaction. So we know that asthma is a type of type 1 hypersensitivity reaction. And there are many different ways our friends at the NBM Es love to bring in asthma questions. They will tell you some story about a person that whenever they exercise in cold weather, whenever they go out and exercise, they have like some shortness of breath, they have a cough that accompanies it. That could be a very classic presentation of asthma.

Or you see a person, they are taking some medication for low back pain or whatever, and then you notice that they start having a lot of respiratory symptoms. That can be a classic presentation of asthma. Or they can give you a question about a person that is taking a bit of blocker. And you notice that they have this really bad hypersensitivity response, like they just have a lot of airway symptoms. They have a lot of airway symptoms because of their... because of their taking some inset-related compound. When you see that, those are all classic signs and symptoms of asthma. So whenever a person has asthma, what's the thing that causes their symptoms again? The key critical thing is they have an antigen that comes in through the airway. And then that antigen meets the immune system cells and then you make IgM first against that antigen. But over time, that IgM is going to, by the action of interlooking four, be class-witched to IgE. And in that IgE, that is sensitized to that antigen, goes and parks on the surface of a mast cell. Right? Because the thing is mast cells, they have what we call Fc-epsilon receptors. Those Fc-epsilon receptors, they have the ability to bind to the constant region of IgE. So when IgE binds to those Fc-epsilon receptors, right? It then kind of hangs out. Right? It just hangs out. The antigen bind the region of the IgE is just waiting.

Once the antigen comes again and binds to the antigen binding regions of those IgE antibodies, they're going to have cross-linking and the mast cell will degranulate. It will degranulate. Right? So the key trigger, the key trigger of you having the mast cell degranulating is an antigen binding to the antigen binding region of the IgE that is parked on the Fc-epsilon receptors that we find on the surface of a mast cell. So when a mast cell degranulates, what are some nasty things? It releases. It releases persta-glundings, it releases luchotrines, it releases histamines, it releases chymotactic factors for eocenophiles. Chymotactic factors for eocenophiles. What's a chymotactic factor? A chymotactic factor is something that attracts, right? It attracts. It attracts eocenophiles. That's part of the reason we have the leapfee of asthma. The mast cells release those eocenophiliate chymotactic factors and then that's going to recruit eocenophiles to the airway and you have more massive inflammation, right? Again, that's largely the pathogenesis of asthma, right? Again, because you have all these things like histamines and bradykines and luchotrines and eocenophiles, just that jumbled mess causing problems. You're going to have all that inflammation is going to cause you to make a lot of mucus. It's going to be producing a lot of mucus, right? The thing is inflammation causes constriction of smooth, it causes smooth muscle to tense up, right?

So you're going to have constriction of the smooth muscle that aligns up your airway so you can have brunco constriction, right? Again, you just have a lot of inflammation, a lot of mucus production, right? So you end up getting a lot of trouble. So if we want to fix this asthma problem, if the thing is if you understand the pathophysiology of asthma, then the drugs we use to treat asthma make a lot of sense to you. They literally will make a lot of sense to you. So let me ask you this, what are the drugs that we classically use to treat asthma? Well, the thing is, you know, there are many drugs you can use to treat asthma, right? But the highest yield once you probably need to know for your exams are your beta two agonists and you inhale corticosterics, your beta two agonists and you inhale corticosterics. If you think about it, you'll see pathetic nervous system medias brunco dilation through beta two receptors, right? If medias brunco dilation through beta two receptors, right? And the thing is when you activate those beta two receptors, right? Then you're going to relieve the brunco-constructive symptoms of asthma, okay? You're going to relieve the brunco-constructive symptoms of asthma. In fact, to start, let me talk about these short because the thing is there are two kinds of brunco dilators. You could see on your exam. They have a short actin brunco dilators and they have a long actin brunco dilators. So let's talk about the short actin brunco dilators first.

So the thing is, if you really think about it just again from a logical perspective, if you're in a fight or flight situation, you need more energy because your muscles have to work great. You need more oxygen for energy production by your mitochondria. Well, the thing is, how do you think you can get this oxygen? You can only get this oxygen when your airways are dilated. If you have brunco dilation, then more oxygen will come in through your airways. You'll get more oxygen for oxygen for phosphorylation and then you can have appropriate muscle contraction so that you can run away from that proverbial lion that is chasing the person. So again, you're going to achieve this through the sympathetic nervous system by activating bit of two receptors. Remember, these bit of two receptors, they're Jeep protein coupled receptors that increase the activity of adenylate cyclists. But if you look at it from the other perspective, right, let's not just be sympathetic nervous system centric. Let's also look at the parasympathetic nervous system. The parasympathetic nervous system raises a rest and digest system. You don't need that much oxygen when you're resting and digest it. Right? So you need the parasympathetic nervous system causes more of a brunco constriction, right? And it does this via muscarinic receptors, right? Muscarinic receptors.

So if we know that all the parasympathetic nervous system is pro-brunco constriction, it would make sense that blocking the parasympathetic system will mediate brunco dilation. So we use muscarinic antagonists for the treatment of asthma, they prevent the brunco constriction that accompanies asthma. And the thing is the reason you need to learn these agents as being short actin versus long actin is that the short actin agents does always for an acute exacerbation, right? So how long acute exacerbation present on you exam? It will just present as an acute worsening of the symptoms of asthma. I will say that again, it will present as an acute worsening of a person's asthmatic symptoms, right? So we use them for acute exacerbations of asthma. We also use them for acute exacerbations of COPD, right? In fact, I will say that the highest yield short actin beta-toygonis you need to know is our beta-row. The highest yield short actin muscarinic antagonist that you need to know is hypertropium. So our beta-row from the short actin beta-toygonis land, hypertropium from the short actin muscarinic antagonist land, right? And really the key side effect you probably want to know with especially your beta-toy agonists, right? Is that they tend to have weak beta-worn effects as well, right? So the thing is when these beta-toygonis are systemically, you know, absorbed, you're usually going to have some kind of tachycardia.

You're also going to have like a mild increase in your blood pressure. That's how you to know for your exams. So they can give you a question about a patient that comes in for an asthma exacerbation. And you know when they came in, their heart rate was like 87 beats per minute. And then they say that you administer pharmacological agents for their symptoms. And they tell you that, wow, like two or three hours later, the person's heart rate is 125 or something. And then they ask for, oh, what is the most likely mechanism behind these new physical exam findings? And then the right answer will be increased sympathetic activity, right? Or increased agonist activity at beta-worn receptors. Again, the thing is the newer NBM Es. I'm going to keep saying this point. In fact, this is a point. I mean, very obviously my testic and strategy scores amongst other key points, right? I tell people this, the NBM Es, they have very big on pathophysiology these days. They have very big on these derivative answers. It's not something you expect, but it will be something related to what you know. They're just trying to see if you're not just an ankywari. That you actually understand what in the world that you're talking about, right? So these are all key things to keep at the back of your mind with these short acting beta-to-agonists. And by the way, don't forget that short acting beta-to-agonist like Albiterol. You can actually use them in the treatment of hyper-kalemia.

You can actually use them in the treatment of hyper-kalemia. Because the thing is, beta-to-agonists, they have the ability to increase, they have the ability to activate the sodium potassium ATP-spomp. And remember, what does this pump do? This pump takes three sodiums out of the cell and puts two potassiums into the cell. So the thing is, if you activate these sodium potassium ATP-spomp, you're going to keep putting two, two, two, two, two potassiums into cells. That's going to take the potassium from the bloodstream and it's going to dump it in your cell. So it's one of those things you use for the acute treatment of hyper-kalemia. Although do not forget, when a president has hyper-kalemia, the first thing you're supposed to do is to stabilize that awesome myocardium. You're going to do that by giving calcium-bluconate or calcium chloride. Essentially, your goal is to just give a salt of calcium. Like calcium-bluconate or calcium chloride, that is going to stabilize the myocardium. When you stabilize that myocardium, you're going to at least help the president not die from a dangerous cardiac arrhythmia. Because many times when people have hyper-kalemia, they're going to have topic two waves and you know, that's bad, but they're also going to start having a white QRS. And if you don't do squat about it, then the EKG is going to progress to them having a sinusoidal waveform. And then if you do nothing about it, that sinusoidal waveform is then going to go to a flat line.

That's easy-stly. That's obviously bad news. I mean, when a president has easy-stly, they're dead. You do not want that. It's usually prudent to give that calcium-bluconate first, but other things you can consider, things like a butyl role, that increase the activity of the sodium potassium AT Pase pump. You can give something like insulin-plus-blucos, because insulin is also an activator of the sodium potassium AT Pase pump. You can also give things like Kx-elite. Kx-elite makes K, exit out of your body. It makes K, exit out of your body. So by giving Kx-elite, it's going to make you get rid of potassium. Because really, a butyl role in your insulin-plus-blucos are more redistribution of your potassium. From the bloodstream where it can kill you to intracellularly wear, you may not kill you. But on the flip side, right, on the flip side, right, Kx-elite helps you actually get rid of potassium from the body. And also dialysis. dialysis is something that can help you get rid of potassium from the body. Or if you even take a loop diuretic, because remember, loops cause you to dump potassium in your urine. That can cause a potassium diuresis. And those are all things you can use to treat hyper-killemia. But many times, you're going to start with the calcium gluconeid first or calcium chloride. And then secondly, you usually go to our butyl role. And then thirdly, you can go to insulin-plus-blucos.

Again, all these things are mentioning they are all derivative points, but they are very high your points to know for your exams. So since we've talked about the short actin-bronkordi leaders, let's talk about the long actin-bronkordi leaders. To be honest with you, these long actin-bronkordi leaders, they work exactly as the short actin-bronkordi leaders. But they have some chemical modifications in their structure that make them have a slower onset of action. But when they start working, they work for a longer period of time. So they have a slower onset of action, but they have a longer duration of action. That's important to know, because they have these chemical modifications. So if you think about it, since these drugs have a slower onset of action, would you make much of any sense to use them for an asthma or COPD exacerbation? I would really hope your telamine divine know. Because if a person's airways closing up, and you're like, hmm, let me give them a long actin-bronkordi leader. Guess what? Your appearance will belong to your parents. God forbid, not your portioning. But the person's patients will be long dead before the drug kicks in. You don't want that. So that's why you start with a short actin-bronkordi leaders first. So again, these long actin-bronkordi leaders, they have a slower onset of action, but you have a longer duration of action. Again, these drugs are not used for acute exacerbations of asthma or COPD.

If you ever see them as answers, do not pick them. I'll say that again, if you ever see them as answers, do not pick them. For an acute exacerbation of asthma, COPD, if you pick those answers, you will get those answers wrong. So what are so high-youted long actin-bronkordi leaders? Well, the long actin-bronkordi leaders, you want to keep in mind, that drugs like Sarmereol, S-A-L, M-E-T-E, R-O-L, and for Moderol, F-O-R, M-O-T-E, R-O-L. And if you're looking at things from the most chronic antagonist perspective, the high-youted long actin-bronkordi leader, long actin-bronkordi leaders, well, actually I can give you a memory and that's just looking in the order of the alphabet. So if we look at better twagalists, the short actin-bronkordi was our Peter Rho. The long actin-bronkordi was our Sarmereol and for Moderol. Our Peter Rho is short actin, it goes with the A, earlier part of the alphabet. Sarmereol and for Moderol, the longer actin, that's an S and an F, San Francisco, later part in the alphabet. And then if you're looking at it from the perspective of the long act of the most chronic antagonists, the short actin-bronkordi antagonist starts with an A, E-Pratropium. The long actin-bronkordi antagonist starts with a T, Tiotropium. T is later in the alphabet, long actin-bronkordi antagonist. A is earlier in the alphabet, E-Pratropium, short actin-bronkordi antagonist. That's important to know.

Now, another key thing you want to know with these drugs, especially the labas, the long actin-bronkordi antagonists, is that you cannot use them as monotherapy. I'll say that again, you should never use Sarmereol or for Moderol as monotherapy for the management of asthma. If you do, it causes a lot of bad things. It's associated with an increased risk of death if you use them as monotherapy. They are actually associated with an increased incidence of fetal asthma attacks. They are either an increased incidence of fetal asthma attacks. So you do not use them as monotherapy. In fact, let me explain something that I call a treatment ladder. When a person has asthma, the first wrong one, your ladder of treatment, is going to be a short actin-bita antagonist, a short actin-bronkordi leader. And then, if that's not controlling the asymptoms, the second thing you need to go to is an inhaled corticosteroid. If an inhaled corticosteroid is not working, so something like budesonide or fluticazone or things like that, then you go to wrong three on the ladder. Wrong three on the ladder is either a lava, a lava, right? So something like Sarmereol or for Moderol, or it can be a luchotrine blocker, something like Monte Lukas or Zafri Lukas or Zaluton. We'll talk about that in a bit, right? So that's the ladder you follow and then obviously if those things don't work, they need to go to the fourth wrong one, the ladder. The fourth wrong one, the ladder is the use of oral corticosterids.

That's how you deal with asthma. That's really asthma management in a nutshell. But if you're looking at things from the COPD perspective, COPD you start off again with short actin-bronkordi leaders. That's the first wrong one on the ladder. The second wrong one on the ladder at the long actin-bronkordi leaders. I'll say this again. In health corticosteroids do not constitute the second wrong on the ladder in COPD management. In health corticosteroids at the third wrong on the ladder in COPD management, but in COPD management the second wrong on the ladder are your long actin-bronkordi leaders. The third wrong on the ladder at the in health corticosterids. At the in health corticosterids. And remember people that have asthma, you know, they're in people that have COPD, right? Some of them are eligible for home oxygen. The home oxygen you're going to be using that home oxygen. If you're in a situation where you know, in room air your oxygen saturation is like, you know, less than 88% or if it's low in room air, if it's pretty low, usually in the 88% range of their abouts, then those people are going to need home oxygen therapy. They're going to need home oxygen therapy. Again, that's pretty high you to know, know for exams, right? So now let's talk about the health corticosteroids. Health corticosteroids really just corticosteroids as just in general. They're pretty high you to know for for exams, right? So let's see.

I mean, I feel like this corticosteroid discussion is going to be long. So I mean, talk about the luchotrain and tagueness in a future in, you know, pulmonary pathophysiology probably series four, right? So the thing is, you know, you know, you heard corticosteroids, you use them for many things, right? They have many roles in the management of asthma. You can use them in the inhaled form, you know, to chronically manage your person's symptoms. You can use them in the IV form. IV corticosteroids are one of the things you have to give when a person comes into the hospital with an asthma exacerbation or a COPD exacerbation. It's one of the drugs that have to be administered. And then, oral corticosteroids can be used outpatient in both asthma management and in COPD management. Well, let me tell you how they're going to present it on exams. From the perspective of asthma, if you have symptoms that have not been controlled by drugs on the first three wrongs of the latter, and they have like just chronic symptoms that rest, then those people need to be on oral corticostero therapy. That's one. But if we're looking at things from the perspective of, oh, an acute asthma exacerbation, when those people come into the hospital, they need to receive IV corticosteroids. I'll say that again, they need to receive IV corticosteroids.

Now, if we're looking at things from the COPD perspective, when a person comes into the hospital with an acute COPD exacerbation, those people are going to need IV corticosteroids as well in the hospital. But, classic, there are many indications for oral steroids in COPD patients. But the one big one I would encourage you to know for purposes of your exam is that they'll give you a question about a COPD patient. They came in with an acute exacerbation. They got the bronchordilators. They got the IV corticosteroids. And then those people are being discharged. And then they say which of the following can be done to reduce the risk of readmission. When you see a question like that, the smart thing you want to do is to give them a few days of oral steroids. The number of days do not matter. You worry about that in residency. Usually it is about three or five days of oral steroids. But those people will get those steroids because you want to prevent lead reactions. You want to prevent because if you just give sterile in the hospital and say go home, no, that's not smart. The inflammation can come back again and bring them right back to the hospital. So the way you keep that inflammation at bay is to give them a few days worth of oral corticosteroid therapy. Okay? A few days worth of oral corticosteroid therapy of oral corticosteroid therapy. So how in the world do steroids work? Well, the thing is steroids remember, they are lipid soluble drugs. So they work at the genetic level.

The thing they do is they bind to receptors because they are lipid, you know, they are lipid soluble. They go into the cell and then they bind to response elements on DNA. They bind to response elements on DNA. When they bind to those response elements, they are going to decrease the synthesis of inflammatory migrators. Again, they work at the genetic level. Basically, what are steroid doses? It prevents the genes that code for things like leukotrients and histamines or TNF alpha to be transcribed. It prevents the transcription of those genes. If you prevent the transcription, you will make those mRNA products and you will not make those protein products like leukotrients, histamines, bradykines and things of that nature. Right? You know, sometimes you may even see an MBM exams. They ask you for the mechanism of action of a steroid and the right answer is, oh, that inhibitor transcription factor called NFKAPAB, NFKB. Again, this is one of those things you think, oh, this is just step one detail. And then you take your step two exam, you take your step three exam, and your eyes are open, you're like, what? Again, I don't want you to have that expression because you heard that on this podcast. And then another thing I want you to keep at the back of your mind with corticosteroids is that the inhibitor enzyme called forceful lipase A2. The inhibitor enzyme called forceful lipase A2.

The thing is forceful lipase A2 helps with the conversion of membrane forceful lipids to arachidonic acid. It helps with the conversion of membrane forceful lipids to arachidonic acid. The thing is arachidonic acid is ultimately the ancestral molecule that is used to make lucotrines and prostaglandins. And as we know, those lucotrines do not do you any favors with regards to asthmatic symptoms. I mean, that is why there is such a thing as a lucotrine antagonist used, right? So drugs like Monte-Lucas, Zafelucas, Zaluton that are using the management of asthma. Now, there are a few key things you need to keep at the back of your mind with steroids in terms of side effects, right? For example, they can give you a question about a person that has been on corticosteroid therapy for asthma, COPD. And then they are now having painful dysphysia, so they have a dynophysia. When you see something like that, I want you to think of orpharyngeal candidaeases, right? So especially if you are not applying those in your corticosteroids correctly, right? That can cause orpharyngeal candidaeases. Can cause orpharyngeal candidaeases? And obviously, we know that we are going to treat that with my starting swish and swallow, or you can use an oral easel, right? And then it's also high to know that in your corticosteroids can cause cushion-goid features. They can cause cushion-goid features, especially if you use it for a prolonged period of time. That's where you get in trouble.

So they can show you a picture on exams, right? You see a person with a large face, you see them in a buffalo hump, you see all those things, right? Those are all things that are pretty classic. They are all things that are pretty classic for the cushion-goid features of pressing, taking a in your corticosteroid therapy. And remember, those people, if they've taken it for a long period of time, the adrenal axis has been suppressed. It has atrophied, right? Because of all the negative feedback from the steroids that they are taking. So typically those people, if they are having like major surgery, or if they have an adrenal crisis, or they're getting the motor vehicle accident, the ICU, and you notice that man, this person is persistently hypotensive. I'm giving them, giving them, pressers, they are not responding. Then you should probably realize at that point that, hmm, because think about if you're in a stressful situation, you're going to need more cortisol. What if you've atrophied your HPA axis? Your HPA axis cannot respond within a couple of hours to start making more cortisol. So those people are going to need a stressed dose of corticosteroids, because again, corticosteroids, they have a permissive effect on the sympathetic nervous system. So you have very poor response to pressers and their visual constructive effects when you don't have enough cortisol around.

So that's why in those cases, you're going to give those people steroids so that you can encourage that permissive effect that cortisol has on the sympathetic nervous system. And also do not forget, if a person is on chronic steroid therapy, and then they tell you that, ah, over the last four to five days, they've been having shortness of breath, they've been having a cough, and then they tell you that chest x ratios, uh, in testically infiltrating their lungs. What are you thinking about? I really hope you're saying, oh, divine. Hmm. This person has the most systems re-vexinumonia. Remember, people that are on chronic immunosuppressive therapy, they can develop the most systems re-vexinumonia, right? They can develop the most systems re-vexinumonia. That's why many times, if people are going to be on prolonged steroid therapy, one smart thing you can put them on is you can put them on trimethoprim sofomethoxazole as prophylaxis against the most systems re-vexinumonia. Or they can give you a question about a person that has been on chronic steroid therapy. And then they tell you that, this person has been having like back pain, if you're having back pain, if you're having back pain, and it's less like an older person or is a person with very low weight. And then you notice that, wow, you look at the back and you'll find a fracture. Hmm.

When you look at the hip and you see a fracture, because many times when people have these kinds of fractures, the most common location is usually in the vertebral bodies, the second most common location is usually in the hip, right? That's osteoporosis. That's osteoporosis. Remember, corticosteroids increase the activity of osteoclasts. Now, what is the job of an osteoclast? The job of an osteoclast is to reserve bone. The job of an osteoclast is to reserve bone. So if your osteoclasts are reserving your bone, your bone mineral density is going to go down. That's why people that are on corticosteroid therapy or people that have really big risk factors, right? Like people that have very low weight because remember if you're non-weight bearing, then your bones are more brittle, right? Or people that are Caucasians, right? Basically, like if a person is on long-term steroid therapy, those people need to be on bisfossinids to reduce their risk of developing osteoporosis. Remember steroids, they're, I mean, bisfossinids, their job is to cause a poptosis because I'm inhibition of osteoclasts. That's why they're helpful in the management of osteoporosis. And then also, if your long-term steroid therapy, remember corticosteroids, they actually increase the production of gastric acid. I'll say that again, corticosteroids increase the production of gastric acid. Hmm, that sounds like an ulcer in the mecan.

So it makes sense typically on imbim exams when a person is on long-term, especially long-term oral steroids or long-term IV steroids, those people are going to need PPI. They're going to need a proton pumping inhibitor to reduce their risk of developing peptic ulcer disease. Okay, to reduce their risk of developing peptic ulcer disease. That's why, really, like many of these corticosteroid effects, especially the urofaryngeal of the, or the esophageal kind of diocese, these are many times you see some of them told that you know what, I've never used any health corticosteroid, just wash your mouth, right? Just wash your mouth so you can essentially wash so that it just kind of helps with, with you not getting some of these, getting some of these problems, right? Getting some of these problems. So I think since we've gone on for almost 30 minutes at this point, we're going to go ahead and pause here. Again, I do offer one or one tutoring on a limited basis for all the USMM exams, step one, that juicy case, step three, I do offer tutoring for pre-clinical medical exam, 30-year clerkship shelf exams, then I also offer review courses. Again, tons of people have taking these review courses, they've done extremely well. Like, literally, I've had people take my review courses and they've gotten even up to the 280's on their USMM exams.

So again, I have an MBA Me test taking strategy course, I have one coming up tomorrow, I have a 20-hour review course that's going to be, and again, it's for step two, step three, complex level two, and three, that comes up next week, all through next week Monday to Saturday, with the exception of Wednesday, and then I have a four-hour bio-statistics bootcamp that will make you an expert in the bio-stat that you need to know as you approach your USMM exams. The bio-stat's bootcamp is more for people taking step one, step two, three, step three, four, pretty much all the USMM's, all the complex exams, complex level one, two, three, and then I have these podcasts on Apple podcasts, on Google podcasts, and on Spotify. So if you want to, at least the most recent 150, you can find them on those podcast apps, and then I have a You Tube channel called Divine Intervention USMMM really podcasts and videos, that is where I post the videos that I make. So if you subscribe, you'll get an email notification whenever I make a new video. Many of my shelf review videos are actually on my You Tube channel, and then I have a new website, many people have said, oh, divine, I love your life lessons. So I started a new website called Divine Intervention, lifelessens.com. It's a Bible-based website, many of you listen to this podcast though that I'm a Christian, so I have, I think I'm pretty sure I have more than 90 podcasts there right now actually, and most of them are 10 or 12 minutes long.

They just address like a common problem that humanity faces, but I show you how to address it from a biblical perspective. The Bible is a very, it's a very complete book, it's a very insightful book. I even have the podcast on Apple podcasts, it's called the Divine Intervention Life Lessons Podcast. So again, just check those out, and hopefully you're blessed by it. So thank you for listening to me today. Have a wonderful rest of your day. God bless you. I'll see you next time. Thank you.

Cross-linking of IgE antibodies that are already bound to Fc-epsilon receptors on the mast cell surface, triggered by subsequent antigen binding.

Short-acting agents (e.g., SABA/SAMA), because long-acting agents have a slow onset and are ineffective during an acute crisis.

They work at the genetic level, binding to receptors and preventing the transcription of genes that code for inflammatory mediators (e.g., leukotrienes, histamines).

Osteoporosis (increased osteoclast activity) and increased risk of peptic ulcer disease/GI bleeding.

To stabilize the cardiac myocardial membrane, preventing life-threatening arrhythmias, without altering serum potassium levels.

Long-acting bronchodilators (LAB As/LAM As).

It drives class switching of initial IgM antibodies to IgE, which then sensitizes mast cells.

Short-acting Beta-2 Agonists (SAB As).

1) Preventing transcription of inflammatory genes, and 2) Inhibiting phospholipase A2 (which prevents arachidonic acid release).

They are associated with an increased risk of death and severe exacerbations if used alone.

Intravenous calcium gluconate (to stabilize cardiac membranes).

Osteoporosis/Vertebral compression fractures.

Proton Pump Inhibitor (PPI).

It drives class switching of initial IgM antibodies to IgE, which then sensitizes mast cells.

Short-acting Beta-2 Agonists (SAB As).

1) Preventing transcription of inflammatory genes, and 2) Inhibiting phospholipase A2 (which prevents arachidonic acid release).

They are associated with an increased risk of death and severe exacerbations if used alone.

Intravenous calcium gluconate (to stabilize cardiac membranes).

Osteoporosis/Vertebral compression fractures.

Proton Pump Inhibitor (PPI).