DIP Episode 300 - Comprehensive Coronavirus/COVID-19 Podcast for The USMLEs (Step 1-3)

Okay, welcome. My name is Devine. This is episode 300 of the Divine Intervention Podcast. And I'm going to be calling this the Coronavirus Slash COVID-19 Podcast for the USML. This podcast, actually, I guess maybe I should first of start by saying, you know, I'm pretty grateful first to be seen the first day of April. I mean, with this Coronavirus COVID-19 pandemic, there's been millions of people that have lost their lives all over the world. So I guess one message I guess maybe I want to put out there today is just be grateful, just be thankful. I know many people about two weeks ago they found out that they did not match or they had to go into the soap process or they did not match to the appropriate program. But remember that when there is life, there is hope. And the fact that you're alive means that you still have something to do on this planet. So, you know, there are many people that there are definitely some people that probably plan to go through the soap process or go through the match process. That because of COVID-19, their lives were taken away from them and not even able to see the match, the soap or whatever. Those people, I'm sure if they were giving the opportunity to be alive now, even if they didn't match or even if they couldn't get through the soap process, they probably choose that. So again, you know, bad circumstances happened to some people two weeks ago. But let's remember to be grateful.

I mean, there's this part of the Bible that says, in all things give thanks because this is the will of God the Father. I encourage you to be thankful. I most certainly am thankful. I mean, I've just heard of so many things, many families. I mean, like I'm a big watcher of the NBA and just people who their family members have perished from COVID and stuff. You know, so it's pretty rough on a lot of people. So the fact that you are complete, so you have a complete family right now is risen enough. Just the fact that you can take a breath is risen enough to be thankful. So I think I'll encourage you to be thankful. I guess I'm also thankful that you know, we've hit a big milestone on the website. This is episode 300. And you know, by the grace of God, I will make many, many, many, many more podcasts. This is just, I don't think we've even started as a podcast website. At least that's my personal belief. I believe that, you know, God is taking us to bigger places, more and more podcasts, even better podcasts than currently exist. But I'm grateful to have episode 300, right? Because, you know, by the grace of God will come a long way. So you know, 300 podcasts in them. I'm very, I'm very happy with that. But again, I guess almost reminds me that divine, you could do better, you could meet, you could have more than 300. So, you know, just, just thankful for that. But you know, also like a reminder to work harder and do better, do better work out there. Okay.

So we're going to be talking about coronavirus COVID-19. So, I'm going to be talking about this podcast. I'm intentionally going to say that this is for all the USM Ls. The thing is, I would discuss many things that you would potentially see on the USM Ls. And I would try to discuss again a lot of pathophysiology because this is just one thing that many people still struggle with. The coronavirus is just understanding pathophysiology. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there.

There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. There's a lot of misinformation out there. And then they will tell you that, oh, you know, the person over the last like 24 hours, the person has, you know, been crashing and burning. They've been having profound shortness or breath. They may have like a dry cough or they may have a productive cough. They may be having high fevers, right? And you notice that, you know, the auto-sats are really low, right? If you see that, you know, again, especially on the newer US Emily exams, you really want to think about a person having coronaviruses, right? Remember, it's an enveloped, linear, single-stranded RNA virus, right? And it actually has a helical capsid, right? So you remember for people that are taking step one, unfortunately, your friends at the MBME, they still love to test those identification things, right? So you know these identification, identification.

But the thing is for coronaviruses, though, there's a lot of stuff they could potentially test, right? And the thing is some of these questions that describe experiments. Those are very easy for the COVID-19, because, and again, it's of same coronaviruses, I'll just say COVID-19, right? Because there's just lots of integrations with immunology that you can really throw in on a test. So again, if you pay attention, take good notes on this podcast. I think you'll find it to be extremely helpful, right? So the thing is when a person gets the coronaviruses, right? What's going to happen? Well, the thing is, you know, many times they'll be symptomatic a few days after exposure, right? They'll be symptomatic a few days after exposure. And you know, many times you're still going to be infectious for about 14 or more days after you've been exposed, right? Now, one other thing you'll find that the MBME care about, right, is knowing what are the risk factors. Again, we live in this MBME era of risk factors, right? So what are some risk factors that put people at, you know, hires for like really bad disease with COVID-19, right? Remember, if you're old, being over the age of 60, like over the age of 60 for the most part, right? It is associated with really bad outcomes, right? So the older you get, the worse the disease you get, and the higher the risk of death, right? But if you also have like just all the bad chronic diseases, hypertension, right?

Puminary disease like COPD, asthma, diabetes, remember diabetes, crushes a person's immune system, right? All those things can place a person or the person's immunocompromised. They say they have HIV, right? Or they have an immunodeficiency disease, or they are immunosuppressive therapy. Because they are transplant recipients, right? All those people, again, these are all risk factors for a person having a really bad disease, right? With coronavirus. Now, how is this stuff transmitted? Well, for the most part, it's transmitted by the respiratory route, right? It's transmitted by the respiratory route, right? So many times people can get this through like aerosols through respiratory droplets, right? You can even get it from contact, right? But again, for the most part, that's not the main route of transmission. The main route of transmission is the respiratory route, right? And the thing is, there are some risk factors that increase your risk of receiving the illness from someone that has it, right? The first one is if you're if you interact with those people closer, right? That's why we advocate for all the social distancing. The closer you interact with these people, the higher your risk, but also the longer you interact with these people, right? So that's why you want to have very quick, efficient interactions with people. If you interact with people during this COVID-19 pandemic, right?

Now, one thing that's actually high to understand is that people that are working health care, it's actually high to understand that these people aerosol-generating procedures can potentially be the thing that gives them COVID-19, right? In fact, many hospitals have implemented many algorithms or many initiatives to try to curb the use of aerosol-generating procedures, or maybe use alternative procedures that give you the semi-effect on aerosol-generating procedures so that you reduce the risk of these healthcare workers getting these problems, right? So, you know, things like, you know, the obvious ones like intubations, right? But other ones, we don't really think about like if you're getting like some kind of nipulite treatment, this is something that happens on many medicine floors in the ICU, people getting like nipulitis, bronchidilators and stuff. Those things that aerosol-generating procedures, they are very high risk procedures for people contracting COVID-19, right? If you're a pulmonologist, if you're performing a bronchoscopies, right? Or you're doing like this non-invasive positive pressure ventilation, right? So like CPAP, BiPAP, right? Those things can increase the risk of a person getting COVID-19, right? So those aerosol-generating procedures, the things you want to keep at the back of your mind, are things that are very high risk procedures in healthcare workers for potentially getting a quarter virus, right? So the thing is, how do we diagnose this stuff?

Well, for the most part, you want to go ahead and pick performing some kind of Nisofarin-Joe swab, right? And remember, you know, in general, when you take these, although you can use sputum samples or whatever, but in general, most people, vasmigrerti, again, the classic thing is to do a Nisofarin-Joe swab, right? And then you'll send that swab for reverse transcription of PCR, right? Usually within a few hours, you can get those test results back, right? So you do RT-PCR, again, reverse transcription, because remember, it's an aeronavirus, right? It's an aeronavirus. So that, you know, that RNA, you make sense that reverse transcription PCR, right? Because, again, you want to do reverse transcription to convert that RNA to DNA, right? I mean, it's kind of amazing how far along PCR has gone in this world. I remember when I just moved to the US, you know, I used to do, you know, some research with PCR and stuff. This was maybe like eight, nine years ago, something like that. And it's just amazing how quickly the technology has kind of advanced, right? Now, you know, they may try to trick you on an MVM exam, and to begin a chest CT. A chest CT is not recommended. Even if you have chest CT results that look like a person, looks like a person has coronavirus. You need to confirm, right, with reverse transcription of PCR. In fact, one very smart thing your friends at the MVM can do is they can make this a bio-stats question, right?

So, the thing is a chest CT is probably pretty sensitive. It is not probably, it is pretty sensitive for identifying people that potentially have coronavirus. But remember, whenever you have a test that is very sensitive, you know, very likely you're going to pick up a lot of false positives, right? So, a chest CT can almost be like a screening test you can employ in an ED, right? But the thing is if you want to confirm, you need to do the RTPCR, right? You need to do the RTPCR, right? So, again, the chest CT is very sensitive, but again, there are many things that have similar findings on chest CT as coronavirus, that are not coronavirus. So, chest CT is very sensitive, but it is not specific. So, you absolutely, absolutely still need to confirm the diagnosis by using a reverse transcription of PCR. And what will you find on a chest CT, right? For the most part, again, because it's like a Pomona interstitial disease, you're going to find bilateral, ground glass, or pasities. And the thing is usually it's typically symmetric, right? So, one side of the lung will not look like a carbon copy of the other side of the lung. And typically it's also pericurer, right? So, it's going to be predominantly subplural. So, just below the plural lining in a predominance, right? So, that's usually what you're going to find on a chest CT. Usually, these people, they actually don't have plural infusions, right? They usually don't have plural infusions, right?

And remember, when people have COVID-19, right? Many of them that die of respiratory failure, ARDS is a thing that usually kills them, right? But again, we're going to talk more about treatment down the line, right? So, let's talk about how do we prevent the spread of coronavirus? Again, the classic public health measures, again, the friends of the NBME with the newer exams, they really, really love public health measures, right? So, you want to keep things like physical and social distancing at the back of your mind, right? So, remember, you want to keep at least six feet apart, right? So, you want to practice, again, social distancing, that's really helpful quarantining, right? So, if, for example, you've been exposed to a person that potentially has the virus, right? You want to at least self-quarantine for roughly around 14 days. You know, again, some of these things I'm seeing in this podcast are very fluid, right? This pandemic has been evolving, there's all these first wave, second wave, whatever wave, right? So, you know, but for the most part, the things I'm going to discuss today are pretty accurate, right? So, in general, if you've been exposed to a person, if a person has been exposed to some individual that has been discovered to have the virus, right? You want to self-quarantine for about 14 days, right? And then remember, hand washing is also a very effective technique.

I mean, basically, like household soap on the most part explodes like the viral capsid, right? So, it pretty much destroys the virus, right? And if you're using a hand sanitizer, you need to make sure that you're using a hand sanitizer that has at least 60% alcohol, right? Now, also using masks, right? It's very helpful, right? Like homemade masks, surgical masks, these are all things that are helpful for preventing the spread. And also preventing from getting it, right? But if you have it, it also prevents you from spreading it to other people, right? And also the vaccine, right? Getting the vaccine is also helpful. I mean, at least, I believe like the Pfizer or Moderna vaccine or whatever has been shown to be greater than 90% effective. And I'll say some more things because again, for people that are taking step one, I can see the NBME going the immunology route with a lot of these COVID-19 questions, right? You'll see why in a few minutes, right? But again, you'll see why the stuff is pretty high, you'll understand, right? And also like increasing ventilation indoors, right? So, I know this is pretty common in certain populations of people who are for some reason. They don't turn on the fans, they don't turn on air conditioning in their homes. If that's a crowded home, and that's why unfortunately this is a problem in developing countries, right? Because I remember in Nigeria, at least back in the day, remember that there'll be times for months no electricity.

So there's no electricity. Obviously your fans are not running, your air conditioning is not running, right? In a crowded environment that significantly increases the risk of people contracting a COVID-19, right? And again, other things that help is, again, don't touch it. If you have an unwashed hand, right? If your hand is unwashed, don't touch your eyes, don't touch your nose, don't touch your mouth. That's a very effective means of preventing the spread of the virus, right? It always just kind of boggles my mind when I see people, they literally have just shake someone's hand, or they've just touched the surface that many other people have touched. And then you see them cleaning out their eyes, putting their fingers in their nose, putting their hands in their mouth, right? Again, those people are just putting themselves at a necessary risk, essentially, right? And then remember, if you're wearing a mask, right? In general, a mask with an exhalation valve, especially if you have the virus, it's not a good thing to do, right? A mask with an exhalation valve, because guess what? Those masks and many of these things that have these exhalation valves are like some of these N95 masks. Again, it's good. It's protecting you the wear, right? But I think if you have COVID-19, those exhalation valves are essentially helping you spread that to others.

That's why for the most part, many of these airlines, or most of these are public buildings, they don't let people that have masks with exhalation valves kind of get into them, right? So I know at least that's a big thing with the airline industry for sure, right? And then remember, if you're a healthcare worker, and you're working with people that potentially have COVID-19, you want to use a respirator. That's the buzzword you want to remember for NBM exams, respirators, right? Respirators. And the respirators you want to use on NBM exams are N95 respirators, right? So the thing is, many of us, you know, in the midst of this pandemic, we've heard of many different respirators, N95, P100, R99, blah, blah, blah, blah. So what in the world do these things mean? Literally, let's let's deconstruct the term, right? So what does the N stand for? The N means that the respirator is not resistant to oil, right? R, which you've seen some respirators, tells you that, oh, it's resistant to oil. But typically, it means that you're only going to use that thin ones, right? You're going to use that respirator ones is like for single use ones, although unfortunately, you know, with the limited supply of PPE in certain healthcare systems, you know, people had to reuse reuse reuse many of these things. But then the P, right, means that it's all proof, right? So N means not resistant to oil. R means resistant to oil. P means that it's oil proof, right? And you can reuse it a lot, right?

I mean, one thing that kind of boggles me out some things about the way healthcare systems work is, you know, you kept reusing these N95s. But the thing is right out there in the world, there's all these P100 respirators that are so quite widely, right? And even provide somewhat better protection than the N95 respirators, right? And you can reuse them, right? So it's like it offers every single advantage. But some healthcare systems say that, oh, you know, it doesn't look cosmetically good. We don't want to scare patients. But the thing is, you know, we're in the midst of a pandemic, right? It's a pretty bad pandemic. You need to make some concessions, right? And you also need to protect your healthcare stuff that are working with you, right? But that's a different conversation, right? So these respirators, they're pretty good because, you know, essentially, the prevent like all these dust or these liquid droplets in the air, especially those that are like roughly on the, you know, around like 0.3 microns, right? They really protect right? So really that that number you see at the end, like N95, it just talks about the efficiency level of the filter, right? So like an N95 mask, right? Again, the 95 means, oh, it's 95% effective at getting rid of these, you know, protecting you or filtering all these lipid droplets, liquid, not lipid, liquid droplets and dust from getting into getting into your airway, right?

So obviously the P100s, the P100 again, it's not 100%, but it's like 99.97% effective, right? Those P100 respirators, they're very cheap, they're widely available, well, they're amazing. The only problem is many of them again, unfortunately, have acceleration valves, right? So again, you'll protect you, the wearer, but if you have COVID-19, it would not protect the people that are necessarily around you, right? And then it's also also high to know that vitamin D deficiency actually increases a person's risk of having like a severe COVID-19 infection. Again, it's limited data, but it is definitely positive data, right? So if a person is vitamin D deficient, right? So let's say a person has like a person has like dark skin, right? Or you're working or ideology, for example, we're in a dark room all the day, or you live in a very cold climate, right? Especially in this pandemic, taking vitamin D is very helpful. I mean, but I mean, these also just helpful for many different things, right? So, that's actually one high you thing to keep at the back of your mind. Okay, so now that we've done away with many of these social science things, let's begin to go into the basic sciences, let's begin to go into the clinical sciences, that your friends at the end of the year, you really, really love, right? So the thing is COVID-19, the virus, right? It has four key proteins, right? These are four key proteins. You want to remember for your exams, and I'm going to use them.

No, I call them like men's, so like M E, M S men's to remember the proteins, right? So there's obviously the end glycoprotein, right? The end glycoprotein is essentially like a protein that actually helps in bringing like new trends into the virus, right? So it helps for like transmembring new trend transport, right? And then there's the E protein, the E protein is the envelope protein, right? And then the end, the end is the nucleic capsid protein, right? And I'll argue that probably the most important protein here is the S protein, right? The S protein is the spike protein. In fact, I'm going to spend quite a bit of time on the spike protein, right? Because it's very helpful to understand quite a bit of pathophysiology with the virus, right? So the thing is, why is that spike protein pretty virulent? Well, let's look at how people get, how people get COVID-19 essentially, right? So remember, in the longs, we have two major kinds of cells, right? Two major kinds of nimosites. There's the type one nimosites, right? That, you know, they're simple scumose epithelium. They allow you have gas exchange. And then there's the type two nimosites, right? Which are cuboidal epithelium? Remember, those type two nimosites, one thing they do is they have the ability to produce surfactant. Remember, they store that surfactant in those lamella bodies, right? That's a high-yield, a little bit of USM information to know, right?

But those type two nimosites, they also have the ability to undergo metaplesia when a person has long injury to type one nimosites, right? So remember, it's a kind of metaplesia, right? Where you're going from one cell type to another, right? So you're going from simple cuboidal epithelium to simple scumose epithelium, right? So they have the ability to undergo metaplesia. The only problem with these, I guess it's not a problem, but many of us also kind of know this basic science detail that angiotensin-1 being converted to angiotensin-2 happens in the lungs, right? Under the action of angiotensin-converting enzyme, right? So the thing is, many of these type two nimosites, they have a lot of ACE-2 receptors, right? And a lot of ACE-2 receptors is a protein, right? They exist on the surfaces of these type two nimosites. The thing that happens is that these ACE-2 receptors on type two nimosites actually binds the spike protein that comes from a COVID-19, right? And the thing is, this spike protein actually has two subunits, right? So it has the S1 subunits, the S1 subunits is the part of the protein that literally binds to the ACE-2 receptor, right? So that's the receptor binding domain for the ACE-2 receptor, the S1 protein. Remember, again, I said the spike protein has two subunits, has the S1 subunit, and it has the S2 subunit, the S1 subunit, is the receptor binding domain, right?

So in fact, the S1 subunits is ultimately what you should think of as the antigen that is in many of the vaccines that have been produced for against COVID-19, right? Because again, if you can make something that can essentially obliterate the S1, you know, obliterate binding of the S1 to the ACE-2 protein, then that will prevent binding of the virus to your type 2 nimosites, right? And then, the S2 is the portion that medits fusion of the virus to our nimosites, right? So S1, again, is for receptor binding to the ACE-2 receptor, the ACE-2 domain of the spike protein medits fusion. If you notice, many of these are any viruses, you'll pre-biased somewhat similar mechanism, right? Again, like HIV virus, we know of many of those receptors, GB41, GPO, those things, right? This is not a HIV podcast, I'm going to kind of hold myself back there so that this podcast does not be common on necessarily long, right? But again, it's kind of high you to understand, high you to understand that. So if you kind of think about it, we know that the type 2 nimosites, the health post-regionary, the long, right? They literally health post-regionary, the long, after injury. So if you're infecting the type 2 nimosites, you can see why it's very hard for these people for their long story, they pair itself after they've had a potential injury, right? After they've had potential injury.

Now, one thing to know is these ACE-2 receptors, we don't only find them on the long, dynimosites, we also find them in many other parts of the body, right? So ACE-2 receptors, you can find them in the heart, you can find them in the stomach, right? Like your gastric epithelium, you can find them on your dwindling epithelium, you can even find them in the rectum, right? So the thing is, you can see that many people can get COVID-related like myocardial injury, right? They can get COVID-related intestinal injury. They can get all these things because again, the virus can potentially be tropic to these organs in the body, right? And the thing is, again, when the virus infects, right, there is a massive inflammatory response. In fact, many times, if you're measuring these people's labs, you'll notice that their CRP, their LDH, their ferritin, their ddimers elevated, right? These are all inflammatory markers. They'll be elevated in these people, right? So the thing is, the massive inflammation, again, is going to cause like, cause like septic shock, right? Increase vasculoprimiability in the lungs, right? So fluid begins to sip into the person's pulmonary interstition, right? And that can cause like a non-cardiogenic pulmonary dimmer, right? In fact, it can also torch the person's kidneys and cause an acute kidney injury, right? So again, I think one thing that's very high you'll to understand here, right?

It is again, that increased vasculoprimiability from the massive inflammation, right? Again, it can put fluid in the lungs, right? So the pressing, that's kind of essentially the battlefield is behind these people getting ERDS, right? Remember, ERDS is an example of a non-cardiogenic pulmonary dimmer, right? It's an example of a non-cardiogenic pulmonary dimmer, right? So those people's pulmonary capillary wedge pressures, right? Which is essentially a surrogate for left-eatural pressures. It's going to be less than 18 on an endemic exam, right? So what, so obviously, right, if you kind of perform histology on these people, you're going to see like a lot of, you know, diffuser of uloid damage, right? Because again, of the massive inflammation and again, the virus is very immunogenic, right? It's super-super-minogenic, right? So it causes lots and lots and lots of problems, right? So let's talk about the vaccines, right? Because again, this is an area where you do need to understand there's a lot of cell biology, there's a lot of immunology of friends that the MBM can integrate with this, right? So let's kind of talk about the vaccines, right? So the thing is actually that lays us off today from non-mistaking, there's been roughly 12 vaccines made against COVID-19, right? So we kind of fall into our, see maybe like four major categories, right? So the first major category are these RNA vaccines, right?

The RNA vaccines, in fact, like the Pfizer Bio N Tech vaccine and also the Moderna vaccine, these are actually RNA vaccines, right? So it means you're okay, divine. Well, this is a new class of vaccine. What's the mechanism of action of these vaccines? Well, it's actually relatively interesting and relatively simple, if you just actually take the time to understand it, right? So the thing is, these are RNA vaccines, you're essentially giving an, I'm giving mRNA to an individual, right? So if you give mRNA to an individual, essentially, the thing that's going to happen is, when the mRNA gets into the cell, the body is going to use its own translation machinery. Inside the cell, right, to make this mRNA into like a foreign protein, right? And then that foreign protein will then be broken down by proteins, right? It can be broken down by proteins, if we're talking about the MHC one response, right? But it can also be presented on MEC2. So essentially, this protein, you know, it can be picked up by dendritic cells. So it injects the mRNA vaccine into an individual, right? It will be picked up by dendritic cells, those dendritic cells, again, you will translate the mRNA into protein. And then the dendritic cells, they'll be able to present that protein on MEC2. So you can develop a human reality in response to the vaccine.

But also, because you can make that foreign protein, right, in the cytosol, you essentially can break down that protein with MHC one, I mean, break down that protein proteins, right? And then when that protein is broken down by proteins, remember, there are these type proteins, right? Type proteins, there's type one and type two, they will get those broken down proteins into the endoplasmic reticulum, right? And then remember, you can ultimately go ahead and load that foreign protein on MHC one, right? And if you loaded on MHC one, obviously, you're going to be able to also degenerate cellular immunity, right? So it's actually very high, you'll know, for example, that the mRNA vaccines have the ability to develop cellular and human reality. And you will notice there are some subtle things I'll talk about here, but again, they're very high, you'll understand. This is especially important for both the reticulum step one, right? Because again, these mechanisms try to think that people don't understand or kind of give up on what you really don't need to, right? So the thing is, again, you're getting an adaptive immune response to this. You're getting cellular immunity to this, you're also getting human reality to this, right? I mean, the thing is, if you'll be like, okay, divine, how does this compare to other vaccines? Other vaccines have the antigen prepared in the lab and giving to you.

But essentially, when you're getting an RNA vaccine, you're essentially creating the antigen by yourself, right? It's almost like you're getting like the starter pack, right? To make the antigen yourself. And then because you make that antigen endogeneously, because you're making it within yourselves, that's why your body is able to generate humoral and cellular immunity, right? And cellular immunity, right? So unlike the lab prepared antigens, right? In this case, you're making the antigen inside yourself, right? You're making the antigen inside yourself. Believe it or not, your cells actually weigh more efficient at creating antigen than trying to make it in the lab. Again, this is one of the reasons why the vaccine was very quick to come out, right? Because again, it is way easier, it is way faster, making an RNA vaccine, than making an antigen like a protein-based vaccine, right? Because you have to like design the organisms that are going to get the vaccine, get the genetic material or whatever into your body. But now you're just learning, given the genetic material, although in many cases, you are delivering them with nanoparticles. Obviously, the nanoparticle information is proprietary information to those companies, right? You know, they're like lipid nanoparticles if I'm not mistaken, right? So, you know, you're going to stimulate cellular immunity, right? Because again, the antigen is produced inside the cell, right? It's not produced outside the cell, right?

And the thing is, you may, some of you may wonder, oh, divine, why did we have to store these vaccines at such ultra-cooled temperatures? Well, think about it. mRNA is very easily degraded, right? I mean, you've probably learned this from your studies that, you know, for mRNA many times, if we won't send it into the cytosol, right? We're going to put the 5 prime, the 5 prime, a methyl-guano-sane cap, right? And they're going to put the polyethyl, right? Like literally, you know, the polyethyl, we add that with poly A polymerase, right? So, we're putting all those things because the cytosol right is a rough neighborhood for mRNA, right? So, if you already think about that, you can already begin to see why, wow, we need to keep these things at cold temperatures because mRNA is not very stable, right? So, it's easily degradable, right? So, you have to store those cold temperatures, right? So, that when you inject it into the patient, you can get, you can have like an effective immune response, right? You can get an effective immune response. Now, the thing is, why is this mRNA vaccine good? The reason mRNA vaccines are good is because, think about it again, you don't have to design some organism, right? You are literally only giving genetic material. In fact, you're giving a subset of genetic material, right? You're giving a subset of genetic material, right? So, you're not giving an actual organism. So, there's actually a lower risk of creating infection, right?

To be honest with you, there's a lower risk of creating infection because remember, in many vaccines, you're giving like some, let's say for example, like a live-attenant-vacine, because you know, live-attenant-vacines have actually very good at creating humoral and cellular immunity. We think about it in a live-attenant-vacine, right? There is a non-zero risk, although it's extremely small, but there's a non-zero risk of that live-attenant-virus reverting to a pathogenic state and causing disease in the patient, right? But the thing is, if you're just giving the genetic material and notice the kind of genetic material that's been given, you're giving MRN, right? You're giving MRN. So, that thing is not, like you're not giving an actual organism, right? So, you're essentially almost eliminating the risk of the person getting infection, right? This is one very good advantage over live-attenant-vacines, right? Because again, essentially what I'm trying to teach here is that MRN vaccines generate humoral and cellular immunity, live-attenant-virus vaccines also generate humoral and cellular immunity, right? But the thing is, live-attenant-vacines, they come at the risk of the live-attenant-virus reverting, right? So, like the intranasal influenza virus is an example of a live-attenant-virus, right? So, you have the small risk, right? It's non-zero, it's extremely small, right? That's why these vaccines are still safe.

It's extremely small, but there's a non-zero risk of the live-attenant-virus reverting right to a pathogenic state. And when you reverse to a pathogenic state, you can cause infection, right? You can have like an outbreak in the lab that's also like actually like creating the vaccine or whatever, right? But these mRNA vaccines were good, right? Because again, you are not given an actual organism, right? So, that risk of reverting to a pathogenic state is essentially eliminating that risk, right? Essentially eliminating that risk. In fact, I would not be surprised in the future because many times, you know, when people have HIV, for example, and the acidity for counters plummeted to less than 200, right? Or people are pregnant, right? Or people are less than a year old, right? We don't give these people live-attenant-virus vaccines. With the advent of these mRNA vaccines, those restrictions may be lifted because again, you're essentially getting the same benefit from a vaccine, but you're getting that much less risk, right? So, mRNA vaccines, I, I, again, this is maybe me being a little prophetic here, but I strongly suspect that they're going to be the vaccines of the future all over the world, right? All over the world, all over the world. And some people may say, oh, divine. Are there other benefits of this? Candice, mRNA, anything going to our genome, right? Because again, that's one common misinformation that is out there.

Candice, thing, you know, integrating to the genome and cause lots and lots and lots of problems and alter DNA and stuff, really, it cannot, right? Because again, first things first, look at the look at what is happening, right? The vaccine that's being given, again, I'm still on the first kind of vaccine, right? The vaccine that's being given, it's an mRNA vaccine, it's an RNA vaccine, right? So because you are giving mRNA, right? Again, notice you're not giving DNA, you're not giving something that can integrate into the genome, right? You're not giving something that can integrate into the genome. And the thing is that mRNA right after it's translated, right? In the cytos or remember, mRNA translation for the most part does not happen in the nucleus. It happens in the cytosol, right? The moment it's done being translated is going to be degraded in the cytosol, right? So again, the risk of that in filtering into the presence DNA and integrating is really low. But again, I know some people that have very good viral knowledge, you will say, um, divine, come on, give me a break. Can't this mRNA encounter like, you know, can't it maybe somehow by some magic, get into the nucleus? Encounter reverse transcripties, be converted to DNA and then integrate into the genome. Yeah, that's a good thought. But let's think about this. The thing is, mRNA, right? You know, let's see, again, by some miracle, it makes it way into the nucleus. And encounters reverse transcripties.

Yes, reverse transcripties can convert that mRNA to DNA and then that DNA can integrate into the genome. But, but think about this. The mRNA vaccines that are being given, many of them are not given with primers of any sort, right? Because again, you need like almost like viral primer to make all those things happen, right? So the thing is for reverse transcripties to work, it almost needs to be activated by primer. So the thing is, even if that mRNA, we're to getting to the presence nucleus, there's literally no primer available for that mRNA to then binds to reverse transcripties to initiate that reverse transcription process, right? So again, essentially, the risk of this at least these mRNA vaccines, integrating to a presence genome is almost zero. It's essentially zero. But, you know, in science, you should probably never say, oh, 100% or 0%, right? But the risk is pretty close to zero, if not almost, if not essentially zero, right? So the thing is for the most part, again, it doesn't really integrate, it essentially does not integrate into the presence genome, right? So again, these vaccines, they're pretty decent. Again, they are made pretty quickly, right? I mean, like the Pfizer vaccine, the Pfizer bio-antique vaccine, I think it was made in like 22 days, although you know, they had to do all this optimization or whatever. The modern vaccine, I think it was even made in a shorter period of time, right?

So again, very high-yield, again, like if you notice, some of these things I'm explaining, right? They're just applications of basic science principles that, you know, most people should know, right? At least people that are studying for step one should know, I would hope, right? So the thing is, so that's the first class of vaccines, right? So again, these mRNA vaccines, there's 12 of them, right? I said they are 12 vaccines total, right? Now, there are four vaccines that actually like inactivated or killed virus vaccines, right? These are inactivated or killed virus vaccines. And remember, if a person has, is taking an inactivated or killed virus vaccine, these vaccines should technically only generate human immunity. They should not generate cellular immunity. In fact, I'm going to take a small sidebar here and maybe kind of me this point very, very clear and obvious, right? It's a concept that I don't know for whatever bizarre reason. People just get the fact in many of these resources that exist out there that, oh, you know, a live-attenant-vacine would generate lifelong immunity, it would generate cellular and human-aluminity. But oh, killed virus vaccine only generates human-aluminity, almost never generates cellular immunity. If it does, it does it in very small measure, right? So many times people just accept this fact, but the thing is, it actually makes sense if you really think about it. So what's the pathophysiology here, right? Think about it.

When you give a person a live-attenant-vacine, you're a given vaccine that is an organism that is not dead, right? You've attenuated the ability of the organism to cause disease, but you've not attenuated the ability of the organism to infect a cell, right? I'll say that again. When you give a person a live-attenant-vacine, you've attenuated the ability of the organism to cause disease, but you have not attenuated the ability of the organism to infect a cell, right? Because remember, there are two kinds of antigens, and again, maybe I'll probably do like a immunology review, so that I can really botress these points. There are two kinds of antigens. There are exogenous antigens, and there are endogenous antigens. Exogenous antigens are antigens that are outside of a cell, right? So you can bring them in by phagocytosis, and you know, you can present them on MEC2. Endogenous antigens are antigens that you make within your cells, right? Those antigens, right, they go through a different pathway so they can be presented on MEC2.1, right? And when something is presented on MEC2.1, then you have the ability to generate cell-mediated immunity, right? So again, the longer shot of this is that a live-attenant-vacine still has the ability to infect cells, right? So it can become an endogenous antigens. It can be presented on MEC2.1, and it can generate T cell immunity. That's what we usually call cell-mediated immunity, right? But on the other hand, a killed vaccine, right?

So see, for example, like the sole, polio vaccine, remember the sole, the care at the end of sole, can help you remember it's a killed vaccine, right? These killed vaccines, they lack the ability to infect cells, right? So the thing is because they lack the ability to infect cells, these antigens remain exogenous, right? They remain exogenous, right? The thing is exogenous can only be presented by antigen-presenting cells on MEC2, right? And in that image, you know, bind to the CD4 positive health-party cells, right? And then, you know, those CD4 health-party cells, they will produce cytokines and stuff for class switching, right? So this is why killed vaccines only generate human immunity. Again, it's a mute point, but this point is floorily high right? I can imagine some people listening to this podcast now like, wow, I've never really understood this stuff before, right? Again, the first time I learned this information a couple years ago, I was like, wow, why does this thing just not show up in any resource, right? So again, this is something that you actually need to understand, right? So believe it or not, there are killed virus vaccines. I almost feel like I'm doing an immunology review right now, but again, I'm going to title this the COVID-19 podcast, right? So they are like four in activated or killed virus vaccines that are currently available actually for COVID-19, right? So again, again, again, I said that the mRNA vaccines, there's two of them, right?

Those generate cellular and humanoid immunity, right? These are activated or killed virus vaccines, right? They only generate humanoid immunity, right? They should not induce cellular immunity. Again, if we're just going with the science here, right? And then there's also four vaccines that are viral vector vaccines, right? Essentially, you're essentially using like a modified virus, right? So it may not even be a coronavirus, maybe like a different kind of virus, right? And you're essentially delivering the genetic material of the coronavirus, right? Like to or like, you know, basically you're delivering material from, I want to say, it's really genetic material, but you're delivering material from the coronavirus using the modified virus, right, to human cells, right? So that the immune system can respond, right? There's again, about four vaccines that kind of fall on that category. In fact, the Astra Zeneca, the Oxford vaccine is a viral vector vaccine. The Johnson and Johnson vaccine is also a viral vector vaccine, right? And actually, one thing that may help you is to actually remember that the Bola, because there is actually a vaccine against Ebola, the Bola vaccine is actually a modified virus vector vaccine, right? So in general, again, these these things, you don't have any integration into your own DNA, right? You don't have any integration into your own DNA with these vaccines. And then there are also proteins subunite vaccines. There's about two of those, right?

So 12 total, right? So the four classes of vaccines, there's four coronavirus, there's the mRNA vaccine, right? There's two of those. And then there's the killed virus vaccines, there's four of those. There is the viral vector of vaccines, there's four of those, right? So that's 10 total. And then there's the, there's the protein subunite vaccine, right? There's 12 of those, that's 12, right? There's 12 vaccines, a total, right? So how do we manage people that have COVID-19, right? For the most part, we manage these people with supportive care, right? We manage people with supportive care. We give them NSAI Ds, right? So help with their fevers and some of the inflammatory symptoms, right? Now, the thing is, if you see any evidence of hypoxia, right? The presence of two sets alone, the big, big thing you want to remember for in-beaming exams is to give these people steroids, give them the Xamethasone. The Xamethasone is actually one of those things that has been shown to improve survival in people that have COVID-19, right? It actually has a mortality benefit. I think there were some studies that were done, I think, in the UK that showed like a 30% reduction in mortality, right? In people that got the Xamethasone, right? In the setting of a severe COVID-19, right? Now, obviously, these people have hypoxic, right? You're also going to give them other stuff like and give them like 100% oxygen, right?

Usually, there's like an oxygen chain that is fully managing these patients, right? Even if they're hypoxic, you're going to start by giving them 100% oxygen, right? By nasal cannula. But then if that doesn't work, you then have to switch to one of two options, right? You can either do like high-flow nasal cannula, right? Again, maybe in the future, you know, God will now make podcasts on like oxygen delivery and how like different methods for delivering oxygen or like ICU machines and all that stuff. Maybe I should even do an ICU series, but again, that's in the future, right? So you can do like high-flow nasal cannula, but another thing you can also do instead of high-flow nasal cannula is non-invasive positive pressure of ventilation, right? So like, bypass essentially. Although in general, high-flow nasal cannula is preferred over a bypass, right? High-flow nasal cannula is preferred over a bypass. I mean, there's actually been studies. I think some of these studies we actually done pretty early when COVID-19 was a thing that showed that high-flow nasal cannula in general was, I believe it reduced the need for intubation compared to taking having bypass, right? And again, I'm not thinking you kind of need to remember about bypass is that it's an aerosol generating procedure, right? So it's kind of a high-risk procedure for healthcare workers, right? And then obviously, if this non-invasive positive pressure of ventilation or high-flow nasal cannula doesn't work, right?

You're going to go ahead and proceed to intubation, right? You're not going to proceed to intubation. And if intubation is not really helping a person, right? And you have like profound hymodynamic compromise, then sadly you have to proceed to ECMO, right? Extra- extra-copyrile membrane oxygenation. Again, I'm really, really hoping that I can have an ICU series in the future where I talk about some of these machines that we're using the ICU. It's actually a lot of fun, right? Like ventilators, ECMO machines, high-flow nasal cannulas, swung-gans catheters, right? Not just telling you, oh, this is what the machine does. Obviously, that that be a waste of your time. You can look that up on your own. We're kind of going into detail of like the pathophysiology, the physiology behind these machines, right? And what they record, right? And how they help. Like, I mean, ECM Os are very fascinating, right? There's like a ton of stuff with ECM Os, like how the oxygen eat, how they take over your heart and your lung function and all that fun stuff. But, you know, that's a future podcast. That that'll be too much for this, right? I mean, this is almost an hour already, right? Now, another thing you also want to think about that you hear is the drug remdesivir, right? Remdesivir. For the most part, remdesivir is used in people that, you know, are not going to require intubation, right? Not going to require intubation.

For the most part, yes, it's approved in certain countries, but in general, it's not super recommended, right? Because the thing is pretty much all it does is it kind of shortens your time to recover, right? But for the most part, it doesn't really, at least as far as I know from my research, it doesn't seem to have much of any mortality benefit, right? It doesn't seem to have much of any mortality benefit, right? So it shortens the time to recover, right? So it's kind of like the way when a person has the flu, if within 72 hours of the onset of symptoms, you give them like, what am I trying to think about here? You give them a tummy flu, wasn't it? Yeah, also time of year, right? Also time of year is a name of year, right? Those things, they don't necessarily cure the infection, but they reduce your number of symptomatic days. That's essentially what basically like think of remdesivir, like in exam terms, in US as almost like the seltami-vir or zanami-vir of COVID-19, right? It shortens your time to recover, but for the most part, as far as I know, at least again from the research I've done, it's not really recommended. In fact, there are certain organizations that do not recommend a remdesivir, right? Now, the thing is, again, these people when you're giving them oxygen therapy, again, you want to give them oxygen therapy and go no more than 96 percent, right? Because again, many people don't realize this, oxygen is a metabolic toxin, right?

Oxygen is a metabolic toxin, right? So just like hypoxia is bad, hyperoxia is also a problem, right? Because again, remember, when you have tons of oxygen around, it can cause a lot of free radical damage, right? I mean, this is one of the reasons why bleomising is such a toxic drop to the lungs, right? Bleomising literally sensitizes the lung to oxygen-mediated free radical damage, right? That's one, that's literally the primary mechanism behind bleomising causing pulmonary fibrosis, right? So hypoxia, I mean, like again, if you even think about kids that have new net or respiratory distress syndrome, right? And you see them developing like right, empathy of prematurity, interventricular hemorrhage, bronchopulmonary dysplasia, many of those things are free radical-mediated issues, right? So hypoxia is a problem. In fact, you would see that in certain circumstances, giving oxygen is not the fix for someone's hypoxia. Again, this is something I'll probably go ahead and talk about in my, you know, in a, I think I'm pretty resolute on maybe starting going ahead and doing some kind of ICU series, but again, I think I want to establish this fact. That's why again, it's really sad that many people are going into, again, it's one of these sad things that happens with this memorization, heavy generation, and currently living. You see many people, many healthcare practitioners, or you know, some people that are, you know, practicing healthcare that are not physicians, right?

They just know certain things, but you don't necessarily understand, right? So that's where you need to be careful. I'm not saying that, you know, we should disenfranchise some part of healthcare. No, no, no. What I'm saying is, as you're learning, put mechanisms in place to actually make sure people actually understand, you know, what's going on. Again, oxygen is not always the fix for hypoxia. Again, I know it's something, maybe like, no, the fine, this doesn't make any sense. If a person has low oxygen, give oxygen, right? But that's algorithm-based thinking. Algorithm-based thinking is not always smart, right? That's why usually some of the best ICU physicians, people that have actually spent time, you see that they actually think about the patient, they think about the signs, they think about the pathophysiology, right? So those people are usually a lot more targeted in the approach to care. They're usually a lot more structured, a lot more prudent in the approach to care, because they just have the cilient understanding, right? They have that cilient understanding. So I think it's kind of an important thing to actually keep at the back of your mind as a physician, right? Or as, again, a healthcare practitioner, right? Even if you're a school that you're going to as a healthcare practitioner, it's not teaching your pathophysiology. Take it as your own responsibility that you know what I want to take good care of my patients, right?

So let me actually understand pathophys. So I don't kill patients for any reason, right? Again, I'll see this, but again, I'll think of an example in this thought more when we go into the ICU series, but in general, there are certain situations, right? There are certain situations where oxygen is not the best immediate treatment for a patient type of oxygen, right? Oxygen is not always the solution to hypoxia again. The meat is in the pathophysiology, right? But again, that's a conversation for a different day, right? And then obviously these people go into shock, right? So again, sorry, I went off on that run, but I think it's kind of a message that needs to be heard, right? But again, I think I also need to be prudent in the way, express some of these messages, right? Again, because again, we're leaving an atmosphere where everything is offensive, right? So, you know, kind of have to be careful with your speech. In this day and age, right? So if these people going to shock, right? Again, obviously we have, they will likely have some kind of septic shock. Remember when a person has septic shock, right? So, you know, it's a it's a it's a distributive shock, right? So these people, they have a decrease in systemic vascular resistance, right? So because the systemic vascular resistance goes down, right? So the cardiac output is going to go up, right? The cardiac output is going to go up because it's just easier for the left ventral go to ejected blood.

That's one factoid, right? And then remember that in people that have septic shock, right? They're a PCWP. So they're pomeric capillary wedge pressures, which is a surrogate for left atro pressure. And they're central venous pressure, which is a surrogate for right atro pressure. Remember, all the veins draining to the right atro, right? So it makes sense that the central venous pressure, the central hop for all your veins pressure, right? It should be a good surrogate for right atro pressure, right? And then it's also high to understand, right? That when people have septic shock, right? Their MVO2 is actually high, right? Their MVO2 is actually high. Again, I don't want this podcast to get unwieldy here, but remember, people that have septic shock because they have that decrease in systemic vascular resistance, blood flows very quickly, right? Flows very, very, very quickly through their tissues, right? And again, as the blood flows very quickly through, you know, they're zips through their tissues, there is inadequate oxygen extraction, right? Happening, right? So because there is inadequate extraction of oxygen, the oxygen tension of the blood that gets to the red e-trim actually ends up being higher than you would imagine, right? So MVO2 is usually high in, especially in early septic shock.

And by the way, for those of you that are taking in beam exams, the numbers, they always request because I know some cubans get a little excessive here and they talk about early septic shock and lead septic shock. On MVO2 exams, if you get a septic shock question, assume that they are testing the values in early septic shock. So the cardiac output is up, the systemic vascular resistance is down, the pulmonary capillary wedge pressure, which is the left-tick-trial pressure is down, the CVP, the central veno-special, which is the right-tick-trial pressure is down, and the MVO2, which is the mixed veno-soto-saturation, is up. Those are the numbers. And again, I've kind of explained the pathophys there. Those are the numbers that go along with septic shock, right? So when people have septic shock, obviously, they're going to give them antibiotic therapy if you can find an infection or a door. Remember, for coronavirus, there's no relant antibiotic that can really help you here, right? So we're going to be going more into pressures, right? So usually, one, I use nori-pinephrine. Nori-pinephrine is the first line pressure in the treatment of septic shock, right? That's what's called livo-fed in hospitals. It's the first line pressure in septic shock. Well, let's say for some reason, nori-pinephrine is not doing did-list support for your patient. What can you do?

Well, your second line pressure in the management of septic shock and these are three very high-youtu-no-for-nb-ming exams is visual pressing, right? Visual pressing is the second line pressure that's used in the management of septic shock, right? And then your third line pressure is the epinephrine, right? So remember, NVE, it's that one, nori-pinephrine. If that doesn't work, proceed to visual pressing. If that doesn't work, proceed to epinephrine, right? So the thing is, back in the day, there were guidelines that said to use dopamine, but don't use dopamine. Again, you may see some old NVE-me questions where, oh, giving dopamine in the setting of septic shock is the right thing to do, but not these days, right? Dopamine is no longer indicated, right? I mean, this has been for years. Dopamine is no longer indicated for the management. Basically, don't use it as a pressure in septic shock, right? And when people have septic shock, go ahead and give them fluids, so if you're giving them fluids, don't try to use colloid solutions, don't try to use albumin. No, don't do any of that stuff. If you're pressing a septic shock, you can use either normal ceiling or you can use lactated ranger solution, although one problem with normal ceiling is that it can potentially cause like a hyperchlorimic metabolic acidosis. Again, the mechanisms behind these things, that's for the ICU series, right? Again, hopefully, you know, God makes it possible for me to make those podcasts, right?

But so if a person is developing like hyperchlorimic metabolic acidosis, one, you may want to go ahead and use lactated rangers, but for the most part, if a person is going through septic shock, normal ceiling usually on NVE-me examis is the right thing to do, right? But lactated rangers, if you don't see normal ceiling as an answer, if they tell you that, oh, the patient has a hyperchlorimic metabolic acidosis, then you can go ahead and those patients and use lactated rangers, right? If a person has hyperchlorimic metabolic acidosis, lactated rangers is great in these people, right? And again, remember, when a person has septic shock, usually your goal for the miniaturial pressure is between, so between 60 and 65, right? The miniaturial pressure, you want to keep it somewhere between 60 and 65, remember? 60 and 65 for your miniaturial pressures, right? And again, obviously, these people, if they're having like very severe respiratory failure, you need to put them on a ventilator, right? So, on a ventilator again, since these people were most about half ARDS, but the most part, you're going to put them on low tidal volumes, right? Because again, you don't want them to suffer by a trauma, right? You want to cut down on this thing called ventilator induced or lung injury, right? So, you put them on low tidal volumes, right? Usually you do like a tidal volume of like six million, six million letters per kilogram of predictive, predictive body weight, right?

So, if for example, a person's predicted body weight is 70 kilograms, right? They should be on roughly a tidal volume of about 420 million letters, right? 70 times, times six, right? And you also want to put these people on high peak, right? You put them on high peak, again, you're essentially going to be recruiting more of your life to participating in gas exchange, right? And usually also, these people that have like really bad respiratory failure, one thing I'm going to also do for them is actually being sure I believe to improve survival is to put them in a prone position, right? So, basically like these people on their chest and on their belly, right? The thing is it essentially reduces the shunt fraction in the lungs. Again, these terms you're hearing me spit out, right? I'm going to talk about them in the context of, in the context of like the ICU series, right? Because again, if you remember, a shunt is where you have regions of lung that are ventilated, but they are not being perfused, right? In general, when you put the person in a prone position, again, usually won't do for about 12 to 16 hours, we put a person in a prone position. That's actually going to increase profusion. I don't know, like maybe to give some people like a hint of why this is important.

Some of you may potentially remember that, oh, wow, like, you know, there's like zone one, zone two, zone three of the lung, and those differences in pressures of the pulmonary capillary versus the avial gland stuff. Basically, when the person gets in a prone position, you're optimizing those pressures to increase profusion of many parts of the lung. So you're kind of calling down on that shunt fraction, but again, we will say some more things about that. Again, remember, shunt is you're being profused, what you're, you know, you essentially have regions of lung that have been oxygenated, but they're not being perfused. Sorry, if I mix that up there. So let me say that again, shunt is when you have regions of lung that have been oxygenated, but they are not being perfused, right? They have been oxygenated, but they are not being perfused. They have been oxygenated, they are not being profused. Right. I don't know, I feel like I'm seeing the wrong thing for shunt. I hope my mom makes him the sub. Yeah, because, okay, let me try to reason the sub, right? So right to left shunt, right? So the blood is basically skipping the lungs. It's not getting oxygenation. Oh, okay. My apologies there. My apologies there. So actually a shunt is when you have the lungs, they have been perfused, but they are not being oxygenated, right? They have been perfused, but they are not being oxygenated. They have been perfused, but they are not being oxygenated. Sorry about that.

My apologies there, right? So those regions of lung again, they have been perfused, but they are not being oxygenated. Right? So, um, basically, by being in a prone position, you reduce that shunt fraction, right? Basically take away that shunt physiology. So that's part of the reason it improves survival, right? And then, so again, low tidal volumes, high peak prone position in low plateau pressures, right? So plateau pressures are basically pressures you get where if a present takes a full inspiration, like literally at the end of inspiration, you pause and then you take the pressures in the airway, right? That's essentially what the plateau pressures are. You want to keep those plateau pressures low again so that you can reduce the risk of barotrum. Right? So it's going to be less than 30. You want to keep that below 30, right? Because believe it or not, for some bizarre reason on step one, they do actually ask about plateau pressures every now and then. And then, just to quit tidbits of information, I want to say here, in kids, sometimes they can have this thing that is related to COVID-19, but it's called pediatric multi-system inflammatory syndrome. It's kind of similar to Kawasaki's disease, actually, right? And um, um, it can actually cause death in COVID-19, although in general, kids that get COVID-19, their mortality rate is way lower. And then the final thing I will say is that the case fatality rate for COVID-19, um, globally is roughly 2.2 percent, right?

So for every 100 people that get COVID-19, about 2.2 of them are going to die, right? Which is really sad, right? So hopefully with the initial of the vaccine, that can already cut down on some of this mortality. So, um, as I do at the end of every, I think I'm going to go ahead and stop here. I mean, this is more than an hour already. So this is not only worldly. As I do at the end of every podcast, please subscribe to the podcast website, divine intervention podcast.com. And I also have, um, uh, basically if I make a new podcast, you'll get an email notification, and all the podcasts from episode one, all the way to, I guess, 300 now, they're always going to be on the website because, uh, you know, I also have these podcasts on Apple podcasts, on Google podcasts on Spotify. The only problem with those is it's like a Word Press role. You can basically only see the first one, the most recent 150, right? So if you want all the podcasts, you'll, you know, have to go to the website and actually like download it there or listen to it from there. And then I have a You Tube channel, divine intervention, USMD podcasts and videos. Uh, that's where I post the videos that I make. So subscribe. And if I make any videos, which I do, uh, you'll be able to view them there. And then, um, uh, if you need tutoring, I offer one on one tutoring for the USMD exams. So step one, step two, CK, step three, uh, preclinical medical exams, third year clerkship shelf exams.

Uh, and if you're a medicine resident, I need tutoring for the medicine training exam or the medicine boards I do also offer one on one tutoring for those. And then for those of you that are taking step two, CK step three anytime soon, I do offer comprehensive course. I have an MBA me testing strategy scores that's 20, half hours is on the 27th of April, um, of this month. And then, um, if we go to the very end of, uh, if we go to the very end of the month from the 20th of April to the first of May, I have a 20 hour, right? So it's five hours for four days, super comprehensive step two, CK step three course covers again, peets, psych, neural, I am surgery, OB guy, and even the new changes that, uh, have shown forth on the, on the exam, bio stats ethics, I cover all those things, healthcare systems, all those things are amply covered, amply covered in the course. So if that's something you're interested in, just shoot me an email through the website and I'll give you more information on the cost and things of that nature. So thank you for listening to this podcast. I will, I will see you next time. God bless you and have a wonderful day and stay safe and practice social distancing. Thank you.

Respiratory droplets and aerosols.

Age >60, chronic comorbidities (e.g., hypertension, diabetes), or immunosuppression (e.g., transplant recipients).

RT-PCR (Reverse Transcription PCR) performed on nasopharyngeal swabs.

MAP goal 60–65 mm Hg; PCWP is low (<18); MVO2 is high.

The host cell translates the delivered mRNA into protein endogenously, stimulating both MHC Class I and II presentation pathways.

Inactivated (killed) virus vaccines.

Norepinephrine (Norepi).

The S1 subunit of the spike protein binds to ACE2 receptors, which are found on Type II pneumocytes and other organs.

mRNA vaccines stimulate endogenous antigen production (cytosol), leading to both humoral and cellular immunity; killed vaccines lack cell-infecting ability, limiting them primarily to humoral immunity.

Bilateral, symmetric ground glass opacities, usually predominantly subpleural.

Keep it below 30 cm H2 O to prevent barotrauma and VILI.

Norepinephrine $\rightarrow$ Vasopressin $\rightarrow$ Epinephrine.

Oxygen toxicity; it causes free radical damage to the lungs (e.g., contributing to ARDS/fibrosis).

S1 subunit (receptor binding domain) and S2 subunit (membrane fusion mediator).

The S1 subunit of the spike protein binds to ACE2 receptors, which are found on Type II pneumocytes and other organs.

mRNA vaccines stimulate endogenous antigen production (cytosol), leading to both humoral and cellular immunity; killed vaccines lack cell-infecting ability, limiting them primarily to humoral immunity.

Bilateral, symmetric ground glass opacities, usually predominantly subpleural.

Keep it below 30 cm H2 O to prevent barotrauma and VILI.

Norepinephrine $\rightarrow$ Vasopressin $\rightarrow$ Epinephrine.

Oxygen toxicity; it causes free radical damage to the lungs (e.g., contributing to ARDS/fibrosis).

S1 subunit (receptor binding domain) and S2 subunit (membrane fusion mediator).