COVID-19 | Coronavirus: Epidemiology, Pathophysiology, Diagnostics

[Music] iein engineers in this video we're going to talk about Cova denied teen are the novel coronavirus that were discovered in 2019 what you guys to know that this video that we're making today all the information that we're going to be talking about is as of up to date as March 15 2020 so I just want you guys to know that in addition this video is purely for educational purposes only we're gonna have a medical disclaimer pop-up here let's go ahead and get started alright guys so let's go ahead and get started on his Cove in nineteen lecture so again I want you guys to remember that we're making this video here on March 15 20 20 from this time until the future as those things change we will try to continue to guys to keep you guys updated with future videos to go into more detail on these things okay but again this is as of right now all right so what should we know about the coronavirus right well we know that the coronavirus are this 2019 coronavirus okay it's similar to specifically the SARS virus if you guys remember what that was there was an outbreak called this the severe acute respiratory distress syndrome and it was corona virus specifically in 2002 and what happened is that they believed that this virus this SARS virus actually had the ability to hop over from a bat okay from that bat it mutated in such a way that it can then infect another host another intermediate host right so it started off with a bat from the bat it then maybe transferred over what do we believe to be a civet and then from that civet a mutated enough to be able to infect a human because corona virus is naturally they're pretty benign and they don't cause a lot of significant effects within a human maybe just your you know your viral rhinitis Viral pharyngitis viral laryngitis but rarely are they going to be causing the severe acute respiratory distress syndrome types of things but again if they mutate enough where they go through some type of animal reservoir they can become mutated enough to be able to cause severe infection in humans and that's what the SARS virus did in 2002 a top a couple years later actually a decade later to 2012 it happened again where the corona virus had the ability to mutate again where we have a bat where we believe to be again the animal reservoir where the virus mutated then transmitted to what we believe to be a camel so from bat to camel as this next intermediate host and then from there it mutated enough where it could then infect a human okay this is the MERS virus and again this is the middle Eastern respiratory distress syndrome that occurred in 2012 hop now to 2019 where we now talk about the corona virus particularly kovat 19 which was the corona virus discovered in 2019 again we believe that this this actual virus underwent a mutation via this zoonosis right so we have a bat it mutated within the bat then it actually had the ability to mutate within another animal as the intermediate host potentially again we're still not completely sure but we believe it could be what's called a Pangolin so we they think that this virus hopped onto a bat as its reservoir mutated enough got transferred to a Pangolin mutated enough that it can now infect a human and cause kovat 19 okay which is the novel coronavirus discovered in 2019 this is what we know about this virus now another thing that we have to understand about this virus is not just these uu enosis effect of it but we also should know some of the case fatality rates because this is becoming a big concern in society right now everybody is very very scared of the corona virus and again we don't want to overreact but we want to make sure that we don't under actor this virus because it is a very serious virus to give you guys a little bit of an example of the case fatality rates if we take the SARS virus in 2002 case fatality rate is just again the total number of cases on the bottom so if you guys want to remember the formula very simple formula the number of deaths divided by the total number of cases okay and then multiply it by a hundred so they see that this virus the SARS virus in 2002 had 8,000 totalled cases with 800 deaths that gives us a case fatality rate of 10% that's pretty decent move on to the next one the MERS virus in 2012 850 died where there was 2500 total cases that's gonna give us a case fatality rate of 34 percent hop on down here to the köppen 19 as of March 15 22 we have 150 3517 cases okay this is worldwide with 5735 deaths that gives us 3.7 percent now a lot of resources the World Health Organization CDC's different things like that say that this number technically could even be lower why you have to remember that there's a lot of people who are asymptomatic with this virus okay in other words they're not presenting with the classic symptoms that we would see with the corona virus so if they're asymptomatic they technically would be one of the cases but they might not present they might not go to the hospital get tested and come up positive for the corona virus so technically if we think about it there might be thousands upon thousands more of cases where people are just asymptomatic thought that they have the common cold or maybe the flu but really they have the corona virus and think about it as this denominator increases the more cases we have that case fatality rate could technically decrease and that's what you want to think about right now yes it is scary the number of cases that we have and the deaths but again this this denominator it could technically be a little bit larger okay all right so that's what I want you guys to understand right now about the basic points of the corona virus when it comes to the zoo and notic effects in other words how this corona virus mutated enough that it could infect humans and cause severe acute respiratory distress syndrome okay if you understand this very of the stars it's pretty much the same kind of thing the bat was pretty much the primary animal reservoir that then passed it on to an intermediate host right which we believe at this point time to be a Pangolin now how does this important pangolins according to a lot of the research showed that this actually it's scales have healing properties so therefore it's highly trafficked all around the world so that's what also makes this very dangerous and therefore increasing the risk of a pandemic okay so again we need to be careful when it comes to these and just realize that this intermediate e host could potentially be one of the things that's actually allowing for this mutation of the virus and making it allow for it to affect humans in such a way all right let's move on to the next epidemiological fad when we talk about the coronavirus when we talk about the coronavirus we have to talk about what's called the are not the are not stands for the reproductive ratio okay special way of saying this is the degree of spread ability that's really all it is how much can one person how many people can one person in fact that's a simple way of saying it so if i take for example let's say here is this one person here okay patient number one he has the coronavirus covin 19 he's been infected he goes around other people he's in the same room with a bunch of people okay if he happens to sneeze or cough and he spreads those respiratory droplets that could be airborne and they somehow get into the mucous membranes of people nearby how many could he potentially infect they say that he can infect three people so therefore the are not of kovin 19 is actually been said to be anywhere from two to three could even be higher we'll talk about that in just a little bit what i mean by that so again what's the are not for Koba 19 we believe it to be anywhere from two to three let's take the worst-case scenario and say it's three okay one person can infect three people right so you start off with one person that infects three people these three feet people each one infects Authority more people that gives us nine patients now infected with Kovan 19 now these nine people can go and infect three people each how many is that 27 so you can see how this is an exponential rise if we look at this on a graph when we look at our knot of Kovan 19 let's do it here in blue if you look here aren't on the y-axis what are you gonna see you're gonna see this number it's going to increase right it's gonna be exponential this is an exponential growth if we compare the are not of influenza which is around 1.3 approximately let's just round it to one and say that one person has the ability to infect one other person so if this person is infected with influenza he's gonna pass it on to home or person that one person is gonna pack pass it on to the next person which is gonna pass it on to the next person right so you can tell right now just by comparing influence and kovin 19 that this is much larger spreadability whereas this has a much lower spread ability okay so if we were to compare that is this exponential is this decreasing or is it pretty much just kind of the same is it a flat line it's a flat line right so we should see the are not here being straight well we prefer for this to look like less than one preferably we don't want this to have such a high spread so if we had a perfect case scenario we would love for this to start decreasing how do we do that how do we make the are not drop you're gonna be quarantine staying away out of large crowds trying to decrease that spread ability by spreading respiratory droplets making sure that you're washing your hands making sure that you're not touching your t-zone and by doing that and self quarantine yourself and staying out of large crowds we can potentially decrease that spread ability that's what we want with this virus so currently right now you can see how our are not is greater than one that's allowing for this exponential growth that's why there's so many cases in comparison to something like flu which is one and what we would like what we prefer is an are not less than one okay last thing I got to talk about here because are not not only determines the rate of transmission or the degree of spread ability but there's also another factor and this is called the series interval so si is referred to as the series interval a special like very simple way of describing this and the son say here's patient one okay patient one develops symptoms okay and let's say from the day 0 that he developed symptoms all the way until day 14 okay let's say that he has settled for 14 days so this is when the symptoms stop this is when the symptoms start let's say that somewhere during his period of infection he spreads that virus to another person so let's call this X 2 right here's X 1 patient one patient to this person gets infected let's say somewhere about right here maybe is day 2 okay maybe day to somehow around that time this actual pay patient X patient one comes into contact with patient 2 and from that point their their symptoms start so now we're at day 0 and let's say that they go through a 14 day period of this actual infection this point here to this point here from the symptoms of onset of patient 1 to the symptoms of onset of patient 2 that is our series interval now the shorter that is the more dangerous the virus's the larger it is a lot better less risk of this becoming such a high speed of transmission so what is the series interval for kovat 19 it actually depends it depends on which source you're looking at some say that it's anywhere from 5 and some will say anywhere from 7.5 if you take influenza for example it's actually approximately 2.5 around that so what does that mean that means that the time of symptom onset from patient 1 okay from when that person actually is infected - the symptoms of patient - start to develop that's a period of 7.5 days whereas the period of infection so right patient 1 who is infected with influenza from his symptom onset until the symptom onset of patient 2 is approximately 2.5 days why would that be dangerous if you have a high or not in a really low series interval within a small amount of time so imagine here within one person infecting 3 it took seven point five days from three to nine at seven point five days from nine to 27 at seven point five days that spreads it out over a longer period of time thankfully however if you were to imagine 2.5 days the symptom onset from patient 1 to patient 2 this would be extremely high okay there would be a severely high spread of transmission at a very fast rate so we got to be at least thankful that for right now the SI is relatively high and are not also hi this is the unfortunate aspect but be thankful at least that we have a high series interval with the are not here this one's relatively low but it does have a relatively low series interval so it can spread pretty quickly okay but this one you have more spread ability and a higher number of infective cases alright so they think that there's two ways right fecal-oral route potentially and that respiratory droplets so fecal or odd asleep one blade that we believe that this could actually be spread okay and what happens with this is that if someone goes to the bathroom they shed the virus they you know wipe their their bottom they don't completely wash their hands and they go and touch other surfaces within the bathroom someone else comes in they touch those surfaces and potentially you know inoculate themselves with the virus that's one way that we think it could potentially happen okay other things that we also have to remember is that if certain like there has been certain things that if someone lives in an apartment building where there's a faulty plumbing system where certain plumbing right so maybe fecal material from someone who's actually an infected individual has the ability to spread through a faulty pipe or faulty drainage system into another apartment room and allow for those virus to also infect certain areas and surfaces within another bathroom that's one other way so again fecal-oral rod is one way of transmission of the virus and the other one is by coughing sneezing right so it could be this airborne way or these via respiratory droplets now one of the things that they say about these respiratory droplets is that they have the potential to spread and actually an effective person may be within three to potentially six feet okay another thing is they think that these respiratory droplets could stay on surfaces and actually still survive for approximately 24 hours and if someone goes and touches that surface and then touches one of their mucous membranes they have the ability to inoculate themselves again newer research is also newer things are also saying that it could potentially be airborne for potentially three hours so if someone actually coughs or sneezes and then someone walks through that area potentially within a three hour period they also could a knock you himself with the virus okay so again fecal-oral route and respiratory droplets are the way that we believe that this is potentially spreading okay now another really interesting thing is that this can also be an asymptomatic carriers so sometimes if someone is actually not showing symptoms they do potentially have the ability to spread this actual virus as well so that's what also is very nerve-wracking with this okay now what happens the virus gets into the respiratory system right once it gets into the respiratory system it loves to attack the alveoli all right so what we're gonna do is we're gonna zoom in on this portion of the lungs and look at the alveoli all right so once the virus comes down into this area what does it do well the first thing that's going to do is it's actually going to come over here and attach to these type 2 pneumo sites you know within the actual alveolus you have two different types of cells type one NUMA sites which are gonna be for gas exchange and type two numerous sites which are going to be their structures that produce surfactant and that's important to remember because what a surfactant do it decreases the surface tension within this alveoli and reduces that collapsing pressure that's gonna come into play in the second so what we're gonna do is we're gonna look at how this virus infects this cell and uses the cellular machinery to make more of our particles and then cause havoc on the respiratory system so if we take a look here we got our virus right now this virus has different types of spike proteins on it right one of the specific spike proteins that we've seen that is actually a little bit significant here is this pink one and we call this the S spike okay we call this the a spike why is that important well these s spikes on this Cove in nineteen virus are right the novel coronavirus discovered in 2018 it binds on to specific receptors on the type to nuuma sites what is this actual receptor this receptor is called angiotensin converting enzyme type two it binds to this and when it binds to this it allows for the virus to actually be engulfed and taken into the cell once it's brought into the cell it then releases its RNA right because in here we have positive-sense single-stranded RNA virus it releases the single-stranded RNA into the actual cytoplasm of this type to nuuma site once it's released guess what it does it can do a couple things one thing is it can actually use the host cells ribosomes and if it uses the host cells ribosomes it can then the what take mrna and converted it into proteins what is that called it's called translation so then what can happen is we can undergo what's called translation and we're going to convert this single-stranded RNA let's write this down what do we have here single-stranded RNA we're going to convert this translated into specific protein molecules so we're just going to draw a bunch of different proteins here different poly proteins here's a poly protein here's a poly protein heck let's draw another poly protein and it's gonna be making a bunch of different stuff right now from here after it synthesizes these proteins guess what else you can do it's actually really really interesting you see that SS RNA the positive sense right positive-sense single-stranded RNA right it has the potential to use another enzyme called an RNA dependent RNA polymerase so what is this enzyme here called it's called RNA dependent RNA polymerase what does that mean it takes RNA and synthesizes RNA so what are we gonna do here aha this is cool guys look it takes this single-stranded RNA and converts it into more RNA so now from this I have a single-stranded RNA I'm gonna make more copies of this single-stranded RNA I'm Chi positive sense now here's my poly proteins I need to make these poly proteins get converted into all the components of my virus that make up my nucleo capsid specific enzymes my spike proteins so I need specific enzymes that are going to Protea lies these poly proteins into the different individual points that I need for making this whole viral structure so we have other enzymes here okay we have enzymes let's pick a blue color this enzyme are going to be proteinases and there's specific type of proteinases that are going to proteolytically cleaved these poly proteins into the different viral components that are making up the nucleocapsid enzymes and Spike proteins now look what I did use the cell's RNA dependent RNA polymerase and use the cell's ribosome to make proteins that are gonna be making up the components of the viral protein structure right then I synthesized a ton of RNA what happens if I combine these two I combined all of these actual nucleocapsid spike proteins enzymes with the single-stranded RNA incorporate that into it and then I bud off of this type to nuuma site I just made tons of virus particles and in the process I'm destroying this type to Numa site if I cause damage to this type to Numa site what's that going to do there's a couple things that are gonna happen one of the things here is that this type 2 Numa site is going to start actually becoming damaged so it's going to release specific inflammatory mediators guess what those inflammatory mediators are gonna do they're gonna tell the macrophage the macrophage once he stimulated he starts to see create specific cytokines that cause a ton of problems from here one is called interleukin 1 another big one is called interleukin 6 and the other one is called 2 manic rhotic factor alpha what these guys do is they actually come over here into the bloodstream and they cause these endothelial cells to undergo dilation so it's gonna cause the actual smooth muscle actually cause the smooth muscle to dilate but increases the capillary permeability by causing endothelial cell contraction and then by doing that you increase the permeability so now look I'm gonna release all these different info taury mediators right what's gonna happen as a response to that I'm gonna lead to vasodilation and I'm gonna lead to increase capillary permeability if I do that what's gonna happen now all this fluid all my plasma is gonna start flowing out and leaking into the interstitial spaces and potentially into the alveoli as all this fluid starts to accumulate outside the alveoli it's gonna lead to trying to compress the alveoli on top of that some of the fluid is actually going to try to enter into the alveoli and what happens if you start to cause a ton of water to accumulate inside the alveoli what does that do to the surfactant production or actually the surfactant concentration so if I cause increase alveolar edema that is going to technically drown out it's gonna drown out the surfactant what is surfactant do for the alveolus it decreases surface tension so if I drown out that surfactant what's gonna happen to the surface tension it's gonna start going up as the surface tension goes up what's that going to lead to remember lapis is law that says pressure is equal to two times the tension divided by the radius as we increase the surface tension we increase the collapsing pressure what's gonna happen this alveoli is gonna start to collapse and now I'm gonna lead to alveolar collapse and look at that there that's a problem because now as I have tons of fluid accumulating around this alveolus impairing the alveolar membrane the respiratory membrane for allowing for gas exchange that's a problem so this is gonna lead to decrease gas exchange that decrease gas exchange is gonna lead to hypoxemia and that hypoxemia is a very dangerous thing especially when it becomes refractory so that's one thing we have to watch out for so again releases a lot of inflammatory mediators that cause vasodilation increased capillary permeability leading to a lot of interstitial edema alveolar edema leading to drowning out there surfactant increasing the surface tension and leading to alveolar collapse that alveolar collapse is gonna increase the work of breathing that's another thing it's gonna increase the work of breathing okay so it's gonna cause hypoxemia and increase the work of breathing why is it gonna increase the work of breathing because now I got to work extra hard to try to inhale as much air as I can to not only reopen the alveolus but open up against all this interstitial edema that's significantly difficult and that's what can leave them going down the hill and leading it to what's called a RDS okay that's one thing the next thing all of these inflammatory mediators also bring in tons of neutrophils so now I'm going to attract in neutrophils so these inflammatory mediators are going to start pulling in neutrophils these neutrophils are gonna start coming to the area and with all this inflammation they're gonna want to start trying to destroy the virus when they start trying to destroy the virus how will they do that they release reactive oxygen species they release protease is whenever I release these reactive oxygen species and proteases yeah maybe I might destroy some of the virus but guess what else I'm gonna end up doing I'm gonna end up damaging all of these cells and as I start damaging all of these different type 1 type 2 alveolar cells what am i doing as a result of that what does the type 1 alveolar cells do guys they play a role in gas exchange if I destroy them am I gonna have proper gas exchange no if I destroy the type alveolar cells what's that going to do it's going to decrease my surfactant production what's that going to do increased surface tension and caused collapsing of the alveoli on top of that though as all of these cells start to get destroyed they start getting sloughing off into this the actual center of this alveolus so now in the center of the alveolus what am I gonna have I'm gonna have all this collection here a fluid and also maybe some protein deposition and cellular debris type one new monocyte cellular debris type two Numa site cellular debris I'm gonna have some macrophages here I'm gonna have some neutrophils into this area and now I just led to a consolidation okay this consolidation is going to be a problem okay because this consolidation is also going to alter gas exchange and if I alter the gas exchange process I lead to hypoxemia okay another thing is again go back this whole thing can also whenever there's the reactive oxygen species it damages the type 1 type 2 alveolar cells right and as you do that that leads to this significant alveolar collapse as well we talked about that right all right now the next thing that you have to also understand is that you're releasing tons of interleukin 1 interleukin 6 within the lung print come on write this interleukin 1 and interleukin 6 guess where it can travel if it's released in large amounts it can travel via the blood to the central nervous system and you know in the central nervous system there's the hypothalamus and the hypothalamus controls your temperature so an interleukin 1 and interleukin 6 aren't high concentrations they tell and to a necrotic factor alpha they tell the hypothalamus to release specific prostaglandins like pge2 and that helps to reset this thurman thermostat right and increase your body temperature and that increase in body temperature is gonna lead to fever right and that's important because this is the one of the most common symptoms in these patients so they present with fever guess what else if someone has consolidations and all this kind of like accumulation of stuff with inside of the actual alveolus eventually as this starts to degrade guess what's gonna happen you're gonna COFF it up and as you coffin up you're gonna cough up this productive mucus and this might be a productive coughs so they might present with a productive cough they may present with a fever and they may present with increased work of breathing which may present as Disney are shortness of breath and maybe they might even have asthma hypoxemia also because of someone's hypoxemic what happens as a result of that what does that trigger if you guys remember really quickly if someone has low partial pressure of oxygen that stimulates what's called the chemoreceptors right so it stimulates your chemo receptors okay whenever the po2 is really low it can stimulate the actual peripheral chemoreceptors and those chemo receptors can do what they can actually trigger a reflex where it actually causes the sympathetic nervous system to become stimulated and try to increase the patient's heart rate so what else might be a thing that you see on this patient they might also have a increase heart rate okay so they might be tachycardic they might have an increased work of breathing what else does a sympathetic nervous system do - if you're low in po2 what do you have to do to try to get more Pio - in increase your respirations so they might have an increased respiration rate they might have a increased heart rate they may have a fever they may have a cough they may have increased work of breathing which can present as Disney or shortness of breath and maybe even hypoxemia right let's go even a step further than that let's say that this starts to become so severe this inflammation of the lung becomes so severe and it starts actually kind of leeching into the bloodstream and spreading and this systemic inflammatory response starts carrying all over to different parts of the body so now this inflammation with the lungs leads to systemic inflammatory response syndrome right or it starts off as ARDS right so you affect the lungs leading to ARDS maybe that progresses to systemic inflammatory response syndrome which can lead to potentially septic shock how if these actual inflammation spreads throughout the entire circulatory system what's that going to do that's going to start causing increased capillary permeability within your systemic circulation as fluid starts leaking out and accumulating within the tissue spaces what's going to happen to the overall blood volume it's going to decrease right on top of that we're going to cause vasodilation of the actual vessels as you vasodilator lot of your systemic arterioles what's going to happen to the actual total peripheral resistance it's gonna drop as you drop your total peripheral resistance and you drop your blood volume what's that going to do to your blood pressure that's gonna tank it and the patient can start to become hypotensive and if they become hypotensive that decreases the perfusion to multiple different organs and this can lead to multi-system organ failure so this can start off with just pneumonia that can then progress to ARDS right we talked about what the alveolar collapse and having difficulty being able to take an air causing severe hypoxia that can become refractory then progressing from systemic inflammatory response syndrome to potentially septic shock the patient become hypotensive after as they become hypotensive they aren't able to profuse their organs how may that present if they can't profuse their kidneys what's going to happen to that be you in a creatinine that sucker is gonna rise right so maybe the ability to get rid of the creatinine from the kidneys and the ability to get rid of the blood urea nitrogen that decrease the kiddies aren't getting enough blood flow so because of that they may have an elevated bu in and an elevated creatinine to show that there is actually kidney damage maybe the liver is also jacked up it's not getting enough blood flow and because of that it starts releasing specific inflammatory enzymes like ast maybe that starts to rise maybe the alt your liver enzyme starts to rise maybe the Billy starts to increase or maybe it starts releasing acute phase reactants what are some of these CRP fibrinogen right interleukin 6 these might all be elevated you might have an elevated fibrinogen and elevated interleukin 6 and elevated CRP elevated liver enzymes and actually this is some of the things that they check for in a patient who maybe comes in with this actual kovat 19 infection we'll talk about that in a little so now that we talked about all the different effects that can come from this virus which is a pretty nasty virus again from the point of the infection okay until the patient develops symptoms that's called the incubation period right what is the incubation period for this virus it ranges right now the incubation period which is the period from when it becomes infecting in a patient to the patient develop symptoms it's believed to be anywhere from four to 14 days so that is our incubation period however some have actually seen it up to 24 days okay but just keep in mind that we potentially say max of 14 days these are the things that we have to take into consideration when we're talking about the novel coronavirus okay let's go ahead and now move on to the Diagnostics all right so we talked about so far epidemiology we talked about pathogenesis we talked about the signs and symptoms that the patients will present with right and out of those what were the big ones that you guys want to remember again the patient comes in they present with fever they present with a cough they present with shortness of breath and sometimes you have to remember these are the big ones with the most important one being fever and then after that cough and shortness of breath but sometimes the patient may present with Uri symptoms or they may present with GI symptoms so maybe they might present with rhinorrhea congestion sore throat maybe a little bit of a headache GI symptoms may present with nausea vomiting diarrhea again it's primarily fever cough shortness of breath but you can't forget that some patients might present with early GI symptoms or URI symptoms okay but either way they come in with these symptoms okay maybe they're also had tachycardic maybe they're too kipnuk maybe they're SS po2 is a little bit lower again maybe it's less than 93 percent or something like that and you started getting concerned okay what's the first step that you should do first thing that you gotta remember sometimes this sounds just like the flu and it could potentially be the flu so the first thing you're gonna want to do is swab the patient and also you're gonna want to ask them questions have you been into contact with anybody who's been infected with the corona virus have you traveled outside of the United States where there's also large amounts of infections again those are questions you're gonna want to try to ask to persuade the patient figure out their actual clinical history now from there run a flu test do a nasopharyngeal swab and test for influenza or influenza B all right influenza A influenza B so first thing you got to do is you got to rule out influenza so rule out influenza A and B and how do you do that you do this nasopharyngeal swab you stick this actual swab up into the nasal cavity and you test for any of that actual mucus seeing if there is in any of the influenza particles so you can do a nasopharyngeal or oral pharyngeal swap there is another thing that you can also do okay let's say that that comes back negative it's not the flu doesn't mean that it's still not the flu but again your suspicion is high for the corona virus because they have a super high fever what's a fever that's also important if a patient comes into the high fever and their temperature is 98.6 that's not a fever okay we technically consider a fever to be greater than or equal to 100 point 4 degrees Fahrenheit right that's what we consider a fever if they're coughing if they're severely short of breath okay they're otwo sap maybe is a little low okay they're tachycardic to kipnuk again you have a high suspicion next thing you can do is is you can do what's called an RT PCR now realize these tests have a sensitivity from what we've seen here anywhere from 30 to 80 percent and they take a lot of time okay so you run this test right away sure but you might not get the results back in time okay when you need them and on top of that their sensitivity really isn't that great it technically is the gold standard of diagnosis and you can get rt-pcr from a nasopharyngeal swab or just remember you can also get this from sputum so from a sputum sample you can also get this from an aspirate okay and you can also get this from blood but again you can do a nasopharyngeal swab as well okay do an RT PCR which is real-time polymerase chain reaction that's the ways that you can do it called the nucleic acid amplification test okay this is very similar to the what's caught in again they abbreviated as NAT it is expensive from what I remember on my rotations they said it could be up to $300 for the tests okay patient comes in they have these symptoms and again don't forget maybe they also present with specific vital signs that is increased heart rate increased respiration low spo2 and then worst case scenario maybe they have low blood pressure okay that's scary though from there what's the next thing that you're gonna do you're gonna want to get some blood work see where the patients at so what are we gonna do we're gonna order a CBC and a CMP and we can also if we want to check specific markers that have been associated with high mortality rates with this disease so first thing we're going to do is we're going to check BC CBC is gonna tell us our white blood cell count a red cell count and our platelets right and then we can get a diff what we're gonna see here with this and this is what's super interesting you see what's called lymphopenia 80% or more of the time you see lymphopenia okay that is really odd because what would you expect if someone's having an infection you'd expect a high white count but again you're gonna see more commonly for some reason lymphopenia okay so that's something to take into consideration you're gonna have low lymphocyte count next thing you can do is you can order a CMP a CMP can tell you a lot of different things right so CMP it can is basically a BMP and lfts okay so let's check our l.f.t.s if we check the lfts guess what we see that in patients who are having this multi-system organ failure or they're an again severe case they can have if they're having decreased perfusion to the liver increase alt increased AST and increased Billy okay that's one thing we can get from the lfts or the cmp technically we can also get a BMP and BMP can tell us renal function it can tell us the electrolytes and they can also tell us our glucose level as well what would the BMP need tell us which is really important if we're not getting proper perfusion to the kidneys are we going to excrete as much of the actual bu in the bloody renature and the creatinine into the area no because we're not perfusing it properly the kidneys are becoming damaged so they might have an elevated bu in and they may have an elevated creatinine that's important the next thing this is a test that you can do now patients who get for example influenza all right they get viral pneumonia they are at higher risk for getting a super infection with a bacteria bacteria though lead to a specific marker that you can see in patients with pneumonia called procalcitonin so sometimes there is a molecule called procalcitonin but remember this is particular to bacterial infections the procalcitonin is going to be normal they will have a normal Protoss at onin level that is important if it's primarily kovat 19 if it's koban 19 with a super infection of a bacteria then they might have an elevated PCT or procalcitonin so again the only time they'll be an elevated PCT or procalcitonin is if there's maybe a cove in nineteen plus a bacterial infection okay and that's important to remember alright the last thing you can do is you can check for these general markers of inflammation okay now what are some of these markers of inflammation again they're not specific but they help us in this in determining the patient's mortality rate one of them is CRP they'll have an elevated CRP another one is they'll have an elevated ESR these are nonspecific markers of inflammation but they're going to be elevated another one is you're gonna see elevated levels of interleukin 6 where did that come from remember the macrophages who are releasing tons of interleukin 1 6 and TNF alpha that's 1 and it's also released from the liver as an acute phase reactive protein another one is when there's severe inflammation an enzyme called lactate dehydrogenase is also in higher concentrations other things is whenever there's massive inflammation there can also be an elevated d-dimer and there may also be an elevated ferritin okay so these are all markers of inflammation that might be found in a patient with Kovan 19:00 and again these high markers may be associated with actual higher mortality rates something is also really important remember if someone is a multi-system organ failure we can see an increase in the BU n increase in the creatinine and we can see an increase in the ast LD alt and the Billy what if there's not enough perfusion to the heart what we may also see we might see elevated so also take into consideration high mortality associated with elevated troponin x' troponin Zion troponin T and elevated ck-mb and again this is an indicator of higher mortality rates which could be indicative that you're not getting enough perfusion to the heart as well leading to a possible myocardial infarction and that can make things worse because you become hemodynamically stable as well unstable hemodynamically unstable all right we do all the labs we get all this information back we're waiting for rt-pcr to come back we didn't get a positive influenza now what we're gonna do is we're gonna do some imaging all right generally you want to start off with a chest x-ray but you're gonna see that CT is actually the most sensitive test at this point time for being able to determine if someone has cope in 19 now it's not specific okay meaning that there could be other infections you can have influenza or viral pneumonia like influenza pneumonia or other different types like adenovirus they can present with actual findings on a CT scan very similar to Kobe 19 but again it's helpful in helping to kind of has a high sensitivity over 95% for in looking at kovat 19 so first thing you can do is you can do a chest x-ray it's not gonna be the best but it can lead you somewhere what are some of the things that you're gonna see in a chest x-ray you might see this area of what's called ground glass opacities so you may see what's called ground glass opacities now from there maybe you say oh this is not a sensitive this is not what I want it's not as good I'm gonna go ahead and do a CT scan I do a CT scan and I see ground glass opacities again in the peripheral lung fields so let's say I see some ground glass and then I go and I run through my actual CT scan a little bit more and then I start noticing some areas of consolidation and if I start seeing these areas of consolidation oh that's not good that means that I also have some pneumonia as well so we have some ground glass opacities which are gonna be a little out a little interstitial edema consolidation which is going to be a lot of those actual accumulation of cellular debris proteins right and then leading to what's called a special term called the crazy paving pattern so we can see ground glass opacities consolidation and you'll see later when we show you on CT scan you can also see what's called a crazy paving pattern it's a special radiological term that they say also could be associated with interstitial fluid thickening and membrane thickening as well as alveolar an interstitial edema okay other things you could do is if you're skilled or you have the time you could do what's called point-of-care ultrasound ultrasounds also can be utilized what you can look for is you can look for what's called pleural line thickening and we'll show you what that means on an actual ultrasound so you can look for it's called pleural line thickening another thing you can do is you can check for again with with interstitial pulmonary edema you can see these specific lines call B lines so we can also look for increasing B lines within a specific zone okay the last thing that we could also maybe see is consolidation with air Branca Graham's so there may also be consolidation with air Branca Gramps and again we'll see all of this on the imaging here in just a second you I ninja nurse so in this video we talked about the novel coronavirus or the corona virus discovered in 2019 which is responsible for the cove in 19 that we talked about here in this video we talked about the epidemiology which included a little point on the zoo and gnosis we talked about case fatality rates we talked about the reproductive ratio we talked about the series interval right we also went into the entire pathogenesis how those pathogenesis produced the specific symptoms that we see in kovat 19 as well as pretty much your diagnostic process that you're going to be looking to go through in helping to diagnose kovat 19 in the next video what we're gonna do is we're gonna start talking about treatment of kovin 19 we'll talk about the different types of ventilation management okay i'm mechanical ventilation we'll also talk about if the patient is in need of empiric antibiotics if there is a super infection we'll go over different prognosis things that affect the actual prognosis things like if someone has an underlying heart disease lung disease so on and so forth and also lastly we'll talk about preventative measures and trying to decrease the spread of this overall very serious virus engineers I hope this video made sense I hope you guys enjoyed it if you guys did please hit that like button comment down in the comment section and please subscribe if you guys get a chance down in the description box we'll have links to our Facebook Instagram and our patreon account alright and engineers as always stay safe and until next time [Music] you

Channel: Ninja Nerd Lectures

Views: 5,365,808

Rating: 4.8689108 out of 5

Keywords: COVID-19, Corona virus, CoV, Corona, SARS, MERS, corona pathology, corona update, COVID-19 update, corona virus epidemiology, COVID-19 diagnosis, novel corona virus, SARS-COV2, corona virus pathology, corona virus 2019

Id: PWzbArPgo-o

Length: 50min 39sec (3039 seconds)

Published: Mon Mar 16 2020

Reddit Comments

[u/[deleted]]

bruh it says "novel coronavirus 2019" but we living in 2020 rn smh my head lol (laugh out loud)