COVID-19 | Coronavirus: Epidemiology, Pathophysiology, Diagnostics

by birtanpublished on June 30, 2020


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


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


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


we have 150 3517 cases okay this is

worldwide with 5735 deaths that gives us

37 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


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 13

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 75 if you take influenza

for example it's actually approximately

25 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 75 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 25 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 25 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


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


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


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


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 986

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 lfts 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


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


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


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



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