We talked about the pathogenesis. The subtyping
of emphysema becomes very important for us.
This will then tell us as to where the damage
is taking place and what the exact cause is,
and this becomes really crucial for us to
then identify other parts of the body that
are also affected. What the heck am I talking
about? For example, if the centrilobular and
then you call this the proximal acinar. The
reason we call this centrilobular is because
the entire lung is not affected. I paused
at the term “entire” because the term
that you use clinically for the entire structure
to be involved is “pan”. So, this is not
panacinar emphysema, it is centrilobular a.k.a.
proximal acinar emphysema. Now, when I say
proximal, please understand, I don’t mean
definition of proximal. I do not mean as proximal
as being the bronchi and the trachea. That
makes no sense. By proximal, I mean that this
is going to be proximal to the actual alveolus
maybe referring to the dilation or destruction
of the? Let’s take a look, respiratory
bronchiole. Are you picturing this?
Next, epidemiology, commonly encountered in
what type of patients? Well, , you want to
put two patients together here and these would
be coal workers and smokers. So, what is occurring
and how do you keep this straight? What do
you mean? Because if it is strictly smoking
and you were to then induce, and we’ll go
through the pathogenesis further, but if you
were to then induce, the recruitment
of your neutrophil causing damage to parenchyma.
Then you know that you’re resulting in some
type of emphysema and this is called centrilobular,
right? Okay, that's obstructive lung disease
and that’s where we are right now, but then
if you shift over to our second differential
here which is your coal workers' pneumoconiosis,
that’s nothing to do with obstructive, does
it? In fact, it comes under what? It comes
under your restrictive. But, may I ask you
something? In real life, clinically speaking,
many of your coal workers who are working
in mines, extremely young, very much influenced
and may not have access, unfortunately, to
proper education. Now we have to be stereotypical
here, so please bear with me. Many of your
coal workers are going to be smokers, let’s
be smart about this. And if they’re smokers,
do you think that they might be suffering
from emphysema? Absolutely.
So, what do you want to keep in mind is from
henceforth, yes, we are going through pathology
in a black and white manner, but then you
also have to apply it in real-life scenarios
and this is one of them.
Continue discussion of pathogenesis. So, what
about these smokers? Well, , imagine now that
you are introducing tons, about tons of antigens
into the lungs. Well, all these antigens
are being introduced to the lungs. And so
therefore, what’s going to happen? They
are going to recruit an acute inflammatory
cell and these would be your neutrophils.
And what about these neutrophils? Well, , it
has certain enzymes in them so that
it can combat these antigens, but if you have
such recruitment and access of your neutrophils
and you’re releasing your elastase, or the
other name for this is a proteolytic enzyme
know, as your proteinase, then understand
that now, you’re overwhelming the entire
system. What entire system am I referring
to? The lungs right now. And so, therefore
the elastase that you’re then now releasing,
stop there and I need you to tell me about
what normally neutralizes the elastase once
the job of neutrophil has been completed?
It’s a anti-protienase, isn’t it? This
is your alpha-1 antitrypsin. Now be careful
here, all that I’m doing is laying down
the normal function of an alpha-1 antitrypsin.
What is it? It’s a proteinase inhibitor.
So, if you’re a proteinase inhibitor then
what does that mean to you? It means that
you are existing to neutralize your proteolytic
enzyme known as elastase. But now, if you
have these elastase in abundance guess what?
You completely overwhelm the system and you
start causing damage to the adjacent lung
parenchyma. What does this mean?
Does this mean that every single elastase
is causing damage to the entire lung? No,
more commonly you’ll have these areas that
are highly concentrated with neutrophils,
that is highly concentrated with elastase,
therefore, usually in the upper lungs in which
it causes damage to the parenchyma, upper
lungs only. So, if it’s only one portion
of the lung that’s being damaged, how could
you possibly call this pan? You cannot.
And so therefore, what is the topic at this
point? Our specific sub-type of emphysema
is? Good, this is our centrilobular, proximal
type of emphysema.
Let’s continue. The loss of tissue is what
happens here and when you lose these elastic
tissue now I need to make sure that you understand
the concepts so that you understand what’s
going on with your pathology. So, here you
have an airway, shall we say a tube, okay?
And this tube has to remain open obviously.
When you inhale has to expand
so that you increase that flow so that you
fill up that alveoli. Sure, okay. Then upon
expiration, what happens? Well, your pleural
pressure is then going to become positive
and the alveoli is going to become positive
pressure, it’s squeezing out the air into
the airway, isn’t it? Okay. Now, at first,
upon expiration or exhalation, think of your
loop spirometry. The top half of the loop
in which at first, air is coming out
really fast, great. So, that’s going to
keep the airway open, but as expiration continues,
well, there isn’t as much air in your alveoli.
Please tell me, at first, what’s maintaining
the patency of the alveoli? That obviously
is surfactant, right? But then, what about
the airway? It’s not surfactant of the airway,
that makes no sense. It’s the elastic tissue,
right? So, elastic tissue literally keeps
the airway open just enough so you get
air in and get air out but then as air decreases
can you ever afford for your airway to collapse?
That makes no sense. So therefore, the elastic
tissue will keep it just open, will keep it
open just enough. Don’t
So, you’re keeping it open, you have to.
But what happens in emphysema? That
elastic tissue, how appropriate, elastic
tissue is being damaged by what’s the name
of this enzyme that’s being released by
neutrophil? Oh elastase, yeah that’s right.
So the elastase, guess what causes damage
to the elastic tissue, gone is elastic tissue.
Now, air is coming out. What kind of disease
is emphysema? Obstructive. Obstructive meaning
what? Difficulty with air getting in or getting
air out? Good, having difficulty getting air
out so now as air is moving out it’s getting
less, there’s no elastic tissue.
What happens to airway? Gone. Airway’s
gone, collapsed. Welcome to
emphysema. Welcome to specifically what I’m
telling you here what’s called as your well
centrilobular type of emphysema. Loss of elastic
tissue, why? Where excess recruitment of neutrophils.
What happens? Increase elastase. What happens?
Damaged elastic tissue, I collapsed my airway.
Everything we just talked about.
Now, what happens here as air is trying to
get out then it’s an obstructive issue it
gets trapped in there. Its lost all ability
to properly handle that type of air travelling
through here. Okay, now, let me tell you something
else. I guess, at some point in time, you
as a clinician, what might you want to do
based on everything that I just talked about
here? What might you want to do, as a clinician,
to prevent this collapse from occurring in
a patient that you know has emphysema because
you saw that their FEV1/FVC ratio was drastically
decreased? Maybe on a chest X-ray you find
that they’re barrel chest, so on and so
forth. What would you recommend a simple,
non-medical type of issue that you could tell
the patient to do? What the heck
did you try to tell your patient to do? That’s
not very nice. Yes it is. You have introduced
a resistor. What did I just do?
Try it at home, it’s pretty fun. It makes
your lips feel really good, So, it’s
vibration. In other words, you pursed your
lips. When you purse your lips, what have
you done? You’ve introduced a resistor,
haven’t you? Are you with me? Seriously,
you’ve introduced a resistor in a series.
Close your eyes, think series, not parallel.
You’ve learned in physio that in a series
when you add a resistor what happens to the
pressure proximally? Increases. Your lips,
that’s the resistor that you’ve added,
purse them. What will happen proximally?
Increased pressure. Yup, so when you increase
that pressure what have you done? You’ve
allowed for the airways to stay open because
guess what happened to this respiratory apparatus?
It’s like a bag. It’s just floating
in the air, really thin, okay? Really thin,
and all it wants to do is just collapse when
there’s no air in there. How do you keep
this open? You purse your lips, you add a
resistor, increase the pressure and you keep
it open, are we good? I don’t think I could
be any more dramatic, you purse your lips
so that you increase that pressure. Who cares
about the pressure distally, outside the mouth
who cares it’s irrelevant. So, will you
take the information that you learned in physio
every single time you give it a clinical tag,
you’re in fantastic shape.
Okay, let’s move on. Loss of respiratory
bronchiole mostly where? In the upper and
middle lobe. Think about this as being smoke
rising. So, when you’re a smoker remember
this has nothing, I repeat, has nothing
to do with alpha-1 antitrypsin deficiency,
is that clear? Perfectly normal amounts of
alpha-1 antitrypsin. This is a patient that
is smoking and so, therefore, introducing
a lot of antigens. And so, therefore, recruiting
neutrophils and hence, elastase. Having fun
yet? Let’s continue.