Now, the pathogenesis becomes important for
us. It’s hyperplasia of mucous glands in
the bronchi. Think about where you are. Okay.
Next, before we move on, well, give me a couple
of ways in which the alveoli might collapse.
The alveoli may collapse, well, a common
method. Let’s say that you are post-surgically
resting in a bed in a hospital.
And as you rest there and you’re non-ambulatory
and at some point of time, maybe you start
developing a fever. Now this is rather
problematic and should therefore, clue you
in that your patient is on the verge of most
likely developing what's known as resorption
atelectasis. What does that mean to you? Resorption
atelectasis, while you lay there, non-ambulatory,
not moving, postoperatively, in a bed for
a long periods of time, you might start developing
mucous plugs in the bronchi. If that occurs,
then what then happens with the alveoli distally?
Called resorption atelectasis. Guess what?
The same kind of issue that also take place
here amongst others. So therefore, if the
alveoli perish, tell me about your patient.
Are they pink puffer or are they blue? They’re
blue, they’re cyanotic early.
Let’s continue. Greater than 50% thickness,
is hyperplasia of the mucosal glands. Greater
than 50% thickness of mucous glands layer
to thickness of wall between the epithelium
and cartilage. Stop there. Take a look at
the ratio here. We are actually looking at
a ratio, this ratio that we’ll then call
Reid index is the following: greater than
50% thickness of mucous glands layer / to
thickness of the wall between, think about
the epithelium please, and the cartilage. So,
when there’s a greater than 50% thickness
in mucosal glands, guess what you’re doing?
Oh, my goodness, I’m occupying the space
that’s in the bronchi. That’s a problem,
ladies and gentlemen. This is chronic bronchitis,
ladies and gentleman. Hyperplasia of mucous,
well guess what? That is going to be productive
cough, ladies and gentlemen. For how long?
3 months consequently over 2 years sequentially.
Next. What else may happen? In the upper airways,
which normally has what kind of cells? Good.
Ciliated columnar cells, may then undergo
squamous metaplasia. Divide this into two
different portions so that you understand
the two different pathogenesis that are taking
place concomitantly. You have hyperplasia
of the mucous glands in the bronchi. That’s
huge. Reid index is what you’re looking
for there with the ratio of the thickness
mucous gland and between the epithelium and
the cartilage. And then number 2, the squamous
metaplasia of upper airways.
What else may happen here? Well, goblet cell
metaplasia and peribronchiolar inflammation.
So once you start undergoing the process
of more of your goblet cells and around the
bronchiole you have inflammation, what’s
going to happen? The bronchioles are a lot smaller
than the bronchi, right? Just like arteries,
well, arterioles are much smaller than arteries.
So, arterioles – arteries, bronchioles – bronchi.
So, if the bronchiole is quite tiny to begin
with and then you undergo peribronchiolar
inflammation, what’s this
called when you obliterate bronchiolitis?
Okay. So, some may call it obliterans brohiolitis
or obliterans bronchioles or bronchiolitis
obliterans. It’s seen in later stages of
chronic bronchitis due to fibrosis. Stop there.
So, if it’s fibrosis, what does that mean
to you? Extremely generic. What does that
mean? Fibrosis up and down our body. Many
causes. Whenever there’s fibrosis,
you know that it’s chronic type
of issue in which there is enough damaging
lesion, whether repair process ended up
depositing tons of fibrosis. What does
fibrosis mean to you? It means contraction.
In this case, here the fibrosis has taken
place around the bronchioles. So, what’s
happened to bronchioles? Go on. Where did
you go? Oh, obliterated. Why? Because of the
fibrosis. Are you with me?
So, we’ve looked at a few different issues
with pathogenesis here up in the upper airways
along with the bronchi and such, you might
add squamous cell metaplasia along with what
we’ve talked about with Reid index with
increased mucosal glands. As you get further
distally into the bronchioles, goblet cell
metaplasia is what you’re looking for and
with increased destruction or fibrosis,
please understand, you have complete obliteration
of the bronchiole. Understand, however, we’re
going to revisit bronchiolitis obliterans
in other pulmonary pathologies that may result
in fibrosis deposition. And during that
time, I’ll refer to back to what we looked
Clinical presentation. Significant V/Q mismatching.
Such a thing may or may not be the case
with emphysema. It was minimal V/Q mismatching
in emphysema, wasn’t it? What happened
possibly with that hypoxemia in emphysema?
Is it possible that you may or may not have
hypercapnia? Yes. In emphysema, I showed you
specifically in that topic where we looked
at the oxygen dissociation curve versus your
carbon dioxide dissociation curve. If you
missed that discussion, please go back and
review that particular topic.
Now, with chronic bronchitis, because of inflammation
taking place and mucous production in the
bronchi, there’s really no chance of you
having regional type of compensation. It is
going to be cyanosis, immediately. Retention
of carbon dioxide, immediately. There
is none of this with or without. There will
be significant V/Q mismatching, wheezing, crackles
Shunt, wait, stop. Shunt, stop. Why? Because
I need you to understand the significance.
Don’t just read stuff, listen, conceptualize.
So with shunt taking place here in chronic
bronchitis, how does that occur? I just gave
you two examples in which that alveoli may perish.
Two. One was, I told you about postoperatively
where patient lays in the bed for long periods
of time, therefore accumulating mucus plugs
and fever, and infection. What then happens
to the alveoli distally? Gone. What do we
call that? Resorption atelectasis. Is that
common? Yes, we’ll talk about that later.
If this is chronic bronchitis, can we say
that it’s pretty much the same pathogenesis?
Maybe they’re smoking, there’s irritation,
there’s goblet cell metaplasia, increased
mucous production in the bronchi. What happens
to the alveoli? Gone. What is that? A shunt
or dead space? Good. It’s a shunt and
gone is the alveoli. Good. Therefore, shunt
results in early onset of hypercapneic, stop
there. Such a instance, because I’m being
really deliberate here, because you need to
be quick about differentiating between emphysema
and chronic bronchitis. You don’t have all
day. In asthma as well. Asthma, remember, many
of times, you can reverse it. Okay. Now, early
onset of hypercapnea, hypoxemia
is going to be present in any type of COPD.
That doesn’t tell you much, but the early
cyanosis and the early hypercapnea, absolutely.
What does that mean? I’ll give you an ABG,
arterial blood gas, where your carbon dioxide
is what? Good, above 40. What’s your pH?
Good. Acidic. What does that mean? Less than
7.35. Do you understand how important this
statement is? It’s probably the most important
in terms of for you to be able
to diagnose your patient quickly.
Resulting in cyanosis, quickly, polycythemia.
Why? If there’s hypoxic chronically,
who’s going to respond? The kidney. What’s
the kidney going to do? Oh, yes, I forget about
that sucker. Who is this that I’m referring
to? Erythropoietin, EPO. So, here
comes my erythropoietin and what kind of polycythemia
is this to be technical? Good, secondary polycythemia.
We call these patients blue bloaters.
Late onset of dyspnea with chronic complications
of, this says, pulmonary arterial hypertension
(PAH). What kind? What do you mean what kind?
Primary or secondary? Good, secondary pulmonary
arterial hypertension. We’ll talk about
this later, don’t you worry. And we have
secondary right-sided heart failure. Are we
clear about the abbreviations? Okay? PAH – pulmonary
arterial hypertension, secondary type. Those
of you who are ahead of me, you know exactly
why. If not, that’s okay, just digest what
I’m giving you. And then secondary right-sided
heart failure. Why? Lungs are offering more
resistance, right ventricular hypertrophy,
may eventually result in cor pulmonale. That
is not good.