Our topic here is
I want you to hone in on vulgar.
Because there are two conditions
that I’m going to walk you through,
and students tend to get this confused, but
not any longer because you’re with me.
And the two conditions
include pemphigus vulgaris,
and then subsequently, I’m going to
walk you through bullous pemphigoid.
Of these two, which ones
are more dangerous?
So, pemphigus vulgaris is the one that
has an increased risk of killing you.
So therefore, increased risk of mortality.
And we talked about the skin,
where if you took a tongue
depressor and you scrape the skin,
there’s one condition in which
the skin would remain intact,
there’s one in which it would
then come right off, split.
Could you imagine as to how, perhaps,
traumatic that would be for the patient?
So guess which one this would be
in which skin would then come off.
Why do students get
It’s this point.
In other words, the
pathogenesis or the etiology.
Both are type 2
What does that mean to you?
It means that the antibodies are then --
autoantibodies are attacking a
particular target or protein.
What you need to memorize is which
protein is involved and which
type of disease as being a
target for that particular IgG.
In pemphigus vulgaris, it is the skin
which is then being scraped off.
It’s the vulgar, dangerous one.
I’ll tell you what this means.
It means acantholysis, and we call
this positive Nikolsky′s sign.
That’s to come.
So now, you start
thinking about the
two different junctions
or two different bridges.
The one bridge is going to be the one that
then connects one keratinocyte to another.
And then you have another
bridge which is then
going to connect the
dermis with the epidermis.
I’ll tell you right now, it’s the
one that we’re focusing upon
in vulgaris in which it’s connecting
one keratinocyte to another.
And this, ladies and gentlemen, please
focus on desmo-, desmo-, desmosome.
You see anything about
or perhaps even the
family of E-cadherin.
Remember that way back
when in neoplasia.
These are the bridges that you
want to keep in mind between
keratinocyte to keratinocyte,
or from cell to cell.
Your focus here will
be on desmosome.
If you lose this bridge,
in other words,
the function of the desmosome
hasn’t been compromised
due to bombing taking place
by these IgGs attacking it.
If the desmosomes are gone, then what do
you think the fate of the keratinocyte is?
Comes right off.
Autoimmune antibody-mediated attack on
desmosome, a type 2 hypersensitivity.
The desmosomes are the ones that are the
bridge or allow for the keratinocyte to --
I don’t want to say communicate --
attach or anchor through
the other keratinocyte.
If this is gone, then
therefore, as is the epidermis.
There is the foundation that
you want to know for vulgaris,
and I’ll quickly describe
to you, bullous pemphigoid.
Spend a minute, make sure
you repeat me a few times
to make sure that you comprehend
everything that I just delivered.
Vulgaris, demographics, who is it?
Where do you see it?
Often seen in middle-aged men and women.
Usually presents first
in the oral mucosa.
Isn’t that dangerous?
So yes, within your mouth,
you can have pemphigus vulgaris
resulting in the same issue,
attacking the desmosome,
so therefore, the integrity of your
mucosa has now been compromised.
The loss of the keratinocyte adhesion
yields superficial blisters.
Both of these are going
to have blisters.
What do you mean both?
Pemphigus vulgaris and the
other one, bullous pemphigoid.
Are there other variants?
Of course, there are,
but I have to at least give you the
foundation and the fundamentals
so that you know at least
what you’re working with.
Both of these conditions are
going to give you blisters,
but the blister that we then call
in bullous pemphigoid are bullae, right?
Now, blisters here, pay attention to
description, are going to be superficial.
A blister is not as big as bullae,
but yet, which condition is vulgar?
So, loss of keratinocyte adhesion will
then yield a fluid-filled structure
which we then call a superficial blister.
Guess what, it will
This description is not the
case with bullous pemphigoid.
What are we looking for?
Everywhere up and
down the body, huh?
You have keratinocytes
in your skin everywhere.
It is the biggest organ that we
have in our body, for Pete’s sakes.
So, scalp, face, trunk,
arm, groin, whatever.
The point is wherever
this problem occurs,
everywhere, we have loss of integrity
of either the mucosa or the epidermis.
Pemphigus vulgaris, if you were to
take a look at this picture here,
you have superficial blisters.
And then what happens on your
right is that histologically,
if you will take a section,
literally, you'll find that the
keratinocytes are going to come right off.
And when they do so,
what is the bottom most
layer of your epidermis?
I’m sorry, what did you say?
So, say that you have
your stratum basale,
your stratum basale which is left
behind after the skin is scraped off.
It looks like a row of tombstones.
A row of tombstones.
So for example, if you were to bury
the dead, and then maybe perhaps,
you’re going to leave
behind a tombstone,
and that’s what the
stratum basale is going
to look like once your
skin comes right off.
Keep that in mind.
This is the vulgar disease.
Well, you want to try to mitigate
effect of the autoantibodies.
Think of immunosuppressant agents.