00:01
Our topic here is bullous pemphigoid.
00:04
I’d recommend that before you come here,
take a look at pemphigus vulgaris,
I have, extensively
and in great detail,
gone through the foundation
of what you need to know
for two conditions here:
pemphigus vulgaris and
bullous pemphigoid.
00:22
With bullous pemphigoid, it is
also a type 2 hypersensitivity.
00:27
The IgG autoantibodies are then
going to attack the bridges.
00:32
Where?
The bridge not between
the keratinocyte
but the bridge between the
dermoepidermal junction.
00:40
Picture that for me.
00:42
Dermoepidermal junction
is a particular bridge.
00:48
Memorize and focus
upon hemi-desmosome.
00:54
So, if you lose the hemi-desmosome or
the function of the hemi-desmosome has
been compromised due to such attacks,
first let me tell you,
you’re going to form a very, very
tight blister that we call a bullae.
01:08
The skin is not
going to come off,
and in terms of mortality,
there’s an increased risk of
mortality with pemphigus vulgaris,
then there is with
bullous pemphigoid.
01:19
I recommend when you’re
doing this condition,
you also, at the same time, spend a few
minutes and review pemphigus vulgaris
so that you’ll never forget which
particular bridge is being attacked
in which condition and how your
patient is going to present.
01:39
The demographics: Elderly,
debilitated patients.
01:43
Usually presents first on
the lower extremities,
whereas in pemphigus vulgaris,
it’s pretty much everywhere.
01:50
Loss of keratinocyte adhesion
to the basement membrane
leads to large tense blisters.
01:59
Why am I being so dramatic here?
Because I was being dramatic
when we did pemphigus vulgaris,
and I told you, those blisters were
raupturing in superficial blisters.
02:09
These blisters that are bullae
are large and taut or tense.
02:16
What’s being affected?
Hemi or desmosome.
02:20
This is the hemi-desmosome.
02:24
Take a look at the bullae here.
02:26
Large blisters,
most likely on the lower
extremity, thighs and such,
maybe the lower abdomen,
and maybe the axilla.
02:36
The management:.
02:37
Once again, immunosuppressants
because it’s an autoimmune disease.