00:01
Before we talk about each of those
other items on our differential,
behooves us to take a look at
the skin layers themselves
to make sure our anatomies is on point here.
00:10
So, as you can recall, the epidermis,
which is all of those
layers on the top there, is divided
into 6 different layers,
starting with the stratum corneum on the
outside, which is essentially dead skin,
the stratum lucidum, the stratum granulosum,
the stratum spinosum, and the stratum basale.
00:29
It's the stratum basale, which is
where new skin cells, new
keratinocytes are being made, and
they're gradually migrating out
to those outer layers until at
the outermost layer, it's
basically just dead cells.
00:41
All the keratinocytes are connected
to one another by individual
desmosomes. That's what basically
provides a nice link
between each keratinocyte. In contrast,
the epidermis is connected to
the dermis at the stratum basale
via hemidesmosomes. These are
basically links that connect
right at the base of those
stratum basale cells
connecting the basement
membrane to the dermis.
01:07
Depending upon where an immune-
mediated attack occurs,
that's going to dictate how tense
the bullae on the outside is.
01:15
So, if the lesion was within
the keratinocytes
in the epidermis, then the
skin is going to be very thin,
and it's unlikely that the
blisters will stay intact.
01:27
Whereas, if the autoimmune attack is at the
hemidesmosomes, at the junction between
the epidermis and the dermis
and the dermis, essentially, the epidermis
is completely intact, and so, those
bullae are going to be tense and are going
to basically stay strong and intact,
rather than falling apart. That principle,
that idea about where this defect occurs,
will help us to think about what
the disease process
that's affecting our patient may be. In
this case, we know that our patient
had very intact bullae, which tells
us that the lesion is probably
between the epidermis and the dermis, rather
than within the epidermis itself.