Basic Dermpath Cases 2 – Explained by a Dermatopathologist

Basic Dermpath Cases 2 – Explained by a Dermatopathologist

These are some random Dermatopathology cases
that we’re going to look at in this video. Just a few things that I came across recently. And last random video did so well, people
were so interested in it, I thought I’d make another one. So here’s a shave biopsy from sun damaged
skin. You can see that there’s a lot of solar elastosis
out here, all that blue stuff replacing the pink dermal collagen. In this patient, the clinical history was
that they had a rash that kind of came and went, and had these small itchy bumps, little
itchy pruritic papules on the trunk mostly. And here’s a biopsy of one of these papules. And what you can see right away, you can see
how it’s a small kind of discrete lesion that would correlate to a small bump on the skin. And there’s a lot of fluid that kind of pushed
the epidermis, the epidermal keratinocytes, apart. If we go closer we can see that the reason
that fluid is filling the space here, this is not really like spongiosis. In fact, this is the epidermal cells falling
apart. They’re becoming acantholytic. And then this is just some serum, kind of
a fluid that seeped up in here and filled in the space. So acantholysis is when the spinous layer
of the epidermis falls apart and basically the keratinocytes lose connection with their
neighbors. The desmosomes, those spines that hold them
together, kind of get stretched, or pulled apart, or broken down for a variety of different
reasons. And what happens is that the cells become
detached and loose, and you can see here it’s starting. At the very beginning, it can kind of look
a little like spongiosis, but then what happens is the cells break free and the keratinocytes
kind of curl up into a little ball. Their cytoplasm gets more dense because it’s
not stretched as thin and so they have this rounded kind of very pink appearance like
that. And you can see that where they’ve become
detached from their neighbors, those cells are also kind of rounded and smoothed on the
edges. And so that rounding of the cells is because
they don’t the tension of being connected their neighbors and pulled kind of taught
by those spines that are usually connecting keratinocytes in the epidermis. So that pattern is called acantholysis and
it’s really important not just for this disease, which is Grover’s disease, we’ll talk about
in a second, but it’s important for a lot of different diseases. So it’s important to recognize the pattern
of acantholysis in dermatopathology. And then additionally some of the acantholytic
cells appear are beginning to die and break down and what’s happening is the nucleus instead
of being kind of large open and kind of pale purple, has become very dark and like almost
dark purple to black in color almost and very condensed. And so these cells, this process is called
dyskeratosis. And it kind of looks to me a lot like parakeratosis,
but when you see it in the setting of acantholysis we call it dyskeratosis. And it takes kind of 2 main forms. It takes the one form where the cells are
kind of thin and stretched out, and those cells are called grains because they kind
of look like I guess like grains of wheat or other types of grain a bit. Old school dermatopathologists had a very
active imagination I think, no offense to them. They basically created this field. But in any case, they came up with a lot of
names that sometimes sound funny to modern day dermpaths. And then the cells over here that are kind
of more rounded are called corps ronds, and that’s my bad attempt at doing the French,
which means round bodies. And so grains and corps ronds are the 2 types
of dyskeratotic cells you see. So in this setting where we have this solitary
itchy little bump with acantholysis and dyskeratosis. And this patient has a history of a rash that’s
kind of coming and going, particularly on the trunk and itchy little papules. That’s a perfect history for Grover’s disease,
or transient acantholytic dermatosis, which often presents as an itchy, kind of papular
rash usually on the trunk, and they often times will have a little bit infiltrate underneath,
including some eosinophils. And I kind of speculate that maybe that’s
part of why they’re so itchy and bothersome to the patient. So that is Grover’s disease. Let’s look at one other example of that. So you might think well this doesn’t look
anything like that case I just showed you. And in fact it is kind of a different more
subtle pattern of Grover’s disease, but I see this often. I think it’s good to recognize because sometimes
you’ll kind of just catch these changes a little bit on one section and if you cut
deeper you’ll find it. So anytime they’re looking at clinically for
folliculitis or something with a kind of itchy, papular, bumpy little rash, I always keep
Grover’s disease in mind as it can be tricky to find. But here the clues, the most important clue,
is look at the granular layer. The granular layer is very thick and very
hyper chromatic, is very purple. So look over here at the normal skin, the
granular layers are very thin, little purple line with these purple keratohyalin granules. It’s a very thin layer of purple granules
in one or 2 cells kind of thick at the top of the spinous layer. It divides the spinous layer from the corneal
layer. But when you get over here, that layer gets
very thick and you have lots of enlarged cells with big, thick, purple granules. You can see those increased granular layer
in a lot of different processes, but when I see it as a little focal area particularly
when I start to see some stuff that looks like parakeratosis or maybe dyskeratosis and
I start to see some cells that are starting to fall apart and get acantholytic, to me
that’s a good sign that you’re dealing with Grover’s. If you cut deeper, a lot of times you’ll see
it. I think that honestly in the right setting
even changes like this are compatible with Grover’s disease in my opinion. And down here in the dermis again, look at
this little infiltrate of lymphocytes underneath the lesion. And again often if you go closer, you’ll find
occasional eosinophils. You don’t have to have them, but you often
find them. Maybe this one doesn’t have any. And look, we go a little deeper and what happens,
you’re starting to see the cells falling apart and rounding up and becoming acantholytic. And then they’re starting to die and turning
into dyskeratotic cells. The corps ronds right here and then some little
grains up there. So another more subtle example of Grover’s
disease. Alright, so let’s show something different. This is an ulcerated lesion from the ear of
an elderly patient. And right here what we see is really thickened
epidermis with a little bit of scale and curst on top, serum and parakeratosis. So the first thought that I had when I see
this on the ear, an ulcerated nodular lesion, is chrondrodermatitis nodularis helicis. And that’s a kind of a reactive condition
that can mimic a squamous cell carcinoma clinically, can look like a little ulcerated, red bump
or nodule on the ear, often on the helix or antihelix. And the thought is that it comes through ischemic
change from pressure. Usually in older patients in that the pressure
causes ischemia and the cartilage starts to die and the dermis starts to die in a focal
area underneath the skin and then you get reactive epidermal hyperplasia. So that was my first stop but this is one
of those times where I’m not so sure that I’m right. So here you can actually see there’s cartilage,
but we have some other unusual changes. And although I’m not exactly sure why this
is happening in this particular case, I think there’s a couple interesting microscopic points,
so I wanted to share it anyway. So here we do see that there’s necrosis over
top of the skin and it goes down all the way to the underlying cartilage. So this is the cartilage, the hyaline cartilage
of the helix, and you can see how it’s got areas at the edges where it’s kind of pink. And the cells are starting to die, so it’s
becoming degenerated and partially necrotic. So all of that would fit well with CNH, but
the couple things that don’t fit well with chrondrodermatitis nodularis helicis is this,
we’ve got huge collection of neutrophils. These little tiny it kind of multi segmented
nuclei, those are neutrophils and they are breaking down and being destroyed and turning
into keratotic debris or nuclear dust. So this finding here is almost like an abscess. So I personally have never seen a case of
a CNH that became abscess before, although I suspect that perhaps that’s what’s happening
in this case. And when we look around a little bit more,
we find in fact that this is an infectious process at least partially. Now whether the infection caused the process
or is a secondary phenomenon is hard to say. But when you look, these little purple nodules
here, these are colonies of cocci bacteria and they’re a little bit hard to get to show
on a video. But let’s try. When I focus in and out, you can see that
this little collection is composed of tiny tiny little dots, those little dots, each
of those little tiny dots is a cocci bacteria. They show up a lot better under the microscope
than they do on a video. And here’s another. You can see them when they’re on thinner layer
on here. Each little dot represents a bacteria. So bacteria are quite a bit smaller than white
blood cells. And the neutrophils are much more massive
than each of these little tiny dots of bacteria. And you can see that there’s layers, there’s
little collections and colonies of cocci bacteria right up here against the cartilage. So it’s kind of interesting it’s an infectious
abscess by cocci organisms. Probably these because this is on the skin. It most likely these are staph or strep, but
of course there’s no way to tell by microscopic exam. The tissue would have to be cultured to figure
out for sure what type of bacteria. And so in a case like that I just described
what I found and said that there’s an abscess with some necrotic cartilage and there are
lots of bacteria colonies and it appears, at least partially, this is either secondary
infection or this is the primary process and they need to do some cultures to figure out
what kind of bacteria’s causing this. So kind of an unusual case but very very beautiful
histologic details. And then over here you can see these enlarged
vessels. And in the background there some enlarged
kind of hyperchromatic cells that even look a little bit atypical but these are actually,
this is granulation tissue so kind of a reactive tissue repair change that’s basically early
scar formation that’s happening around the abscess. You got these large, these are dilated capillaries
that have thicker walls and they have plump endothelial cells and in between you have
a mixture of inflammatory cells and plump myofibroblasts. And sometimes granulation tissue can get kind
of robust and scary looking. I actually did a few stains here to make sure
that this wasn’t a subtle poorly differentiated cancer infiltrating the tissue but all of
those were negative. So it’s kind of a robust granulation tissue
response right next to this abscess with bacteria and ulcer and necrotic cartilage. So here’s a nodule on the arm of the patient
and it was clinically thought to represent either a cyst or lipoma or some other sort
of skin tumor. And what you can see actually is it’s as large
a nodular aggregate of cells with dead material in the middle, this dead pink stuff. And looking closer. These cells are histiocytes. And in particular not just regular histiocytes,
but actually multinucleated giant cells. And the reason the multinucleated giant cells
are there is because there’s foreign material. Each of them you can see there they’re ingesting
little fragments of pink stuff. So that’s dead keratin material. So keratin is great on the surface of our
skin, but once it gets down in our dermis or deeper tissues, the body does not tend
to like it very much and the immune system is activated against that and usually forms
this really intense foreign body granulomatous response to try to remove the keratin. So each of these little spaces here these
are from where keratin, so that’s kind of washed out or fallen out during processing
in cutting, but these are each multinucleated giant cells, and which are basically a form
of histiocytes or macrophage, and they’re trying to clean up this keratin debris. And that’s just a really extensive exuberant
of foreign body reaction to keratin. So usually when you see this it’s because
there’s been a ruptured cyst or hair follicle nearby. This is a pretty exuberant example of a granulomatous,
or we can call this a keratin granuloma if you wanna have a name to give it. And here in the middle, this dead stuff, this
isn’t necrotic tumor anything worrisome like that, instead see all these little flaky things,
those are all dead keratin flakes, just like you’d see on the surface of the skin. So again this is what you would see in the
middle of a follicular cyst or what people sometimes call epidermal inclusion cyst or
surgeons call incorrectly a sebaceous cyst. So I am not trying to point out the surgeons
but I think they’re the only people that I see ever say, “Oh it’s a sebaceous cyst.” It’s not actually anything to do with sebaceous
glands. So all of this is histiocytes and look, ah
there we go, we look around you can find here is the cyst. And the cyst is lined by a stratified layer
of squamous epithelium just like the skin surface. You know if you didn’t know any better, I
can tell you that this is the top of a skin biopsy but it’s actually down deep in the
dermis here. So this is stratified squamous epithelium,
it’s benign. It’s got nice loose flaky keratin over the
top of it and so that keratin in the middle of the cyst, you can see it better for low
power, all that stuff in the middle, if the cyst ruptures, it spills out into the dermis
and surrounding tissue and that creates this really robust host response. So keratin granuloma from a ruptured cyst. So at first glance you can think that this
is another example of a ruptured cyst, so much flaky keratin here and detached fragments
of dead keratin, but there’s actually some tissue here. And this is really a big shave biopsy of a
large scaly thickened area. And so from low power, when I see something
like this with the epidermis really pushing way down and kind of sending little extensions
down into the dermis, that really worries me for squamous cell carcinoma. But you always have to be really careful because
reactive squamous epithelial changes, what we call pseudoepitheliomatous hyperplasia,
that those kinds of reactive changes the epidermis can be seen in a variety of conditions and
they can really closely mimic squamous cell carcinoma. So there’s a tendency to sometimes overdiagnose
as a squamous carcinoma. You can see those changes in the setting of
different inflammatory conditions or reactive conditions and you can also see it in the
setting of some infections like leishmaniasis, blastomycosis, these other types of deep fungal
infections have a tendency to get reactive epidermal changes. And a variety of other things too of course. And when we look closer, you can see actually
this is indeed a reaction to something. And right here, look there’s pigment in the
dermis. And I want you to pay close attention to the
color of this pigment. This pigment is not brown, it’s black. So although melanocytic lesions and a lot
of other things in the skin surface look black to the naked eye, when you go microscopically
you’ll find that there are always some shade of brown or yellow or orange. Our bodies can make a variety of different
pigment colors, particularly brown, which is what melanin is, and it can make some different
variations of reddish orange color, but our body cannot make black pigment. If you find black, truly black pigment, somewhere
in the body, it is almost always from outside the body. I can’t think of any instance where it’s from
inside the body. There’s a variety of different things you
know that you can see this from. You can see from amalgam from dental fillings
that happens to get down implanted in the gums or the oral mucosa. You see this black stuff in the lungs which
is carbon, that’s from breathing in pollutants in the air, particularly if you live in big
cities, but almost all of us have a little bit in our lungs. You can see it from different types of metal
that gets deposited in the skin. Some people drink colloidal silver because
they believe it has magical health properties and I would advise against that. It’s probably not a good idea because what
it’ll do is turn your skin blue looking because it will put black pigment in there that makes
the skin look blue to the naked eye. But this is none of those things. This is something much more common, and this
is actually tattoo pigment. So this pigment was put here on purpose. That’s black tattoo pigment. And then you can see there’s a really robust
brisk inflammatory response, lots of lymphocytes and histiocytes and dilated blood vessels. So this granulation tissue here and scar formation. Really the body is very unhappy with the tattoo
pigments in this particular case. And if I can find it, ah here it is, this
is not just a black tattoo, this is a multi color tattoo. And this is red tattoo pigment and this really
bright red. It’s kind of granular under the microscope. It’s hard to get that to show up on a video,
I’m gonna try to, you can kind of see it through refractile and red. So that’s red tattoo pigments and red tattoo
pigment tends to be the one that is most likely to cause an allergic response to the tattoo
or an immune response to the tattoo. It doesn’t do that for everyone of course
but it is the most common offender. And red tattoo pigments are often made from
cinnabar, which is kind of the ore that mercury is made from. So it’s different from metallic mercury
but is related to mercuric compounds. But in any case, it tends to stimulate the
immune system a lot in some people. And in the clinical history was that this
patient had a tattoo and it was the red areas the tattoo in particular that were getting
really inflamed and they were getting thick and scaly because the epidermis was over growing
and reacting to the underlying dermal inflammatory change. So I don’t see this very often, but from time
to time we’ll see really extensive tattoo reactions and sometimes they can, I mean really,
they can mimic a squamous cancer. I’ve seen one that had really abundant lymphocytes
going into the epidermis that looked like mycosis fungoides. And obviously with the history it’s real easy
to avoid those problems or those misdiagnoses, but keep your eye out for tattoo pigment. That’s a black tattoo looks like and red tattoo. And this case is a particularly exuberant
example of a tattoo reaction. So I’m not saying you can’t get a tattoo,
that’s between you and your doctor and your tattoo artist but do keep in mind that occasionally
they have side effects. All right. Here’s a nice example of a seborrheic keratosis. There’s kind of this thickening of the epidermis. And it’s covered by orthokeratin, not parakeratosis,
and you could draw a kind of a line right underneath it, or run a string underneath
it from end to the other. It has a very flattened bottom that’s a helpful
clue for seborrheic keratosis. I cover the features more in one of my other
videos and you tend to see these little horn pseudo cysts. There’s another one over here. Those are nice clues for seborrehic keratosis. So no problem right. Well you can see that they’re someone’s used
the marker at point out something on the slide. So that’s always a good clue. Unfortunately slides do not come to us in
the pathology lab prelabeled like this, and we have to still look at them without any
marks and coming to show us where the cancer is. But here’s a really subtle example of a tiny
little superficial basal cell carcinoma. It’s kind of hitchhiking right underneath
this seborrheic keratosis. Now this is probably just an incidental finding
and it’s probably been cured just by this shave biopsy. I imagine this won’t cause any problems for
the patient but it’s an important point to remember that just because you find one diagnosis
on a slide doesn’t mean that you should stop looking. I always try to keep my eyes open for subtle
melanoma in situ at the edge of a basal cell carcinoma biopsy or little areas of basal
cell carcinoma in biopsies or excisions for other things. But you can see the cells have a little bit
more atypia, kind of a basaloid appearance. Some palisading around the edges. And they’ve got that clefting artifact and
that kind of loose mucinous stroma underneath. So basal cell carcinoma kind of hitching a
ride underneath a big benign seborrheic keratosis. Right here is something else that looks a
little bit like a seborrheic keratosis and may in fact be related depending on your point
of view. This is a solitary lesion from the face and
it’s a shave biopsy. And you can see that it’s got that pink appearance
that’s kind of like a seborrheic keratosis, made of pink keratinocytes. You can see some areas that look like horns
pseudocysts that are filled with orthokeratin. But this lesion instead of having kind of
the flat bottom that most seborrheic keratoses have, it really pushes down. You can see that it’s kind of pushing down
with a kind of copper bowl shape. Here you can see it again, and pushed up and
above the epidermis but also is kind of bulging down into the dermis. And although the first part that we saw over
there was that was kind of cut across the bottom, you can actually see the base of the
lesion here on this a section. It looks like it’s got a smooth border and
no infiltrative growth, so that’s helpful. And when you look closer, some of the spaces
are artifacts unfortunately, but when you look at closer here what you find is this
really unusual pattern. The keratinocytes are making these little
tiny whirled balls. You can see that each individual keratinocyte
cluster, they’re kind of swirled together in these little balls or whirls and these
are called squamous eddies. And you can see these in irritated seborrheic
keratoses but when you see something that looks like a seb and it’s pushing down into
the dermis with kind of a cup shaped or bowl shaped kind of a high profile and then it
has lots of these squamous eddies, the other thing you can think of is what’s called an
inverted follicular keratosis. And the reason it’s called that is it tends
to be centered on hair follicles and I think that’s probably what we’re seeing right here
is a portion of the follicle that’s kind of been replaced by this tumor. Or maybe even here, maybe there’s kind of
more than one branch of the follicle that’s got this tumor growing. And these are benign tumors and the biggest
problem I think with them is that occasionally they can get some reactive atypia and oftentimes
on a shave biopsy they’re transected at the bottom, you can’t see the base. So in old sun damage person, I always worry
a little that could this maybe be a squamous carcinoma. And if I’m uncertain and I feel this kind
of some atypia there I might occasionally say, “Well keep an eye on the patient and
if it grows back, then you need to go biopsy yet again,” or if I’m really worried I’ll
tell him I just really can’t tell and please do a small reexcision. So that’s how I handle that issue. Everyone has their own way of addressing atypia
and uncertainty when we run into them in dermpath. But I try to be as definitive as I can but
sometimes we just can’t know if we can’t see the whole lesion. But these are really pretty. I really like these kind of squamous whirls
and eddies. And I think that’s a very very beautiful pattern
that you can see where the squamous cells come to swirl around. And they could get confused potentially I
guess with keratin pearls that you often see in squamous cell carcinoma. The biggest difference is that here these
little whirls and balls are in the middle of the tumor itself. They’re kind of up in the epidermis or in
the protrusion of the tumor from the epidermis whereas keratin pearls and squamous cell carcinoma
usually are kind of individual invading nests of keratinocytes down in the dermis, kind
of separate from the main tumor mass. But again look at that, you can just see each
one of these. Each one of these little discreet swirls or
whirls were eddies of keratinocytes. So again from low power kind of looks like
a seb but growing down often centered on a kind of a follicular opening here, and has
this little squamous eddies. Inverted follicular keratosis or IFK as we
often abbreviate it. We like to abbreviate names in dermpath. All right. Now this is another biopsy from a single lesion
on the face and it’s a little bit pale, I apologize but I think it’s a pretty good example. We can see here is that there are zones of
very pale almost clear cells that are filling up the whole epidermis. And kind of pushing down hair follicles and
down the sweat ducts and other adnexal structures. So these clear pale cells, we have to figure
out what they are. They’re not normal. Let’s look up here. And then in addition to them filling up the
whole epidermis, in some places they also have this tendency to scatter and spread upwards
towards the skin surface. So we refer to that as padgetoid spread and
the reason for that is that it’s similar to what we see in Paget’s disease of the nipple,
which is breast cancer that grows up through the epithelium of the ducts and out on the
skin surface the nipple. And it’s actually intraepithelial cancer and
you can also see Paget’s disease in the skin away from the nipple and that’s usually in
the genital or anal genital regions. We call that extra mammary Paget’s. So other things that have that same scattered
you know single scattered atypical cells that are spreading up in the epidermis, there are
3 main things and a few others. But the 3 main things are Paget’s disease
whether of the nipple or extra mammary, looks pretty much the same. Number 2 melanoma, melanoma often has pagetoid
spread of melanocytes. And then number 3, squamous cell carcinoma. And so we see these things a lot where we
have biopsy with pagetoid spread. By far the most common thing I see pagetoid
spread in is actually squamous cell carcinoma but a lot of people forget this. They focus on Paget’s and melanoma, but
squamous cell carcinoma at least in my patient population of older white patients who’ve
been sun damage, many of them we see squamous cell carcinoma so much more commonly even
though we do see quite a bit of melanoma actually. So when you have pagetoid things you can do
immunostains to try to sort them out. So you could use something like melan A or
MART1 or SOX10, which are melanocytic markers to look and see if these are melanocytes. You could use a stain like cytokeratin 7,
which is a low molecular weight keratin that usually is negative in most squams and strongly
positive in Paget’s disease. And then if you’ve ruled those things out,
what you’re left with is squamous cell carcinoma. p63 is a good marker for squam if you want
to use something or p40. But here’s an easy clue to find that you are
probably dealing with squam, if you have the full thickness of the epidermis filled by
atypical cells, that’s almost always, not always, but almost always, going to be squamous
cell carcinoma in situ. So if I just see an area with pagetoid spread,
I often have to do immunostains. If I’m in the genitals or the nipple, or
if I had any doubt about melanoma, then those are times where I’m going to do immunostains,
probably regardless just to be sure. But here, you can see really nice example
of squamous cell carcinoma in situ with pagetoid spread. And notably, this is an example of that has
really prominent clear cell change. So these are probably glycogen filled squamous
cells and we can see that sometimes that squamous cell carcinoma can become clear cell. So you can also see clear change in basal
cell carcinoma and a wide variety of other tumors. And this tumor is not actually limited only
to the epidermis, which would make it in situ, but if you look down underneath, you can see
all these areas are islands of invading tumor, it’s invading the dermis. Quite sneaky here because the tumor is so
pale, it would be easy to overlook this and just think it’s all reactive stuff. Anytime you see spindle cells and a little
bit of mucin and some inflammatory response underneath an in situ tumor, always look closely
to make sure that you’re not dealing with invasion. So this kind of stuff around here is a kind
of desmoplastic response by the body against these invading cancer cells. And see there’s little island of cancer here. This is cancer here. Some cancer here involving a sebaceous glands,
so it can be very very tricky to see. And if you have any problems with it, you
can do a keratin or again a P-63 or P- 40 to look for the invasive, subtle invasive
component in a squamous cell carcinoma like this. So again a beautiful example of clear cell
squamous cell carcinoma. This is the in situ area. We just saw the invasive area. And then again, this also has some cells with
that upward scatter so what we call pagetoid spread. So a nice example of several different features
here in this unusual pattern of squamous cell carcinoma. Right. It’s kind of an oddity but it’s something
I like. Now this is on the scalp and this is from
a patient with a nevus sebaceus. So they have this kind of greasy yellowish
hairless plaque on their scalp since childhood. It’s gotten bigger over time and nevus sebaceus
is kind of a benign hamartomatous process but sometimes a variety of different tumors
can grow in the middle of it, particularly skin adnexal tumors like hair follicle or
sweat gland tumors. And so this right here is an area that started
to grow and eventually kind of crusted and started to bleed. So they were worried that maybe there is cancer
rising in here or something. So they went and did a biopsy and here what
you see is on the outside you can see this epidermal acanthosis thickening, that’s probably
partially reactive change and partially the background nevus sebaceous. But here in the middle, you can see that the
color changes to a darker purple, and we have something else going on. There are these little branching spaces that
are kind of pushing their way down into the dermis. And when you go closer, you can tell that
what the spaces actually are is ducts. So see here and in these areas, they’ve become
very similar to sweat ducts. They have a lumen, an empty space in the middle
that actually has a little bit of pink sweat secretion in it. So these are sweat ducts here. And they are lined by a double layer of cuboidal
to columnar cells. So there’s kind of an outer basal or myoepithelial
layer, and then an inner apical layer, and then there’s that secretion in the lumen. So that’s what, when they get kind of compressed
at the base, they look like sweat ducts. But as they go up, you can see that they become
dilated and they kind of branch and they eventually empty all the way out on to the skin surface. See there’s the surface of the skin and then
there’s a bunch of scale and crust, then kind of debris up there. So these dilated kind of frond like branching
spaces that are lined by a double layer of cuboidal to columnar epithelium, are of sweat
duct derivation. That’s one feature and when you have these
branching spaces, what happens is in the middle you get little islands, little finger like
projections of tissue, they get kind of caught in the middle. And we cut through it, it looks like they’re
little stranded islands. They’re actually like little papillary structures
but papillae when you cut through them on a tissue section they end up looking like
little islands. So these little islands are papillary structures
here are stranded in the middle of these cleft like, or these frond like branching spaces,
and in the middle of the island, this is basically the dermis. Little islands of dermis caught in middle
of these papillary structures. You can see that there’s a bunch of inflammatory
cells and particularly the cells are, let’s see if I can get in focus, plasma cells. They have a very kind of amphiphilic bluish
purple cytoplasm. They have that very speckled kind of clock
like or cart wheeling, there’s a lot of different names for it, chromatin pattern. They’re like little purple blobs here, each
nucleus, it’s hard to get it in focus on this power I apologize. We’ll go up maybe a 40 X. See here you can see the chromatin better
here. So those little speckles or people think they
look like the numbers on the face of a clock, those are characteristic of the chromatin
pattern of plasma cells. And then the other thing that you’ll see in
plasma cells, if we get a good section, is that they tend to have this little pale nodule
or this little pale area right next to the nucleus, and that’s called the perinuclear
hof. And it’s a golgi apparatus that is needed
to transport all of immunoglobulins a plasma cells is making out into the body so that
it can be released into the circulation. So anyway there’s tons of plasma cells here
in the middle of these islands. And so you have those frond like spaces, double
cuboidal lining, and a bunch of plasma cells. This is called syringocystadenoma papilliferum. That’s a long name so we call it SCAP. S-C-A-P. SCAP is an easier way if you don’t mind using
abbreviation but syringocystadenoma papilliferum is a benign sweat gland proliferation that
often arises in the scalp in the middle of a nevus sebaceous. So kind of a cool pattern and an interesting
thing to know about. Now here is a biopsy. This is a child who has a multiple hyper pigmented
papules on their trunk and they’re very itchy. And so the dermatologist did a biopsy here,
and there’s a little keratin granuloma down here from a ruptured follicle, that’s incidental. But what we’re most interested is that the
dermis here is not normal, it’s filled with some type of cell. So get it closer to see what kind of cells
these are. And they’re kind of oval to spindle shaped
cells and their mixed in with a lot of pink collagen. And you can see that they’re totally within
the dermis, they do not involve the epidermis at all. And mixed in between these kind of oval to
spindle cells, see here’s these kind of oval to spindle cells. And then there’s also a bunch of bright pink
or orange eosinophils scattered in there. Right. So whenever we see an infiltrate in the dermis,
and eosinophils and it’s a child, we always think about Langerhans cell histiocytosis. That’s one thing. The one difference is that Langerhans histiocytosis
is that usually is going to involve the epidermis. It’s going to get up into the epidermis because
Langerhans cells normally live in the epidermis. They’re built to get into the epidermis. But this infiltrate is filling up the dermis
and not involving epidermis. And then when you look closer at the cytoplasm
of the cells what you can see is they have a very finely granular texture to them. It can be a little hard to appreciate on video
but let’s see if we can get it to show up. So they have this kind of slightly bluish
cytoplasm that is falling apart there and has kind of a granular nature to it. So I think when I see cells like that, I always
think about mast cells. They have these bluish purplish granules in
their cytoplasm. So mastocytosis is also something that can
occur in children and it can make multiple itchy papules like we just described. And so what we did is some stains to make
sure. So the one stain that you can do for mast
cells is a CD117 or c-kit. Now word of caution c-kit will stain mast
cells beautifully but it’s not specific. It will stain a lot of things, melanocytes
and lots of other things can be positive for c-kit. And here is a beautiful example their strong
diffuse staining of all of these mast cells in the dermis. Beautiful. Very nice. You can also use mast cell tryptase which
is a little bit more specific, so that works pretty well too. Or you can even use a giemsa stain which highlight
them. But wait what about these on CK7 positive
cells up here in the epidermis? We said that there were no cells in the epidermis. See these are background melanocytes, normal
melanocytes better in the background of the skin. So again remember the normal melanocytes and
a lot of melanocytic lesions will express CD 117, so be careful. But here we have diffuse strong staining of
the dermal cells for CD 117. And we also did a CD1a and an S-100 protein
which are stains for Langerhans cells. And you can see, sorry this section’s upside
down, these cells in the middle of the epidermis those are actually Langerhans cells there
and then the ones along the base of the epidermis those are melanocytes. So both expressed S-100. So we got a nice normal positive internal
control but the dermal cells are almost completely devoid of S-100 staining with the exception
of scattered cells here and there. And those also represent Langerhans and other
dendritic cells in the background. But it’s totally normal to have a little scattered
staining in the dermis for almost anything actually. But the rest of the infiltrate all the cells
that are c-kit positive are negative on S-100, I’m sorry, that was actually CD1a. So I miss… No, no it was S-100. And then here we have CD1a. And that you can see beautifully does that
Basal layer. Basal layer melanocytes, the normal background
are not staining, but by the mid level cells in the epidermis, those are staining and those
are the Langerhans cells. So that’s S-100 listing Langerhans cells but
also melanocytes and some other things whereas CD1a pretty much only stains Langerhans cells
in the skin. That’s about the only thing that stains both
normal and neoplastic Langerhans cells. So it’s a real nice example of cutaneous mastocytosis. And the form that this child had with that
kind of an itchy hyper pigmented papules and nodules, that’s called urticaria pigmentosa. Just kind of a confusing name because it microscopically
doesn’t look anything like urticaria, but in any case that’s a nice example of that. And I usually let dermatologist make the clinical
distinction between the different subtypes of mastocytosis because they added the clinical
picture is much more important for classifying which type of mastocytosis it is. So let’s try our hand at one or two inflammatory
dermatoses here. So here’s a shave biopsy. It’s a very broad shave. And you see the epidermis normally would be
kind of like that but here the epidermis gets really thickened and it’s not the whole epidermis
that’s thickened, but just individual areas that’s thick. That’s thick. That’s thick. That’s thick. So we have these areas of really marked acanthosis. And then in between the epidermis is kind
of more or less normal in thickness. And on the surface there is a lot of thick
keratin and most of its orthokeratin, meaning it lacks nuclei. You see there’s a few little bits of nuclei
here and there, so a bit of parakeratosis but really it’s kind of this dense compact
orthokeratin. And look at these dilated blood vessels here. This is a clue to us that were probably on
the lower leg and that’s where we are. This is actually from the shin. Patient has these plaques that are very itchy
on the anterior shins. So these vessels are called stasis change. It’s just from our gravity related blood flow
pushing back down on the blood coming up the legs. And it makes this kind of a reactive proliferation
of capillaries. So we see that all the time, it’s kind of
a normal variation as people get older they get more and more stasis change. And so whenever you see that, this cluster
capillaries in the papillary dermis, useful clue even without being told that you’re probably
on the lower leg. Sometimes on exams, it’s really helpful to
be able to tell the clinical information by knowing there’s a background clues even if
you’re not given the information. And then also in real life it’s helpful
because sometimes you know the things get mislabeled and once you see, you realize,
“oh wait, this can’t be from the scalp, it has to be from the lower leg.” And then you go investigate and see what’s
going on and why the label switched up. So when we look down here at the base of these
are areas of acanthosis, we can see that there’s a band like infiltrate made of, a dense band
like infiltrate of lymphocytes, kind of hugging along the bottom of the epidermis. And its most predominantly noted at that the
tips of these acanthotic regions. And when we got even closer, we can see that
this is actually a lichenoid infiltrate, it’s not only a band of lymphocytes but it’s a
band of lymphocytes that’s kind of chewing up and destroying the basal layer. So normally there’s a real clean division
between the basal keratinocyte layer and the dermis and that’s the basement membrane, but
here the basal keratinocytes and basement membrane are being destroyed by the lymphocytes. And what’s being left behind are these little
bubbles, these vacuoles. We call those of vacuolar change or liquefactive
change. And then little pink blobs which represent
dying keratinocytes. See there’s a little pink blob there. So you can call those cytoid bodies or Civatte
bodies, there’s a bunch of different names for them, but they basically represent dying
keratinocytes that are dying here because of the lymphocytes that are attacking the
basal layer. So again see dying keratinocyte, you can even
see its retained nucleus there, you can see all these vacuoles and you can tell that the
line between the dermis and epidermis is very blurred and difficult to distinguish. So that’s the definition of an interface change
and when there’s interface change with a thick band of lymphocytes, we call that lichenoid
interface dermatitis. So here on the anterior lower legs, itchy
plaques and papules and nodules that have a really thick acantholytic epidermis and
then a band-like lichenoid infiltrate underneath, this is called the hypertrophic variant of
lichen planus. So hypertrophic lichen planus is usually on
the lower legs and it usually has not only a lichenoid band but also these little kind
of skipping areas of really thick acanthosis. So that’s a really useful finding I think
that you go have acanthosis and then not that much acanthosis, and then there’s more acanthosis
and then it kind of skips. So I find that really helpful and that you
have interface change and lichenoid change that’s most prominent down at the tips of
these elongated acanthotic rete. And one other thing that’s a little different
in hypertrophic lichen planus that’s different from regular lichen planus is that you can
see eosinophils and plasma cells. Those are usually not very abundant in regular
lichen planus but we often see them in the setting of hypertrophic lichen planus. So there’s an eosinophil right there and there’s
a plasma cell, see its little pale perinuclear hof there. So that’s a really nice example of hypertrophic
lichen planus. Occasionally they can present as kind of solitary
lesions on the lower legs and not be as diffuse and rash like and will get biopsied because
that they can mimic a basal cell carcinoma or squamous carcinoma clinically. So real nice example of hypertrophic lichen
planus. And then, here’s a punch biopsy. And this is from the abdomen and this is an
area of kind of thin atrophic looking skin that’s kind of thin and papery. And what you can see is there’s a definite
abnormality here in the superficial layers of the dermis. The epidermis for one thing is atrophic. Now how do we know it’s atrophic? Atrophic means it’s thinned or decreased in
the number of cells present. Well you don’t have to go and count the layers
of the cells or anything like that. All you have to do is recognize that there
are no rete ridges. Normally they’re rete ridges in skin that
extend down from the epidermis. But here, the epidermis is totally flat with
an absence of rete. So when I see that, that means that the skin
is atrophic. Either because it’s been injured before like
a scar. Over scar you’ll see atrophy like that usually. Or because there’s some sort of the underlying
process that’s causing it to become atrophic. Here it’s the latter situation, where you
have an underlying inflammatory process. And what you can see is there’s this dense
band of really dense pink sclerotic hyalinized looking collagen. Look at that. Just totally smudgy pink, that’s what you
mean by hyalinized, it’s just kind of smudgy glassy looking pink that’s very homogeneous. And it’s not as easy to see down here in the
deeper dermis. You could see individual pink collagen bundles
up here, those collagen bundles are all smushed together. And if you flip the condenser you can kind
of see the collagen bundles better. There still are collagen bundles up here but
they’re packed really closely together and they’re hard to tell apart. Down here, you can see the normal reticular
dermis. And what divides this sclerotic zone at the
top that’s replace both the papillary dermis and the upper portions of the reticular dermis,
what divides that’s sclerotic zone from the more normal dermis down beneath is this band
of lymphocytes. So there are a lot of lymphocytes in here,
sometimes you can see some plasma cells as well and some histiocytes. There’s some histiocytes. And what’s happened here is that this process
started as an interface dermatitis up at the skin surface. Let’s see if I can show you. See, there are still some little vacuoles. So kind of like lichenoid change I just showed
you in hypertrophic lichen planus, this started as a lichenoid process early on but what happened
then unlike lichen planus, this process of the inflammatory change moved away from the
epidermis. And kind of burned its way down through the
dermis. Kind of like you know destroying the dermis
as it went. So the inflammatory change started up here
and you can still see the little vacuoles that are left over from where it started. And as it pushed its way down, it left kind
of a wasteland of hyalinized sclerotic collagen behind it as it marched further and further
south into the dermis. And so this is called lichen sclerosus. And in the older days, people often called
it lichen sclerosus et atrophicus or LSA. We often just call it lichen sclerosus now
and it’s one of those many diseases in dermatology that has the lichen name and this can be quite
confusing because they don’t always show a lichenoid change microscopically. But anyway this is one that often does start
lichenoid. By the time it’s biopsied, usually the lichenoid
infiltrate is much much deeper down but it’s left this very distinct band of pink collagen. So the most commonplace to see this is in
the genital region and particularly of women, but you can also see it on the penis where
it’s called out balanitis xerotica obliterans is the fancy name for it there. And then you can also see it in extra genital
sites like in this case which is on the abdomen. So this is lichen sclerosus et atrophicus
and it can be kind of a problematic and uncomfortable disease to have particularly when it’s in
the genitals, but it’s an inflammatory process and it has a very distinct look. Once you’ve seen it a few times and recognize
that band of pink collagen, you’ll remember it forever. So those were some basic random dermatology
cases and I hope you enjoyed.

14 Replies to “Basic Dermpath Cases 2 – Explained by a Dermatopathologist”

  1. Thank you very much, excellent teaching, could you please kindly show some clinical dermatology photos and some DD in each case as well. And also if you could consider creating systematic lecture series in dermatopathology that would be very useful for people setting dermatopathology exams.

  2. hi – old school dermatopathologist here (using for some CPD). I’m watching, writing down answers on first view and seeing if we agree (pretty good so far 😂). Looking forward to doing the 100 Board Case one! Thanks for doing these – the histology is really well demonstrated. (Think your lab does good tech work👍) Thanks again.

  3. Dermatopathy is the window of health in a patient yet all too submerged as in hidden or arcane. Auzgezeichnet, Arst Gardner. Ich mag viele dein Metier!

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