Basic Dermpath Cases  – Explained by a Dermatopathologist

Basic Dermpath Cases – Explained by a Dermatopathologist

Right today we’re going to talk about some
random Dermpath cases that I came across recently. These are kind of bread and butter cases,
what you might see in a normal day of sign out of skin biopsies at the microscope. So the first case that we have here this is
a seborrheic keratosis. These are kind of benign keratinocyte proliferations
that usually occur in older people and have this kind of stuck on appearance. Usually they’re dark in color. And microscopically there’s a variety of different
patterns you can see. This was kind of an acanthotic pattern. The epidermis is really thick. Look here’s the normal epidermis. You can see the thickness of it right there. And then here’s the lesion, look at how thick
and how elongated the rete ridges are there, really thick and fat and filled with cells. And the rete ridges all kind of interconnect
together as they come down. Let’s find our arrow here. See they come down, kind of interconnect and
kind of spread along merging with each other. And what is left behind are these cystic spaces
that are filled with usually with loose orthokeratin. So this is dead keratin like you would have
up here in the corneal layer. It’s the same stuff that you have it’s accumulating
down here. And these are not really cysts, these are
pseudocysts because if you cut deep but of what will happen is these cysts actually connect
up to the surface. So this is kind of a funny artifact of the
way we cut through and section the tissue. So these are called horn pseudocysts. So you get a thickening of the epidermis and
it’s made of these kind of small some people say basaloid, I don’t really like that term
personally because I think these look a quite a bit different basal cells, but they’re kind
of small keratinocytes, they’re usually very uniform and monotonous. And they often have pigment in them, and that’s
why these lesions look dark brown clinically. You can see that pigment there, that’s melanin
pigment. Now remember that melanocytes make melanin
and then kind of feed it to their neighboring keratinocytes. So just because he’s a brown and it doesn’t
mean that they’re actually melanocytes, it’s actually keratinocytes. And you can see this little halo that they
have. If you have a little halo with the naked nucleus
in the middle, that’s a good sign that you’re probably done the keratinocyte not a melanocyte. Alright, so this is a seborrheic keratosis. And these are benign sometimes they can clinically
look like melanoma or other melanocytic lesions. Here’s another cut from the same lesion, look,
again there’s a thickening of the epidermis and these horn pseudocysts that are filled
with that orthokeratin. Now if you start seeing a bunch of dense pink
keratin with retain nuclei, parakeratosis, in the middle of these pseudocysts, then you
have to stop and think about up the possibility of a subtle squamous cell carcinoma. Because squamous cells they tend to make little
keratin pearls but instead of it being loose orthokeratin like this, it usually has parakeratosis
in the middle. When seborrheic keratoses get inflamed or
irritated they can also make parakeratin down in those horn pseudocysts. So you don’t want to use that as a hard and
fast rule, but it is a thing that’s worth considering. And another thing I think is useful about
seborrheic keratosis, let me get in focus here, is that they usually kind of grow up
from the surface of the skin. They kind of push up. And that actually if you can kind of draw
a straight line across the bottom of the lesion, most the time. See if we go to the top piece, it gives you
the same thing. The lesion looks like it’s growing down, but
it’s actually not. It’s actually pushed up like a little dome
above the skin. And you can draw a straight line across the
bottom. So seborrheic keratosis usually do not infiltrate
down the skin, they kind of push up. See again the same thing on the third piece
here, you can draw a straight line underneath. So thickening, a thickened lesion that’s kind
of a rising for the epidermis, made of bland small keratinocytes, often with melanin pigment
and then horn pseudocysts. That’s a seborrheic keratosis. Let’s do the next case. We’ll make it right side up. This lesion is so big that we can’t actually
even put the whole thing underneath the microscope, but let’s look and see if we can figure out
what this says. It’s a lot bigger than the previous case and
all that bright red stuff, that’s keratin, just like the last case. It’s just a little more dense, that’s why
it looks so red and also I think this slide I may have just picked up some more of the
eosin stain. But look if you see the epidermis is thickened,
the rete ridges are really elongated and fusing together, and what you’re left with are these
horn pseudocysts again. These kind of pseudocystic areas in between. And look, when you get a certain cut here,
you can see those cysts aren’t really cysts at all. They open up to the surface, that’s why we
call them pseudo cysts. And here it almost looks a little bit warty. So you can sometimes think about a verruca
or a wart with this lesion. But look right here, you get kind of a straight
line across the bottom. I think this is another example of seborrheic
keratosis. This one is very irritated and inflamed. It’s got an area over here that you can see
is really thick. And has got a lot of lymphocytes, a lot of
inflammation. So sometimes these lesions get really inflamed
over time and when they do they can sometimes mimic squamous carcinoma clinically. And look at all that pigment there, this is
why they look so dark. Not only is the pigment in the keratinocytes,
which you can see up here, there’s pigment in keratinocytes, but there’s also these little
branchy thin dendritic cells. Dendritic means as little branches arms. Sorry just let me adjust the light a little
bit. And those are actually melanocytes, those
are pigmented melanocytes that are kind of dendritic, you can tell because of their little
branching processes. So melanocytes usually aren’t very darkly
pigmented, but sometimes they are. So there’s always exceptions to every rule
in dermatopathology, and sometimes dendritic melanocytes get caught up in the middle of
a seborrheic keratosis, and they further contribute to the dark color. And also when seborrheic keratosis s get inflamed,
they often will do this, they will drop melanin pigment out of the epidermis and into the
dermis, and then macrophages come and eat that up. And so those are called melanophages. So if you see real dark cells in the dermis,
usually they’re going to be melanophages, which are pigmented macrophages that are eating
up the melanin. Usually they’re not melanocytes. Again, exceptions exist for all these rules,
but that’s kind of a good rule of thumb if you see real dark cells in the dermis, most
the time they’re melanophages. So go back to lower power here again, even
in this area that’s more inflamed, you can see it’s a thickened lesion arising from the
epidermis. You got horn pseudocysts which are really
useful clue for low power. And again, when they look kind of darker blue
or purple, sometimes squamous cell carcinomas can have the same kind of pattern. So go a little closer and look, but I still
think of the cells here are very uniform and monotonous looking. And I think that’s good. And sometimes they can get a little bit of
atypia and some mitotic activity when a seborrheic keratosis is gets really inflamed. And you see when you get irritation or inflammation
in a seborrheic keratosis, sometimes the horn pseudocysts do begin to produce parakeratin. And so again I always look a little closer
when I see that just to make sure I’m not missing a squamous cell carcinoma, but in
this case I think what we have is just a very big robustly irritated and inflamed seborrheic
keratosis. This is a very large one. And I can imagine that if I had that on my
skin, I would want it to be removed as well. Probably very uncomfortable. All right. And these lesions don’t look really pretty
on someone’s skin but I think they’re actually quite beautiful under the microscope. And I guess that’s why I am a dermatopathologist. Alright, so here’s another case, and this
is just kind of a routine bread and butter dermpath case. Here we have again with the lowest power and
I still can’t fit the whole lesion under the scope, but you can see on this is kind of
a dome shaped lesion that protrudes from the skin. And the dermatologist said it was flesh colored
or skin color and kind of soft and fleshy to the touch. You could push it on it was not firm. And you can see this is normal dermal collagen
here, this kind of bright pink stuff. This is the type one collagen of the normal
dermis. And here’s a sebaceous gland and hair follicle. Here’s a sweat duct. And then over here you can see that that normal
dermal collagen goes away in the dermis changes color. It becomes more spindled, more cellular, and
it’s got a kind of lighter pink color. If we going closer look at the cells, we’ll
see these are not normal dermal fibroblasts. These cells look a little different. So these cells are bland cells that are kind
of thin and elongated, so we call those spindle cells. And some of them have kind of a kind of curved
or crooked nucleus like the nucleus is kind of elongated and it looks kind of bent or
buckled or curved. And these are schwann cells actually. They’re schwann cells and they’re mixed
together with some other cells like fibroblasts. And this is actually a neurofibroma and neurofibromas
have these bland spindle cells. They have really pale collagen that they produce. And they often will make a little bit of bluish
mucin or myxoid background which is hyaluronic acid. We don’t really see that in this case but
you can often find that. And this case particularly was a nice one
because a lot of times in neurofibromas you’ll see a background population of mast cells. Let me see if I can get them to show up here
on the video. Because I thought they were actually pretty
nice in this case. Adjust the lighting a little bit here. So this little guy right here in the middle
that looks like a little fried egg, that’s a mast cell. And you can’t really appreciate it on the
video, but it’s got a very kind of delicate granular cytoplasm. And I think that’s really helpful to detecting
mast cells. Here’s another mast cell here. Another mast cell down here. Mast cell there. So mast cells can be seen in lots of things,
but they are often kind of scattered throughout the background of neurofibroma. And again look at these nuclei, they’re
very bland. Some people say that Schwann cells are pointed
at one end and kind of blunt at the other end, that they look a little bit like a sesame
seed, like this little seeds that you get on a bun of a hamburger. And I kind of like that analogy. One of my mentors Mark Edgar taught me that
and I think that kind of works pretty well. So these bland Schwann cells, this kind of
fine light pink collagen background, sometimes with myxoid change, this is a neurofibroma. And the mast cells are nice little clue as
well. And I think this one and another feature that
was useful. Let’s see if I can find it now. No. Once you’re recording a video, then you’ll
never find it. So let’s see. Ah here we go. So right here in the middle the field, and
again let’s see if we can get it to come up and show up nicely, this little pink bundle
right here, that’s a little tiny nerve twig. And here’s another one. So there’s a little tiny nerves that are in
the middle of the neurofibroma. And that’s normal. Neurofibromas normally have nerve twigs in
them, where Schwannomas for example are made totally of Schwann cells and don’t have any
nerves. And so this is a little nerve here. That’s a little nerve here. That’s a little nerve here. And you can see a little touch of that light
kind of bluish color and that’s mucin hyaluronic acid. You often find that around normal nerves but
also in neurofibromas. I feel like it tends to get a little accumulation
around the nerves. And then here’s a little mast cell over there
too, which I can’t quite get in focus but I promise it’s there. Alright and that is a neurofibroma. And that people often sporadically get neurofibromas
and it’s of no worry or concern. Of course people with neurofibromatosis get
neurofibromas as well, and most important neurofibromas they get is a plexiform neurofibroma,
and usually those are deeper. You sometimes see them in the dermis, but
most of the time they’re going to be deeper in the subcutis or the deep soft tissue. So that is neurofibroma. And usually from low power you can recognize
these just from the fact that it’s this kind of pale color of pink and it’s a spindle cell
tumor that’s pale and filling up the dermis and kind of replacing the normal collagen. One kind of potential pitfall is that there’s
a sarcoma called dermatofibrosarcoma protuberans, DFSP. And you can have cells that look a good bit
like the cells of a neurofibroma, very bland, even though it’s a malignant tumor, it doesn’t
have atypical cells. It lacks the nuclear pleomorphism and atypia
that a lot of other sarcomas have. And it can look an awful like a neurofibroma. I think that tumor usually stains with a stain
called CD 34. And the pitfalls is that neurofibroma, a lot
of people don’t know this, but they also often stain strongly with CD34. So if you do a CD34, you could potentially
be confused. But if you used an S-100 protein, or Sox-
10, both of those are very good neural markers, and they will very nicely stain neurofibromas
and be totally negative in dermatofibrosarcoma protuberans. So that’s a little trick to make sure that
you don’t confuse neurofibroma with DFSP. Because neurofibromas sometimes can go down
and entrap… Sorry I’m getting out of focus a little
bit… Can sometimes entrap adipocytes like this
and that’s what DFSP does, so it’s an easy mistake to make if you’re not familiar with
that mimicry. And an S-100 stain will easily keep you out
of trouble if you have any doubts. And now here’s the area I think that even
better. I can see the mast cells already. There. See those little pinkish purple fried eggs
there. Makes me hungry for breakfast. So there are these little cells right here
you can see the little light pale granules, they are not the bright orange granules of
an eosinophile. These little fine granules they contain things
like histamine and that’s what mast cell do if they get activated, they release as granules
and it causes swelling and leakage of blood vessels and stuff. And that’s another mast cell. Another mast, and another one. So really really beautiful example of background
mast cell population that’s kind of scattered throughout a neurofibroma. And again look at the nice buckled or bent
nuclei. I really like that someone took a little spindle
cell and grabbed it and kind of twisted it into a little crooked bent shape and so that’s
a really nice feature when you see that little bent cell like that. That’s a really good feature to suggest that
you’re dealing with Schwann cells, and Schwann cells are one component of a neurofibroma. So there’s neurofibroma. So this case, here’s biopsy of skin and look
the dermis instead of being the pink color it’s supposed to be, is this blue gray color. The entire dermis has changed color and th
reason for that is that all of the normal collagen, or almost all of it, that used to
be here… Let me find a little area here… That’s the color that dermis should be, that
little bright pink color right there, type one collagen, but instead this dermis is totally
replaced with blue gray disorganized tangled up elastic fibers. So this is called solar elastosis and that
indicates that this person has probably been out in the sun all day everyday of the week
for many many years. It takes a long time to build up this much
solar elastosis. I mean the entire dermis is basically replaced
with it here. So this is probably an older person who’s
spent lots of time in the sun. And the clinical impression was that maybe
this had like a hard kind of nodule in the dermis, and they wondered if maybe there was
a foreign body, like maybe they had gotten you know cut on something and a little piece
of metal or glass or something broke into their skin. And I wonder if that might be the case. Right here the epidermis looks kind of thickened
and reactive. There’s some scarring and blood in the dermis
here. And so I thought maybe it was a foreign body
that was underneath the shave biopsy. And then I saw an extra piece here, and now
we actually can get to a diagnosis. So here there are some kind of blue, a little
basaloid cells in the outside. In the middle there’s pink keratin but this
keratin is kind of special. It doesn’t just look like loose flakes of
keratin. It actually looks like you can see the outline
of individual cells. Sometimes it’s hard, so let me put the condenser
back up so you can see. You can see like a shadow or a ghost outline
of dead keratinocytes. And those are the same kind of cells that
are here, those cells have kind of died off and converted into the sheets, of a ghost
or shadow cells, and these are very very characteristic, very useful clue to the diagnosis that we’re
gonna make here. The other thing you’ll often see in this
entity, see here’s more these kind of shadow or ghost cells. More of them still. And then the other thing that you’re gonna
see are these areas here, blue basaloid cells are very blue because they have nuclei but
little cytoplasm. And the blue basaloid cells are kind of converting
into these areas sheets of ghost cells. And this right here, this one picture, this
is diagnostic of pilomatricoma or pilomatrixoma. You could put either a “c” or an “x”
in that word, which ever you like. And pilomatricoma is a benign hair follicle
tumor. Sometimes it’s kind of cystic and it can be
hard and firm because it’s often calcified. So that explains clinically why it kind of
looked like a firm nodule that might have been a foreign body. But what you have is varying amounts of these
blue basaloid cells which are kind of what these are these are called matrical cells. They’re recapitulating or kind of imitating
the kind of cells that you see in the root, or bulb, of a normal hair follicle. And what normal hair follicle matrical cells
do is they turn from blue cells like this and kind of die off and become dead keratin. That dead keratin organizes into a hair shaft. That’s the normal process that happens in
hair follicles, and this tumor is trying to kind of recapitulate or imitate that process,
it’s just not doing a very good job at it. So instead what you get is blue matrical cells. And these cells are usually uniform, they
might a small nucleoli but they don’t usually have marked pleomorphism or atypical mitosis. They may however have quite a few normal looking
mitosis and I think that that sometimes because they’re blue and cellular and because they
often have a lot of mitotic activity in them. Mitosis can be very brisk here as well. There’s another one there. Because you can see so many mitoses, if you’re
not familiar with this tumor where you can get very scared and worry that it’s malignant. And there is a malignant form of this, but
it’s quite rare. And usually you’re going to have marked
atypia and really infiltrative growth which we can’t really see here because this is fragmented. And these are the sheets of kind of ghost
or shadow cells. So the blue basaloid cells and the ghost and
shadow dead keratinocytes are here, pilomatricoma. And this one has even got a little bonus. These little red things, these are called
trichohyalin granules and again that’s a finding that you see in the inner root sheath of a
normal hair follicle. So if you’re really into dermpath, you’ll
appreciate that. I think that’s cool and it makes me happy
when I see those at least. So really nice example pilomatricoma. These are most common in young kids, often
in the head and neck area, but they can be seen in people of all ages and even this person,
he was older totally find out pilomatricoma. I see them in older adults all the time. And anyway this a really nice example and
if I see the blue basaloid cells, and the metrical… I mean the shadow or ghost cells, that’s really
great but sometimes all you’ll see is kind of a granulomatous reaction and just some
fragments of these shadow or ghost cells. And for me personally I’m happy if I just
see some of these ghost cells, I’m happy to say that it’s suggestive of or consistent
with a pilomatricoma, because it is a very characteristic finding to see these shadow
or ghost cells. Very very unusual to see quite this pattern
and anything else really other than a pilomatricoma, or a couple of similar entities. Okay. Let’s go to the next case. Here’s a shave biopsy of a patient with itchy
bumps on their trunk. And I really like this entity. I think it’s really kind of nice, easy thing
to diagnose microscopically. It has very distinct features and it’s kind
of cool looking. So I will show it here. It’s a good example of what we call Grover’s
disease, or transient acantholytic dermatosis, which is why we call it Grover’s Disease
because that other name is too long for most people to use or remember. And Grover’s disease is a nice example of
2 different microscopic patterns. And it’s good because you either learn these
patterns in there some other diseases that have the same pattern. One thing that we see here is the normal epidermis… Get in focus. I apologize for the lighting issue. The normal epidermis, the rete ridge is a
kind of elongated but what you see starting to happen here is that the keratinocytes are
falling apart, they’re losing contact with their neighbors and leading white space in
between them. And they’re starting to kind of round up and
get this dense pink cytoplasm. That dense pink color so that’s called that’s
called acantholysis. Acantholysis means that the spiny layer of
the skin, the desmisomes are losing contact with one another and the cells are kind of
rounding up and balling up and down that’s what acantholysis is. And you can see here that the basal layer
is still stuck down here onto the dermis. But all of the cells above kind of detached
and broken loose. It’s almost similar to the pattern that you
see in pemphigus vulgaris, and in fact pemphigus vulgaris is another disease that does have
acantholysis. So here we have acantholysis and then we also
have another thing that’s happening up here, that is acantholytic cells, they’re breaking
free and they’re turning into… They’re dying and turning into these dense
bright pink little bodies that have dense purple dark nuclei. And this pattern is called dyskeratosis. It’s kind of a funny pattern of the cells
undergoing cell death and the nuclei get real crunched up and purple and the cytoplasm gets
really really bright pink. And so the acantholytic cells, they get called
two fancy names. If they’re long and thin, and look like parakeratosis,
people call them grains, like they look like a grain of wheat or something. And if they’re more round like this, people
call them Corps ronds which is the French word for round bodies. And so corps ronds and grains are these little
cells up here, and that’s dyskeratosis. So acantholysis plus dyskeratosis. And a patient that has little itchy bumps
or papules on their trunk is great for Grover’s disease. And there are a handful of other diseases
that have both acantholysis and dyskeratosis. The other one ‘s called Darier’s disease,
which is a genetic syndrome and has a different distribution, large plaques often on the trunk. And another disease is called Hailey Hailey
disease. Hailey Hailey disease has a lot of acantholysis
but doesn’t have as much dyskeratosis usually. And it usually involves kind of the fold areas,
like the groin, around the neck, or underneath the axilla. It’s also a genetic disease but has lots of
acantholysis. And then pemphigus can have acantholysis as
well, but it’s due to an autoimmune reaction, autoantibodies that are attacking the desmisome
spines in the spinous layer of epidermis. So that little combination, this little small
lesion acantholysis and dyskeratosis, beautiful example of Grover’s disease. Grover’s disease often gets inflamed. Often has some scattered eosinophils in the
dermis, under it and that is part of the reason probably that they’re in the kind of itchy. So if I see a little focus of inflammation
of the dermis within eosinophils, I’ll often look carefully in the epidermis or maybe cut
deeper levels to see if there’s a little papule of Grover’s disease there that I haven’t seen. Because sometimes they can clinically mimic
a cancer. Right. Here’s the next case. Well this is a really nice example. This tall lesion here has a lot of keratin
on top of it. So when you get piles of dead keratin on the
surface of a lesion, we call that a cutaneous horn, and clinically it looks a little horn
growing onto someone’s skin. So a handful of different entities can make
horns. Warts can, squamous cell carcinoma, actinic
keratosis. And the only way to really know what’s making
the horn is to do a biopsy and let us see what kind of living cells are underneath it
giving rise to the horn. So here you can see that that’s the skin
surface down here, and this lesion is growing straight up from the skin surface. Making a single papule. And on the surface it does look a lot like
a wart, and clinically they were thinking it was the wart on the face of a middle aged
patient. And it’s got these kind of elongated tips
here, fingers that are sticking out. So we call that papillomatosis. And on the tips of those we see parakeratosis,
little nuclei retained in the corneal layer, and other areas look more like orthokeratosis
without as many nuclei. So that’s good for a wart. There’s also some little foci of blood or
serum in the corneal layer. So those little hemorrhages we often see that
over top of warts. So a lot of things here to make you think
of warts, but when you actually get down to the base of the lesion, we see something interesting. We see this kind of smooth protruding bulging
border that’s pushing down into the dermis. It’s made of pale almost clear cells, and
these cells are pale because they contain glycogen, sugar that dissolves and washes
away during our routine processing, and leaves the cells looking like the kind of almost
empty. And then around the outer surface, the outer
layer of cells are kind of lining up in into a little row, we call that palisading, kind
of like the palisading you see in a basal cell carcinoma, just not quite so dramatic. So that little palisading around the outside,
and then these clear or pale cells in the middle the lesion bulging down, and then a
warty surface, all of those things come together for what we call a trichilemmoma. Trichilemmoma is a benign hair follicle tumor
that often looks a lot like a wart clinically, and in fact some people believe that these
really are a variation of warts. And there been some studies that show that
they have a human papilloma virus and other studies show that they don’t, so I think there’s
some debate over that. Some people believe their warts that are kind
of involving hair follicle and that’s why you’re seeing this area like here, is that
the glycogenated cells, this is basically mimicking the outer root sheath of a normal
hair follicle. So other people believe these are benign follicular
tumors. Whatever you believe, whatever you want to
call them, it’s good to recognize because occasionally these can get confused with other
cancers both clinically and microscopically. But I think finding that little palisading
and then the clear cell in this kind of bulging or pushing border is really useful. In patients who have multiple trichilemomma,
sometimes you see that in the setting of Cowden syndrome, which is a genetic syndrome that
involves the PTEN gene. So patients with multiple facial trichilemmomas
make you always think of Cowden syndrome. Cownden syndrome is associated with a variety
of internal cancers. So it’s a good syndrome to know about. When you just see one lesion, I don’t get
very worried about that personally. Alright here’s another little bump that was
on someone’s face. This was on the top I think of the nose and
they thought this is going to be a basal cell carcinoma may be clinically. A basal cell or maybe a wart, something like
that. And what you can see it as that the epidermis
is a little thickened here, and has a really thick purple granular layer. And the corneal layer is thickened and has
this little dense line of pink there. So when you get a really thick purple granular
layer in this kind of thick light or dark pink zone right over it, we call that lichenification. It means that someone has been scratching
or picking or rubbing at the at the skin, and the skin is growing thick and is starting
to look like that skin you see on the palms or soles, acral skin. And that’s kind of a defense mechanism the
skin making itself thicker to protect against the irritation. But the reason that this person is rubbing
or scratching at their skin is not because the problem’s the epidermis, the problem
is actually here in the dermis. The dermis has this dense dense pink collagen
and so there’s not much normal dermis here. But this is a very dense pink collagen deposition
in the dermis, and there are these dilated kind of branching looking blood vessels. And then if you go closer, you can see that
embedded in the collagen are these larger kind of hyper chromatic cells. Great example right here. They kind of large, they have a lot of cytoplasm,
and that kind of star shape or stellate or triangular shape, whatever name you like for
them. They kind of have multiple little branchey
arms stretching out. And some of them, right here even look, kind
of like a nice little triangle. See these very triangular or what we call
stellate cells. So dense collagen in the dermis, these kind
of stellate cells, these are actually kind of funny fibroblasts is what they are, and
then dilated vessels, those 3 things together are what we call an angiofibroma or fibrous
papule. These usually occur on the nose but can also
occur in other places and they clinically often mimic basal cell carcinoma, so really
important thing to recognize. These are common. You’ll see them on biopsies all the time. And this is a really beautiful example and
these little stellate cells sometimes can get kind of atypical looking and make people
worry for something atypical or malignant. And my mentor, Doug Parker, who taught me
dermpath and fellowship, he actually said that he thinks he’s all triangular shapes
look like that the little Star Trek insignia that all the people on the USS enterprise
wear on their uniforms, to show that they were part of the federation. And I thought that was cool. So if you’re a sci-fi nerd like me you might
like to remember that a Star Trek insignia. So I give that credit to Dr. Parker for teaching
me that and many other cool ways to remember derm path. So this is a fibrous papules and it’s totally
benign. The one time that it might be kind of important
is if you see a younger patient, like a child or teenager with multiple reddish brown lesions
on the face and on biopsy they all look kind of like this. In that setting, those are suggestive of tuberous
sclerosis. So the lesions that are called adenoma sebaceum
of tuberous sclerosis. They’re neither adenomas nor are they sebaceous,
so it’s kind of the total misnomer. What they are is they’re actually angiofibroma,
and patients with tuberous sclerosis get multiple angiofibromas on the face, and get a variety
of other cutaneous findings as well as neurologic issues. So I’m obviously don’t bring that up when
I have a solitary biopsy from an adult where there worry about a basal cell, but do keep
in mind that if you have multiple little papules like this in a child, you know maybe talk
to the dermatologist to make sure that there’s no other signs that would suggest a tuberous
sclerosis. Usually that’s pretty obvious clinically,
but that’s worth bringing up and it’s good for exams for our residents and medical students
to think of. Okay let’s do the next case. And this case was thought to be a basal cell
carcinoma on the nose. And in fact this is another example of a fibrous
papule, not quite so robust as that last case, it’s a little smaller and this is probably
what they look like more often. What you see here is there’s kind of some
dense dermal collagen centered around these couple of hair follicles. And you might say, “Well how do I know that’s
dense dermal collagen?” Well look, we have a nice trick here. Look at this patient. This is what this patient’s dermis looks like. Again, it’s almost completely replaced the
pink collagen and normally what you’d see is this pink collagen like up here but it’s
almost entirely replaced by this blue gray solar elastosis, but here in the middle that
elastosis is basically gone away. It’s been pushed out of the way by collagen. So in really badly sun damaged patients who
have a thick layer of solar elastosis, if you see a zone where suddenly the blue gray
elastosis goes away and is replaced with pink collagen, you should look at that area and
ask why is that collagen there? Is this damaged or biopsied or excoriated
previously and now it’s healed with scar? Is there a tumor nearby that’s producing desmoplastic
stroma? Or is there a fibrous lesion like a fibrous
papule? So it’s really useful you can see this pink
collagen in here and again look it over here we’ve got elastosis. Pink collagen, so you can tell there’s really
a lesion here, something has happened here because that. Go back here, back to elastosis. So that’s a really useful trick to use in
patients that have a lot of sun damage. So when there’s not solar elastosis, you can’t
really use that trick. And then look here, we have dense collagen. It’s kinda centered around follicles. And that’s often what you see in fibrous papules. We got dilated vessels. Let’s look closer. Kind of these dilated telangiec vessels of
blood and endothelial cells. Benign looking totally normal endothelium. So just dilated vessels, there’s a couple
more over here. And then in the dense stroma we got those
larger kind of funny fibroblast. Now these aren’t quite as stellate or is triangular
as we saw in the previous case, but it just goes to show there’s kind of a range of findings. It’s really nice when their big and stellate
and triangular or star shaped, but a lot of times they just kind of look like plump around
a spindle fibroblasts. Kinda scattered here in this dense collagenous
fibrotic stroma with these dilated vessels. And this is a little bump on the nose again,
so that’s the most common place you can see them in other locations, but the nose is by
far the most common site that I see them from. And again got a little bit of that hyper granulosa
as in that stratum lucidum there that indicates the patient’s probably rubbing, or kind of
picking or scratching at the lesion. And that’s probably because some irritation
change. So that’s another fibrous papules or angiofibroma
if you prefer. And this patient had a second biopsy and it
was also though to be basal and behold, it’s another fibrous papule. This one looks a little different than both
the previous two. It’s pedunculated like the first example
I showed you, but this was notable because it’s got very prominent to telangiec or angeic
dilated vessels here. So you first can even think of this as a hemiangiomas
or a little vascular malformation, cherry angiomas, but the thing that sets it apart
is it clinically looked like a little pink pearly bump like a basal cell. And unlike most capillary hemiangiomas or
cherry angiomas, whatever you are going to call them, there’s a lot more of a stromal
component in between the vessels. So you don’t just have dilated vessels like
you might have in a telangiectasia or a vascular lesion, but what you have here is that dense
collagen in the backgrounds. And in this case, you have again those kind
of plump stromal cells, the fibroblasts, that are embedded in there. Again, they’re kind of that some are spindled,
some are kind of oval shaped, none of them are quite as triangular as that first example,
but it’s a really nice example. And here I think you probably have a kind
of a funny cut of the endothelium. You’re cutting right up against the edge,
that’s what that stuff is filling the vessel, or alternatively could be histiocytes in the
vessel. You can see both those things. So usually a funny cut of a vessel wall can
sometimes make it look like there’s a bunch cells in there, but you’re actually just kind
of skimming against the backside of the lining of the vessel. And there’s a little inflammation here. There’s little small dark dots are lymphocytes
of course, and you can get inflammation in your fibrous papules. So there’s a nice example of another fibrous
papule here, kind of as we get to the edge of it. It’s a little less prominent and kinda looks
just like more less just like telangiectasias, but when you go on this area you can see the
fibrosis there, the larger kind of spindle fibroblasts in the background and the dilated
vessels centered around hair follicles making a little bump on the nose. Fibrous papule or angiofibroma. Okay. Look at the next case, we’ll shift gears here. And when you look at your tray of dermpath
slides that’s often what you’ll do. You’ll have to go from one type of lesion
to a totally different type of lesion and back and forth and you have to learn to be
able to shift the way you think out between cases. That’s I think to me part of the fun of dermpath
is that wide variety of things you see everyday. So this was a kind of fleshy pedunculated,
kind of raised lesion on a patient’s, I think it was somewhere on their scalp. And this lesion is a really nice example of
congenital pattern nevus. So this is an intradermal nevus or mostly
intradermal at least. And you can see this is raised, it was fleshy
and flesh colored clinically, and you can see there’s a bunch of increased cells here
the dermis. And so I know from low power you might say,
”Well I can’t tell those are melanocytes” but after you do enough dermpath or any pathology
for that matter usually from very low power, you can from the silhouette, Dr. Ackerman,
a famous dermatopathologist, liked to talk about the low power silhouette of lesions
and that that’s a really important clue to being able to figure out what the diagnosis
is by looking at the kind of overall shape of the lesion from low power. And I totally love that approach, that low
power look at the lesion and try to figure out what it might be and then you go down
to higher power to confirm it. So in this case, you can see, you know from
low power you might first pick up on these big sebaceous glands and you might think all
this is something to do with sebaceous glands but those are just actually kind of a reactive
increase in sebaceous glands that you sometimes see over top of nevi. And it is kind of long thin strands coming
down those are just elongated rete ridges or elongated portions of follicles. Again it’s a reactive epidermal change that
we sometimes see over nevi and over other entities like dermatofibroma. It’s a kind of related to what we call follicular
induction, it’s a kind of reactive process where hair follicles and skin surface grow
because of something in the dermis. So let’s look down a little closer and see
how we can prove this is a nevus. Well when you look at the cells up here that
are filling the superficial portion of the dermis, you can tell that they’re kind of
gray in color and they’re arranged in little clusters. We call those nests. When you see gray cells that are clump together
in nests in the dermis or epidermis, that means you’re probably dealing with a melanocytic
lesion. There are some other things that can nest
but in the skin when you see nests of cells like this, the first thing you should think
of is either nevus or in the right setting, maybe melanoma. We’re not gonna talk about melanoma today. It’s a bit too complicated for this video
and kind of requires some more time. But these nest cells , they’re melanocytes. Let’s look a little closer. They have kind of round or oval nuclei and
they sometimes will have small kind or punctate nuclei in the center of their
nucleus. And they have gray to pink cytoplasm. Sometimes you get a little bit of brown melanin
pigment, but a lot of times the cytoplasm is totally devoid of any visible pigments. And that might be kind of surprising if you
haven’t done dermpath yet to think well melanocytes make melanin pigment, why aren’t they pigmented. But oftentimes they’re not pigmented. They make their job, the job of a normal melanocyte
is to make pigment and feed it to the neighbor keratinocytes. So a lot of nevi don’t have a bunch of pigment
in them. And the other thing that you should know about
melanocytes is that sometimes they like to cluster together and make little multinucleated
cells. These can look at a similar multinucleated
giant cells but these are actually not histiocytes or giants cells, these are actually just clustered
melanocytes kind of fused together. The reason it’s important to know about those,
you often see those in benign nevi, particularly big congenital looking nevi. But from low power, sometimes those cells
can really catch your eye. They look really dark and big and so you might
think all it’s a pleomorphic atypical nucleus and you might inadvertently start thinking
that this is a malignant lesion because it looks big and dark from low power. But higher power, you can realize that it’s
actually just a bunch of nuclei all closely associated with one another. So these are nests of melanocytes. Okay. Now the next thing I’m going to show you
here, and again we can’t really give the full of spectrum of melanocytic lesions today,
but when you have a nevus, the typical feature of nevi, and you can see this really well
on these big thick nevi, the congenital pattern nevi, is that when you go from the top, you
start with large plump epithelioid melanocytes and a lot of cytoplasm and arranged in nests. And as you go deeper, the idea is that the
melanocytes get smaller. They have usually less cytoplasm, and they
tend to have smaller nests or even trickle out into little singles cells or even little
spindle elongated cells the deeper you go to the dermis. We call that pattern maturation. So let’s see we’re starting with these larger
nests up here. And as we get deeper look what happens. The cells are still there, but they’re a bit
smaller and now instead of them being in nests, they’re trickled out as little single cells
that are kind of scattering out into the dermis, and that’s perfect. In a lot of tumors, when you see little single
cell scattering out, you start thinking oh it’s infiltrating or invading that’s a bad
sign. Like for a lot of epithelial tumors but in
melanocytic lesions, this is totally a normal pattern. It’s a good pattern. It’s a reassuring pattern usually. When you see the cells get smaller and become
single and kind of trickle out into the dermis in between dermal collagen bundles or have
like little tiny nests, you go down and most of the cells there may still be some larger
cells here that a lot of cytoplasm, like these guys over here, but a lot of them are much
smaller than the cells that we’re looking at the top of the lesion. So getting smaller nests and smaller cells
as you go deeper that’s called maturation that’s a normal pattern in nevi, intradermal
nevi, and compound nevi. And also I will point out that often melanocytes
have these little vacuoles in the nucleus, they’re called nuclear pseudo inclusions. They’re not actually a full vacuole, what
they are is a little… Sorry I’m going to get it centered here… A little blob of cytoplasm. See how the color is kind of gray just like
the cytoplasm outside. What this is is like a little blob of cytoplasm
that’s pushed into the nucleus and then when we cut through the nucleus, it actually
looks like it’s a little bubble there but it actually is a bubble that connects back
out to the cytoplasm. Imagine if you take a baloon and push your
fist into it, it kind of invaginates into there, it makes a kind of a cup shape and
then if you were to take in 3 dimensions and cut right through that, what it would look
like is a circle in the middle of the balloon, but it’s actually not a full vacuole. So anyway these nuclear pseudo inclusions
you often see in melanocytic lesions both in nevi and also sometimes in melanoma. So they don’t always tell you that much by
themselves but I think it’s worth noting that they’re often there and if you see them and
you’re a beginner and you wonder what’s that cell, well now you know. Nuclear pseudo inclusions in melanocytes. Okay so this nevus is a normal benign looking
nevus and when nevi trickle way down deep into the dermis and track around sweat glands,
excuse me sweat ducts , or around hair follicles, or around blood vessels or nerves, we call
that a congenital pattern. Now that doesn’t mean that the nevus was definitely
there when the person was born, but when we see nevi in babies, in nevi that babies are
born with, we often see those features that the dermal melanocytes track way deeply in
the dermis and surround the normal structures. And to me that makes me think that this nevus
kind of grew along with the person’s skin embryologically. I don’t know if that’s exactly what happened,
I’m sure there are people that are skin biologist that understand in great detail the embryology
the skin, but the way I imagine in my mind and it makes it easier to remember is that
these melanocytes kind of grew up as the skin was developing in the baby so they’ll get
intermingled with all the normal skin structures. You can even see them kind of the infiltrating
into the middle of arrector pili muscles and an unusual things like that. And those are kind of signs that we often
see a congenital nevi. And I don’t think this case really shows it
but sometimes the cells, but others it shows a little bit I suppose, sometimes as you go
down deeper the shape of the cells changes from the round cells with cytoplasm or what
we call epithelioid looking melanocytes, to kind of more elongated spindle looking melanocytes. And they can become so spindled in fact that
they look very much like that neurofibroma we showed earlier in the video. And look ,there’s a little mast cell right
here. So actually you can get very spindled or what
we call neurotized nevi that look just like a neurofibroma. At high power they can be almost identical
actually. So again that’s why low power helps if you
see nests of melanocytes anywhere in the lesion, it’s probably a nevus and not a neurofibroma. Both are benign in their distinction or rarely
matter clinically, but I think its useful diagnostic pearl to know. So here again on low power, a nice example
of an intradermal nevus. From the scalp of patient. Alright. Let’s move on to a different case. And here is a red scaly growing lesion on
the skin of a sun damage patient. And it’s kind of cup shaped, or crater shaped,
and it looks like almost a little volcano with a bunch of pink keratin in coming out
of it. So whenever you see a cup shaped lesion with
a lot of keratin coming out of it in sun damaged skin on older patient, you always have to
think about squamous cell carcinoma. And there’s another entity called keratoacanthoma
which some people believe is benign and some people believe is a variant of squamous. I personally tend to regard it as a variant
of squamous cell carcinoma but that’s a more complicated and controversial topic than we’re
going to discuss here. But in any case I think that whatever you
see this cup shape kind of a lesion filled with keratin in sun damaged skin, always stop
think could be squamous cell carcinoma. Because if you look here, there’s not much
that’s very atypical, right? The surface looks actually kind of lichenified
and reactive. The patient’s probably been scratching, and
see that really thick band of purple keratohyalin granules, that’s the clue that’s been scratched
and rubbed. And there’s not much atypia in the cells. And as you go down look the nuclei don’t look
very bad at all in the cells, these are keratinocytes. How you know the keratinocyte, they’res
are coming off the epidermis, they have abundant bright pink cytoplasm. Look at high power, look which you can see. See all those spines, those are desmisomes,
desmisome spines that are holding the keratinocytes together. Really beautiful example here and those spines
and the dense pink cytoplasm characteristic of keratinocytes. Now look, these are keratinocyte nuclei that
have some nucleoli which is normal for keratinocytes and a lot of cytoplasm, they don’t really
look very ugly or very atypical, but they do have a bunch of pink cytoplasm. So when we see that really abundant dense
pink cytoplasm in keratinocytes, we say that they look kind of glassy. And when I see a proliferation of glassy keratinocytes
in sun damaged skin, oftentimes that ends up being squamous cell carcinoma. So I think it’s really important to recognize
that you’re looking kind of a different sort of feature where a lot of other tumors you
look for nuclear pleomorphism and atypia, and you can see that in squamous cell carcinoma
also, but to me I think you also have to look out for these very bland lesions that don’t
have much nuclear atypia, but at this real glassy cytoplasm. And also look at the growth pattern. This is really pushing down into the dermis
and look what happens at the bottom of the legion. It trickles out a little nest of invasion
that are invading into the dermis. So up top, when you have a superficial shaves
biopsy, these lesions are often very difficult to diagnose and that’s why I see kind of a
crater filled with keratin and if I can’t see the bottom or anything definitively to
make diagnosis of squamous, I’ll often put a comment in, “Hey this lesion has some
features that worry me that there might be a squamous cell carcinoma underneath” and
then the dermatologist can decide how worried they are. They can either go back and repeat biopsy
the lesion or do some additional work on the lesion or they can follow the patient closely
and see if the lesion goes away or comes back. So I like to at least alert the dermatologist
I have some concern that there could be a squamous cell carcinoma. This biopsy they were clearly worried about
it and they got a nice deep shave biopsy, and we can see that down at the bottom what
we have is more atypical cells. The nuclei are more atypical. And some mitotic activity in there, there’s
a mitosis here, which you can have mitosis and benign squamous lesions too. But this growth pattern, these really angulated
irregular nests invading the dermis with nuclear pleomorphism, and here look, this little nest
is making a little ball of keratin with some retain nuclei. So this is kind of what we call squamous pearls. They like to talk about that in med school
and this is a squamous pearl, not the best one maybe, but I think it works in invasive
squamous cell carcinoma. Here, this one might even be better. This is kind of a squamous pearl too, where
the keratinocytes are kind of getting glassy and making a little swirled nodule in the
middle of a nest. But look at this invasive kind of angulated
pattern. Again, I think from lower power it’s easier
to see the invasive trickling growth here and this is squamous cell carcinoma. But I think it’s important to point out that
the crater shaped keratin filled area and how on a shave biopsy that can easily be mistaken
for a cyst or something benign. See over here, it doesn’t really look that
atypical, but that pattern of kind of complex cystic growth glassy keratinocytes pushing
down into the sun damaged skin always worries me. Right away the first thing I think of squamous
cell carcinoma. And then look over here, I mean here, there’s
really not much at all to suggest squamous cell carcinoma. The epidermis is very reactive and very thickened
with a thick granular layer. This is actually very similar to what we call
prurigo nodule or lichen simplex chronicus, which are two kind of variations of the same
thing. Reactive thickening of the epidermis from
chronic scratching or picking, or rubbing of the skin. And this makes sense, we often see this change
right next squamous cell carcinomas are other skin cancers because the lesions are irritating
as they invade the dermis and then the patient feels pain or discomfort and so they scratch
or pick at the lesion. So we often, very often I would say, almost
always in fact, see reactive changes in the epidermis next to a squamous cell carcinoma. So that’s why it’s really important if you
got a big biopsy and you can’t really see all of it maybe do deeper levels. Look right here actually. If we look closer. It’s very focal but we can see the squamous
cell carcinoma, it’s right there. Let me get in focus here. There, see there’s a base of little islands
there. And there. So at the top, it doesn’t look like much. It looks very reactive and again that’s why
I’m always very careful with warty or prurigo nodule or seborrheic keratosis like lesions
that are kind of glassy, and where if the biopsy’s thin and I can’t see the bottom,
I always think will could there be a squamous that we’re not seeing underneath. Because I feel like we often see this ,particularly
in the sun damaged skin on the extremities. Squamous cell carcinomas often have that more
glassy look and are not the really wildly atypical things that we sometimes see on other
sites. On the lower leg, or on that hand, the dorsal
hand, or the distal arm, this is the kind of squamous cell carcinoma you often see. So this is bread and butter dermatopathologoy
what we look at every day. Let me show you another example. Here’s another one, it’s crater shaped, cup
shaped, in this view very similar to what a lot of people call keratoacanthoma because
it’s kind of got smoother borders and it’s got the glassy keratinocytes that’s pushing
down in. Sometimes lesions that had this kind of keratoacanthoma
look this cup shaped crater shape look that don’t have real marked atypia, some of them
progress on their own and that’s why there’s this belief that maybe they’re different than
squamous carcinoma, that they kind of regress and go away on their own. And while I’ve certainly see that happening,
I’ve seen other ones that look kind of like this, that do progress and still continue
to grow like a cancer. So I feel like to me it’s safest to usually
consider them as squamous cell carcinomas for the purpose of follow up and treatment. But again that’s just my opinion. There are other dermatopathologist that disagree
with that, so I’m going to admit you right now there are different schools of thought
and you can go and learn those schools and decide for yourself which school you want
to follow. And then over here you can see there’s kind
of more obvious islands of invasion, but again look at the pattern is invasive from low power,
which is what tells you that you’re dealing with the cancer. But look at the cells, they don’t have much
nuclear atypia, that they have that really dense glassy cytoplasm. Really abundant dense pink cytoplasm and you
got some parakeratin formation. So when you have little whorls or nodules
of parakeratosis, where the nuclei are retained in the keratin, way deep down in a pushing
or invading squamous lesion, that’s a really good clue that you’re probably dealing with
squamous cell carcinoma. It’s not a hard and fast rule, but it’s a
clue that when I see little nodules with nuclei retained, that means this lesion is probably
kind of growing quickly and did the kind of pattern of keratins and maturation is abnormal,
and it worries me that we’re dealing with an invasive squamous cell carcinoma, which
is exactly what we’re dealing with here. So most squamous cell carcinomas of the skin,
if they’re treated when they’re smaller, usually have a good prognosis and as long as they’re
treated appropriately, usually the patients do fine. But if you have squamous cell carcinoma on
the ear or the cutaneous lip, those have somewhat higher risk of giving rise to metastases. So you can have sometimes aggressive squamous
cell carcinomas of the skin but usually with appropriate treatment the progress is quite
good. All rights and let’s see another case here. Alright. Now here’s another lesion on sun damaged skin. And note that there is kind of glassy, pink
keratinocytes here. So you could think well maybe this is squamous
cell carcinoma. But in this case actually again at a high
power, it’s almost impossible to tell this apart from a squamous cell carcinoma. But when you go to lower power, the clue is
in the shape. Look at this lesion, it’s kind of mounding
up from the skin and you could take a line and draw a line directly underneath it, straight
underneath it. It’s got a straight, kind of flat bottom,
you can draw a line right under it. This is in fact a seborrheic keratosis. See, it doesn’t have well developed horn
pseudocysts, but these kind of little pockets full of keratin are kind of analogous to the
horn pseudocysts. They connect up to the surface and you can
see a few of them look kind of cyst like here. Alright. And look there’s this really brisk dense band
of inflammation here, these are all lymphocytes. And the lymphocytes are kind of attacking
the lesion, it makes the lesion looked more atypical when you see that. And look what’s happening if you get closer,
you can see there’s actually kind of a lichenoid pattern of inflammation, a dense band. And then there are little pink dying keratinocytes
in there, which are kind of similar to the cytoid bodies or apoptotic keratinocytes,
there’s lots of different words for this. But these are dying keratinocytes and these
little bubbles and vacuoles along the basal layer, those little bubbles right there, this
is called interface change. So we see that in lichen planus and in a lot
of inflammatory dermatosis, but you can see the exact same pattern of lichenoid inflammation
underneath keratinocytic lesions that are being attacked by the immune system, particularly
seborrheic keratoses and lentigos and other things like that. So here at lower power again the flat bottom
helps us and the fact that even though it looks kind of glassy, a little atypical down
at the base, if you look up at the top, the top looks nice and has a lot of orthokeratins
and it doesn’t have a lot of parakeratosis on it usually. And again, the overall shape of the lesion
is what tells you this is a seborrheic keratosis that’s inflamed, not a squamous cell carcinoma. Admittedly I still on an almost daily basis
struggle with lesions like this if they’re not biopsied deep enough and I sometimes have
trouble telling inflamed irritated wart and inflamed seborrheic keratoses and squamous
cell carcinoma apart. I’ve been doing dermpath for you know a few
years now and have been trained well, I think, but it’s still something that even though
it seems so basic it’s still ends up being difficult because the lesions get a lot of
features that overlap with each other. So that just takes a lot of practice but it’s
good to know that those lesions can be troublesome even for people who see lots and lots of skin
biopsies everyday. So this is an inflamed seborrheic keratosis. And then for the final lesion, this is something
that clinically was thought to be a skin cancer. It was red, irritated painful lesion and with
ulcer and crust on the surface. And see that thick layer of purple pink stuff,
that’s what scab looks like microscopically. It’s called scale crust. It’s a mixture of parakeratosis and serum
and neutrophils and probably some bacteria too. So this lesion doesn’t actually have anything
here that looks like squamous cell carcinoma, so clinically it was worrisome, but when we
look microscopically, we see there’s a big ulcer of the epidermis. So we have to wonder why is the ulcer there. Well it’s hard to say at first glance. The clue is down here in the dermis. There is an ulcer and there’s all that scale
crust like I said. There’s serum, the pink stuff, the little
dark things are degenerated neutrophils, these little purple blobs here actually cocci bacteria,
probably staph organisms that are staphylococcus that normally grow on the skin as flora, just
kind of colonizing this lesion. We often see that on the surface of ulcers
in the skin. But the key is in the dermis. In the dermis we have really dense lymphocytes
around the superficial vessels and also even around the deeper vessels, and not only do
we have lymphocytes, but we also have lots and lots of these bright orange little guys
with orange granules. These are eosinophils. So there are tons of eosinophils in here. We have a bunch of lymphocytes and then bunches
of eosinophils. And eosinophils aren’t just up at the top,
they get deep down into the dermis. I’m sorry. They get deep down the dermis, they gotta
go out away from the vessels in between the collagen. Let’s look at the other piece. Even away from the ulcer, you see the same
thing, eosinophils. So this is actually probably an exuberant
bug bite, a bug bite that got really inflamed and the patient scratched and itched at. And it ulcerated and then it got bacterially
infected, or impetiginized and it made it look even worse. And so when they came to the doctor, you know
they might not even remember that they got bit by a bug or even known it. All they know is they had this itchy painful
lesion they kept picking at and then it kept getting worse. And so they came and the dermatologist said
let’s make sure it’s not a skin cancer and biopsied it. And we see that often that a bug bite that’s
really exuberance can look a lot like a skin cancer clinically. So usually what I call these is arthropod
bite reaction. Some people like to say arthropod assault
reaction because that covers both bites and stings. I think that’s kind of a fun way to say it,
but I used to say arthropod bite reaction and it’s a good thing to know about because
we see a lot of them in my part of the country. We have lots of insects here and a lot of
times people get bug bites. And people that can particularly get really
inflamed exuberant bug bites are young kids around the age of 2. Their immune systems kind of still developing
and learning to react to different things, and sometimes they get really big really inflamed
bug bites. And also in older individuals with a chronic
lymphocytic leukemia, CLL, for some reason because their immune system is altered, they
also tend to get really exuberant bug bites. So those are some random basic dermpath cases,
and if you learn something new from every case, you’ll eventually be an expert.

4 thoughts on “Basic Dermpath Cases – Explained by a Dermatopathologist

  1. Medicine Gardner, bon travaille! Se fait la dermapathy très bien et extraordinairemente narrée. Vous devez devenir un bon maitre d'academie et je serai votre testimoigne…..

  2. Good list of cases. Once I start watching(sorry.. learning) your videos, I am not able to stop in-between right till the end. Kudos to you..

Leave a Reply

Your email address will not be published. Required fields are marked *