Chapter 28: Rashes & Skin Lesions Assessment

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Welcome back to the Deep Dive.

Today we are tackling a subject that is simultaneously the most visible part of medicine and paradoxically one of the most confusing.

Oh, for sure.

It literally covers us from head to toe.

It's the first thing you see when a patient walks in the room and yet for so many clinicians, especially those just starting out,

it can be incredibly intimidating.

We are talking of course about the skin.

It is the largest organ in the body and you are absolutely right about the intimidation factor.

There is this, I don't know, this misconception that dermatology is just cream and steroid medicine or that it's purely about vanity, but when you sit down with the source material, specifically chapter 28, rashes and skin lesions from the advanced health assessment and clinical diagnosis and primary care, you realize that the skin is this high fidelity dashboard for the entire body.

That is such a great way to put it, a dashboard, because it's not just about a pimple being a pimple.

It's about infections, immune responses, systemic diseases, environmental exposures.

The skin is basically a tattle -tail for what is going

Exactly.

Our mission today is to decode that dashboard.

We are going to follow the structure of chapter 28 very, very closely because it lays out a roadmap to move you from that panic of, oh my gosh, it's a red bump, what do I do, to a sophisticated clinical diagnosis.

We want to get you to the point where you can look at a rash and not just name it, but understand the mechanism behind it.

Before we start memorizing Latin names for bumps, let's zoom way out.

The text opens with a big picture,

the mechanisms of disease.

It categorizes dermatologic problems into four main buckets.

What are we dealing with here?

This is foundational.

It really is.

If you don't understand the mechanism, you're just memorizing pictures.

The text identifies four primary drivers.

First, you have inflammatory mechanism.

Okay.

Second, infectious mechanism.

Third, immunologic mechanisms.

And fourth, environmental factors, which includes things like trauma and exposures.

Okay.

Let's unpack those a bit because in the real world, biology is rarely that tidy.

These buckets have holes in them, right?

They leak into each other.

They absolutely do.

Real life is messy.

The text makes a point to say that these mechanisms often overlap.

Let's take a really common scenario.

An insect bite.

Simple.

Right.

Sounds simple.

A bug bites you.

That feels environmental.

It is environmental because it's an external exposure.

But what happens next?

Your body reacts to the saliva or the venom.

You get redness, swelling, maybe some heat.

That's inflammation.

That is an inflammatory response.

So you have a single lesion that is both environmental and inflammatory.

And if you scratch it with dirty fingernails and it gets full of bacteria.

Then you've added an infectious mechanism right on top of it.

So why do we bother distinguishing them if they're just going to mix together anyway?

What is the so what here?

The so what is about risk prediction?

It's about looking forward.

Identifying the dominant mechanism tells you about the patient's future, not just the present.

The text gives a fantastic example regarding eczema.

Eczema or atopic dermatitis is fundamentally an immunologic or atopic condition.

If you identify that mechanism in a child, you aren't just treating itchy skin.

You now know that this patient has an atopic constitution.

Which means they are at risk for other things in that same category.

Precisely.

They're at significantly higher risk for asthma and allergic rhinitis.

By understanding the mechanism immunologic, you're predicting what we call the atopic march.

You're treating the whole patient, not just the patch of skin.

That is a great perspective.

It elevates the diagnosis from skin deep to system wide.

Now the chapter lays out a very specific roadmap for how to work up a skin patient.

And this is where dermatology kind of goes rogue.

It breaks the standard rules of the physical exam, doesn't it?

It really does.

And almost every other body system, cardiac, respiratory, GI, the rule is rigid.

History first, exam second.

Yeah, that's drilled into us from day one.

You talk to the patient, you get their story, and then you touch them.

But chapter 28 says not so fast.

Right.

For the skin, the text suggests a brief physical assessment or an initial focused look before you dive into the history.

Why flip the script?

What's the advantage?

Because the vocabulary of the skin is visual.

It's a visual language.

If you start with the history, the patient might say, I have a rash.

Which could be literally a thousand different things.

Exactly.

It could be anything from hives to skin cancer.

But if you look first, even for just 10 seconds, you categorize the lesion.

You see blisters in a line.

Okay.

Now my history questions are super specific.

Did you have trigger pox as a kid?

Do you have burning pain?

Versus if you see a generalized red rash all over the back.

Exactly.

Then my question shift to, did you start a new medication?

Do you have a fever?

The visual anchors the history.

It makes you a much more efficient detective.

Okay.

So let's talk about that first glance.

This brings us to section one of our outline,

the initial focused physical examination.

And to do this, we have to speak the language.

We have to understand morphologic criteria.

This is the hurdle.

This is where students often get overwhelmed because it really does feel like learning a new language.

But if you break it down like the text does in table 28 .1, it's actually very logical.

It's like a decision tree.

The text lists a systematic analysis, location, distribution, primary versus secondary,

shape,

margins, pigmentation, texture, and size.

But the bread and butter, the starting point is the primary lesion.

Correct.

This is the lesion that pops up first, right?

Before the patient has scratched it or put cream on it or anything.

Right.

It's the lesion in its original unaltered state.

And the first fork in the road is simple.

Is it flat or is it raised?

Let's start with flat.

Imagine I'm closing my eyes and running my finger over the patient's skin.

Okay.

If you run your finger over the lesion and you cannot feel it, if the skin texture is completely normal and it's just a change in color, that is a flat lesion.

If it is small, specifically less than 1 .5 centimeters, we call it a macule.

A macule.

Like a freckle.

Is that a good example?

A freckle is the perfect example.

Or a flat mole, little brown spot.

And if it's bigger than 1 .5 centimeters, it's still flat.

I still can't feel it with my finger, but it's large.

Then it graduates to a patch.

Think of a cafe au lait spot or a Mongolian spot on a baby or the white areas you see in Vidaligo.

It's just a big macule.

Okay.

Easy enough.

Small flat macule,

big flat patch.

Now let's get 3D.

What if I can feel it?

Now we are in the world of raised lesions.

And again, there's a fork in the road.

Is it solid or is it filled with fluid?

Let's start with solid.

Okay.

If it is a solid bump raised above the skin surface and it's small less than 1 centimeter, that is a papule.

Give us a mental image.

A standard mole, a nevus that bumps out, a wart,

an acne pimple that doesn't have puss yet.

It's like a little braille dot on the skin.

And if that raised area gets bigger, specifically if it's larger than a centimeter and feels kind of flat on top, like a plateau.

That is a plaque.

Plaques are interesting because they are often formed by a bunch of papules merging together what we call confluence.

Okay.

The classic textbook example is psoriasis.

You have these raised red scaly areas that cover a large surface like the knee or elbow.

That's a plaque.

Okay.

What if the bump feels deeper?

Like it's not just sitting on top of the skin, but it's anchored down in the dermis.

That is a nodule.

It's firmer, deeper, and usually larger than a papule.

You can almost feel it more than you see it sometime.

And if it's really big?

Then we call it a tumor, which, you know, sounds scary, but in dermatology, it just means a large mass.

It doesn't automatically mean cancer.

Right.

Now we have to talk about fluids

because sometimes a bump isn't solid.

It's a bag of something.

This is a critical distinction.

If you have a raised lesion filled with clear, serious fluid and it's small, less than one centimeter, that is a vesicle.

Like a tiny blister.

Exactly.

Like what you see in herpes simplex or chickenpox, a little fluid -filled bubble.

If that blister is huge, like the size of a quarter or bigger?

That is a bulla.

You see these in severe burns or really bad contact dermatitis from poison ivy, or in some autoimmune blistering diseases like bullous pemphigoid.

And what if the fluid isn't clear?

What if it's cloudy, yellow, or green?

That changes the name to a pustule.

The fluid is purulent, which usually, though not always, implies an infection is present.

Think of a whitehead in acne.

That's a pustule.

There are two more specialty primary lesions the text defines.

One is the wheel.

A wheel is unique.

It's what we see in hives or urticaria.

It is a raised erythematous red area caused by edema or swelling in the skin.

The key feature of a wheel is that it is transient.

It moves.

It moves.

If you circle a hive with a pen, come back in three hours, it might be gone from that spot, and a new one has popped up somewhere else on the body.

It's fleeting.

And finally, the cyst.

A cyst is distinct because it is encapsulated.

It's a sac filled with fluid or semi -solid material like keratin.

It feels resilient when you push on it, kind of like a grape under the skin.

Okay, so that's our primary vocabulary.

But by the time a patient comes to see us, they've usually been living with the rash for a while.

They've scratched it, picked at it.

Maybe their cousin told them to put some rubbing alcohol on it.

Now the lesion has changed.

And that brings us to secondary lesions.

These are the aftermath.

As a clinician, you have to mentally subtract these changes to figure out what the primary lesion was to begin with.

Let's look at the debris first.

Stuff that's sitting on the skin.

Okay.

If you see dried fluid serum, blood or pus that has hardened on the skin's surface,

that is a crust.

We colloquially call it a scab.

And the color tells you a lot, right?

It tells you everything.

If you see a honey -colored crust, your brain should immediately think impetigo.

It's almost diagnostic.

And if it's flaky, like dry skin.

That's scale.

Scale is actually thickened stratum corneum.

It's an accumulation of dead skin cells that are flaking off.

You see this in psoriasis, saborect dermatitis, which is dandruff, or fungal infections.

Then there are the lesions caused by trauma, the self -inflicted damage.

Right.

If you see linear scratch marks, that's excoriation.

It tells you one very important thing.

This rash itches.

The patient is literally tearing at their own skin to get relief.

What about a crack in the skin, like on your heel in the winter?

That is a fissure.

It's a linear break all the way down into the dermis.

You often see these at the corners of the mouth, which is called angular chylitis, or on very dry hands or heels.

They can be quite painful.

There's one term in the secondary list that sounds very serious, like canification.

It sounds complex, but it's basically a callus from scratching.

If a patient has chronic eczema and they rub and scratch the same spot for months or years, the skin thickens in response.

It starts to look leathery, and the normal skin lines become really exaggerated.

That is like anification.

It's a hallmark sign of chronicity.

So we've identified the what, but the text says the where and the how are just as important.

We need to look at shape and arrangement.

You have to step back.

Don't just look at one lesion.

Look at the whole pattern.

This is often where the diagnosis just jumps out at you.

Let's run through the big ones from tables 28 .1 and 28 .2.

Annular.

Annular means ring -shaped, but specifically it implies a ring with a clear center.

If you see a red scaly ring with a normal -looking middle, your brain should immediately scream, ringworm, tinea corporis.

Zostraform.

This is a classic board exam favorite.

It is for good reason.

Zostraform means the rash follows a nerve dermatome.

It looks like a band or a belt of rash, and the critical feature is that it does not cross the midline.

It stops dead center.

If you see that, it is shingles, herpes zoster, period.

Linear.

In a line.

This usually points to an external cause.

The most common is poison ivy or roost dermatitis.

A clant leaf brushed against the skin in a straight line, and the rash appears exactly in that path a few days later.

Iris or target lesions.

These look exactly like a bullseye.

You have a dark center, a pale ring around it, and then a red ring on the outside.

Three distinct zones.

This is the hallmark of erythema multiform.

And morbilliform.

This means measles -like.

It's a generalized rash composed of pink macules and papules that often merge together into bigger patches.

We see this in viral xanthums, but also very, very commonly in drug eruptions.

Okay, we've done our first clants.

We've categorized the bump.

We've noted the pattern.

Now, finally, we get to talk to the patient.

We move to section two, the focused history.

But the expert guidance here is very specific.

Before you ask, when did it start enterly,

you have to make sure the patient isn't dying.

Safety first.

Always.

There are dermatologic emergencies.

You need to screen for them immediately before you get the whole long story.

The text lists the must -ask questions.

Do you have a fever?

Are you short of breath?

Is it hard to swallow?

Is the rash tender to the touch?

And critically, are your mouth, your lips, or your eyes involved?

Let's explain why these specific questions matter.

What are the monsters in the closet?

Okay, the first monster is meningocrasemia.

This is a bacterial infection of the blood.

It kills fast.

And what does that rash look like?

How do you spot it?

It's petechial or purpuric.

These are purple or red spots that do not blanch.

If you press on them with a glass slide, they stay red.

If a patient, especially a child or young adult, has high fever, irritability, and non -blanching spots, you call 911.

You do not wait.

That is a life -saving immediate treatment situation.

Then there's anaphylaxis.

That's where the shortness of breath comes in.

Right.

If you see urticaria or hives, that's an allergic reaction.

But if it's paired with angioedema swelling of the lips, tongue, or airway and wheezing, that is anaphylaxis.

The text notes that the speed of onset correlates with severity.

If the hives popped up five minutes after eating a peanut, you're in deep trouble.

And then there's a group of conditions that sound like something out of a horror movie.

Toxic epidermal necrolysis, TAN,

and Stevens -Johnson syndrome, SJS.

These are arguably the most terrifying conditions in all of dermatology.

They are usually severe reactions to medications, often antibiotics or anticonvulsants.

The immune system basically attacks the skin.

What are the red flags we should be looking for?

A tender rash.

Usually, rash is itch.

They don't hurt to touch.

If a more biliform rash is painful, be very alert.

Also, fever and oral ulcers or mucosal involvement.

The defining feature is that the epidermis, the top layer of skin, separates from the dermis.

The skin essentially peels off in sheets.

And the difference between SJS and TA is just the body surface area involved.

Exactly.

If it's less than 10 % of the body, it's SJS.

If it's more than 30%, it's 10.

These patients are treated in burn units because they've lost their skin barrier.

That is incredibly sobering.

So once we have ruled out the life -threatening stuff, we settle into the standard diagnostic detective work.

What are the key elements of the history we need to gather?

We need the timeline,

onset and duration.

Is it acute, like minutes to weeks, or is it chronic, months to years?

Hives are acute, psoriasis is chronic.

We need evolution.

We need the evolution.

How did it start versus how does it look now?

Herpes simplex starts as a tingle, turns into a vesicle, then it breaks and forms a crust.

If you only see the crust, the history of the tingle and blister is the only way you'll diagnose it.

Spread is another good clue, according to the test.

Yes.

Centripetal spread means it starts on the limbs and moves to the center of the body.

Centrifugal is the opposite, starts central and moves out.

And caudal means it starts at the head and moves down.

Measles, for example, is a classic cephalocodal rash, starts on the face, moves to the trunk, then the limbs.

Let's talk about the symptom that drives patients absolutely crazy, pruritus or itching.

The text has a box, box 28 .2, that groups diseases by how much they itch.

It's a great heuristic.

It really helps you narrow things down.

There's the always itch group, atopic dermatitis or eczema is the captain of this team.

We call it the itch that rashes, because the itching often comes before you even see the rash.

And the never itch group.

Warts, vitiligo, most moles.

If a patient comes in with a classic wart and says it's intensely itchy, you should probably think about something else.

There's a specific type of itch that points to a creepy crawly cause,

nocturnal itch.

Yes.

If a patient says, I okayed her in the day, but the second I lay down in bed, I want to tear my skin off.

Your brain has to go to scabies.

The mites are more active at night when the body is warm, and the lack of other distractions makes the sensation incredibly intense.

And scratching just creates that vicious cycle.

The itch scratch cycle.

You scratch, you damage the skin cells, they release inflammatory mediators like histamine, which makes you itch more.

It's a loop you have to break, often with medication, to let the skin heal.

Okay, section three, environmental factors and exposures.

This is where the clinician has to put on their Sherlock Holmes hat.

You have to ask about things the patient might not think are relevant at all.

Absolutely.

You have to investigate their living situation.

If a child has an itchy rash, you have to ask about daycare or school.

Daycares are little petri dishes for lice, scabies, and impetigo.

Travel history is huge, especially for vector -borne diseases.

It's critical.

If a patient presents with a fever and a rash, where they have been in the last month, determines your differential diagnosis.

If they were hiking in the woods in Connecticut or the Midwest, you have to worry about Lyme disease.

And what does that look like again?

It's the erythema cronicum migrans.

The bullseye rash.

It appears about four to 20 days after the tick bite.

But here is the catch the text emphasizes.

Only about one -third of patients remember the tick bite.

The tick, the exodes tick, is tiny, so you can't rely on the patient knowing they were bitten.

What about Rocky Mountain spotted fever?

This is more common in the South Atlantic states.

It's also tick -borne.

It causes a patechial rash that classically starts on the wrists and ankles and moves inward toward the trunk.

It's accompanied by high fever and headache.

It's very dangerous if not treated.

The text also mentions some more exotic things like leishmaniasis from sandflies and leprosy.

Right.

Rare in the continental US, but in a globalized world, you have to ask about travel to endemic areas if the picture doesn't fit a common diagnosis.

Let's talk about occupation and hobbies.

What do you do all day?

Farmers working with cattle are at higher risk for certain types of ringworm.

People handling imported animal hides could theoretically be exposed to anthrax.

Hikers and gardeners get poison ivy.

And pets.

People love their pets, but they bring passengers.

Fleas usually bite around the ankles and legs.

You see these little urticaria lesions with a tiny central dot.

And dogs with mange can transmit a form of scabies to humans.

The text also lists triggers factors that make an existing condition worse.

Stress is a universal exacerbator.

It flares eczema, psoriasis, and acne.

For rosacea, the trigger is vasodilation.

Anything that makes you flush heat, sunlight, spicy food, alcohol, hot coffee, will make rosacea worse.

And medications.

This is a big one.

A huge one.

We already mentioned the severe reactions like SJS -10, but meds can cause milder issues too.

They can cause light sensitivity, what we call photosensitivity, simple hives, or commensal eruptions.

Commensal eruptions?

What's that?

Like when you take antibiotics for a sinus infection, the antibiotic kills your good bacteria and that allows yeast to overgrow.

You get a vaginal yeast infection or thrush in your mouth.

That's a drug -induced skin issue.

There's a specific note about vaccinations in the chapter.

Yes, specifically the measles vaccine.

It can cause a mild measles -like rash about 10 to 14 days after the shot is given.

Parents will freak out thinking their kid has measles from the vaccine, but it's just a normal expected vaccine reaction.

Finally, family history.

Genetics load the gun.

Environment pulls the trigger.

The atopic triad, asthma, eczema, allergies runs very strongly in families.

Psoriasis has a definite genetic component.

And if you see a child with lots of cafe au lait spots, you need to check the family history for neurofibromatosis.

Okay, moving on to section four.

The focused physical examination in detail, the actual execution.

We've talked about the first glance, but now we are doing the full exam.

The expert advice in the chapter is avoid people diagnosis.

It's so tempting to do.

The patient says, look at the spot on my arm and they pull up their sleeve.

You look at the arm, but you miss the fact that they have the same rash on their knees or behind their ears or on their scalp.

You need to see the whole picture to understand the distribution.

And distribution helps distinguish between the big chronic conditions.

The book emphasizes flexor versus extensor.

Memorize this rule.

Just burn it into your brain.

Atopic dermatitis, eczema, loves the flexor surfaces, the folds, the inside of the elbow, which is the antecubital fossa, and behind the knees, the popliteal fossa.

Okay.

Psoriasis loves the extensor surfaces, the pointy parts, the tip of the elbow, the kneecap.

That simple location check is often the diagnostic clincher between those two.

What about the palms and soles?

Most rashes spare the palms and soles.

So if a rash is there, your lord of suspects shrinks dramatically.

You should think about erythema, multiform, secondary syphilis, or hand, foot, and mouth disease.

And the hidden areas.

You have to look where the sun doesn't shine.

Check the mouth.

You can find lichen plinus or signs of drug reactions there.

And you absolutely must check the hair.

For children with hair loss, there is a specific triad to look for.

Yes.

If a kid has hair loss or alopecia, plus scaling on the scalp, plus swollen lymph nodes in their neck, that is, tinea capitis ringworm of the scalp, until proven otherwise.

The text suggests the hair pull test.

You gently pull a clump of about 50 hairs.

If more than a few come out easily without pain, that's a positive test and suggests active hair shedding.

We also use palpation.

We are feeling for texture.

Is it rough like sandpaper that suggests scale or keratin plugging?

Is it soft?

Is it firm?

Is it hard like a rock?

And oddly enough, the text says we check the abdomen.

Right, because the skin is a window.

If you have a rash that suggests a systemic infection or a lymphoma, you might find an enlarged liver or hepatomegaly or an enlarged spleen's monomegaly on your abdominal exam.

All right.

Sometimes looking and touching isn't enough.

We need to get scientific.

Section five, laboratory and diagnostic studies.

Let's open the toolbox.

First tool, diastrophe.

This is a low -tech, high -yield test.

You take a glass slide and press it firmly against a red lesion.

You're looking to see if it blanches or turns white.

What does that result tell us?

Why do we care if it blanches?

If the redness disappears or blanches, it means the blood is inside the blood vessels.

When you press, you're just squeezing the blood out temporarily.

This is typical of inflammation or dilated vessels like a telangiectasia.

And if it stays red?

If it does not blanch, it means the blood has leaked out of the vessels and is trapped in the tissue.

That is petechia or purpura.

That's the danger sign for things like vasculitis or meningocasemia.

Next up, wood's light.

This is the UV lamp.

It feels a bit like CSI.

It is useful, but it has some traps you need to be aware of.

You shine the UV light on the skin in a dark room.

Certain things will fluoresce.

Microsporum, a type of fungus, glows a blue -green color.

Erythrasma, a bacterial infection you find in skin folds, glows a brilliant coral red.

Pseudomonas can glow green.

What is the trap?

You said there's a trap.

The trap is that trichophyton tonsurans, which is currently the most common cause of ringworm in the US, does not glow.

So negative wood's light does not mean no fungus.

You can't rely on it to rule things out, only to rule them in if you get a positive fluorescence.

So to really confirm fungus, we need the KOH preparation.

Yes.

Potassium hydroxide.

You scrape some scale onto a slide, you add a drop of KRH, maybe warm it up a little, and look under the microscope.

The KOH dissolves all the human skin cells, but leaves the tough fungal cell walls intact.

And what are we looking for?

We're looking for the famous spaghetti and meatballs sign.

The spaghetti corresponds to the hyphae, which are the long filaments, and the meatballs are the spores.

If you see that, you have confirmed a fungal or yeast infection.

Then there is the Zank smear.

This is specifically for vesicles, for blisters.

You unroof a blister with a scalpel blade and scrape the base.

You're looking for multi -nucleated giant cells.

If you see them, it confirms a herpes virus infection.

But which one?

And that's the key.

It doesn't tell you which herpes virus.

It could be simplex, which is a cold sore, or genital herpes, or it could be zoster, which is shingles, or varicella, which is chicken pox.

It just tells you it's in that family.

Here, finally, the definitive test.

Biopsy.

If you don't know what it is, take a piece of it.

A punch biopsy uses a little circular blade, like a cookie cutter, to take a core sample down to the fat.

It's great for inflammatory rashes to see the pathology.

And an excisional biopsy.

An excisional biopsy cuts out the entire lesion.

That is mandatory, if you suspect melanoma, because the most important prognostic factor is how deep the cancer goes.

And you need the whole lesion to measure that accurately.

OK, we have our vocabulary, our history, our exam techniques, and our tools.

Now, let's apply them.

We are going to walk through the Rogues Gallery, the specific diseases detailed in the chapter.

Let's start with section six, Follicular and Infectious Eruptions.

Let's start with the teenager's nemesis, acne vulgaris.

It's a disorder of the polyspacious unit, the hair follicle, and its oil gland.

The hallmark lesion, the thing you have to see to diagnose it, is the commedone.

Blackheads and whiteheads.

Exactly.

Blackheads are open commedones, and whiteheads are closed ones.

How do we distinguish that from rosacea?

Because adult patients often confuse them.

Rosacea affects the central face with persistent redness, flushing, and telangiectasia, which are little broken blood vessels.

You can get papules and pustules, just like an acne.

But UT, and this is the key differentiator, you do not see commedones in rosacea.

If there are no blackheads, it's likely rosacea.

Also, remember the triggers.

Heat, alcohol, spicy food.

Moving on to bacteria.

On pedigo, usually in kids.

Caused by staph or strep.

The lesion starts as a fragile vesicle or pustule.

It breaks, and the exudate forms that classic honey -colored crust.

It is highly contagious.

Moleculitis.

This is an infection of the hair follicle itself.

You see a pustule with a little hair sticking out in the center.

Usually caused by staph.

But there is a fun variant.

Hot tub folliculitis.

Sounds nice.

Pseudomonas aeruginosa.

This bacteria thrives in warm under chlorinated water.

So a few days after being in a hot tub, you get this itchy pustular rash under the bathing suit area where the water was trapped.

And if a follicle infection gets really deep and nasty?

It becomes a furuncle, or a boil, a tender red fluctuant nodule.

It's a skin abscess.

If several furuncles join forces and connect under the skin, it's a carbuncle.

These are very painful and often need to be cut open and drained.

Antibiotics alone might not be enough to penetrate the abscess.

Okay, section seven.

Macular, papular, and viral.

This covers the childhood xanthums.

The classic viral rashes of childhood.

Let's do a rapid fire on the key features.

Fifth disease.

Parvovirus B19.

The child looks surprisingly well but has bright red cheeks.

The classic slapped cheek appearance.

Then, a few days later, a lacy, reticular rash appears on the body and limbs.

And is dangerous.

Not usually for the kid, but it is dangerous for pregnant women because it can cause fetal high drops.

And also for people with chronic anemia, like sickle cell, where it can cause a life -threatening aplastic crisis.

This is a sick kid.

High fever.

The preces.

Cough, chorisa, which is a runny nose, and conjunctivitis, or red eyes.

Look inside the mouth for coplic spots, little white grains of salt on a red background on the inside of the cheek.

The rash starts at the hairline and moves down.

Cephalocotl.

Rubella, germ, and measles.

Milder than measles.

The key physical exam finding is swollen lymph nodes behind the ears, posterior, and at the base of the skull, which is suboccipital.

Raziola.

The pattern is the diagnosis.

High fever in an infant for about three to four days.

The baby is cranky, but otherwise looks okay.

Then, the fever breaks abruptly, and as the fever leaves, the rash appears, usually starting on the trunk.

Scarlet fever.

This is a reaction to a strep throat infection.

The rash feels like sandpaper.

You might also see a strawberry tongue, which is red and bumpy, and pastilla lines, which are red streaks in the skin soles of the armpit or groin.

Also, classically, the area around the mouth stays pale, which we call circumoral pallor.

And the most artistically named rash, pittoriasis rosea.

This one is fascinating.

It starts with a herald patch.

A single large oval scaly plaque, usually on the chest or back.

The patient often thinks it's ringworm.

But then, about one to two weeks later, they explode with the generalized rash of smaller oval lesions on the back.

They align along the lines of skin tension, creating a Christmas tree pattern.

And does it need treatment?

Nope.

It looks traumatic, but it resolves on its own in six to eight weeks.

You just reassure the patient.

Okay.

Section eight.

Vesicular, bullis, and fungal.

Back to the blisters.

Hand, foot, and mouth disease.

Usually, Coxsackie virus A16.

You see painful ulcers in the mouth and vesicles on the palms of the hands and soles of the feet.

Kids often stop eating and drinking because their mouth hurts so much.

Herpes simplex.

HSV.

Grouped vesicles on an erythematous base.

That is the classic description you have to know.

A bunch of grapes on a red plate, usually on the lips, HSV1, or genitals, HSV2.

It's painful and it's recurrent.

Herpes zoster.

Shingles.

Reactivation of the chicken pox virus.

We already talked about the key feature.

The dermatomal pattern.

A band of painful blisters on one side of the body that does not cross the midline.

And there's a specific warning about the nose here in the chapter.

Hutchinson's sign.

Yes.

If you see vesicles on the tip or the side of the nose, it implies that the nesiciliary branch of the trigeminal nerve is involved.

That nerve also supplies the eye, which means the eye is at high risk for involvement.

This is an ophthalmologic emergency.

They need to see an eye doctor immediately because they can go blind.

And varicella chicken pox.

The classic lesion is a dew drop on a rose petal.

A clear vesicle sitting on a red base.

The key feature for diagnosis is that you see lesions in all stages of evolution simultaneously.

You'll see some new blisters, some crusted scabs, and some healing spots all at the same time on the body.

Let's briefly touch on bugs again.

Bed bugs.

The bites themselves are not diagnostic.

They can look like any other bug bite.

You diagnose bed bugs by finding the evidence in the room.

You have to tell the patient to look at the seams of their mattress for the rusty spots, which is dried blood and the bug's feces.

Lovely.

Let's move to fungal infections.

Candy diocese.

Yeast.

Yeast loves warm, wet environments.

So think diaper area under the breasts in the groin.

The rash is beefy red.

And the telltale sign is satellite lesions.

Little red papules or pustules scattered just outside the main red area.

Tina ringworm.

We know this one.

Annular, a scaly border, and central clearing.

A red ring.

And pediureus is versicolor.

Also called tinea versicolor.

It's caused by yeast called malicencia.

That's part of our normal skin flora.

It interferes with melanin production.

So you get these hyperpigmented patches.

They can be tan, pink, or white, usually on the trunk.

They become more obvious in the summer because they don't tan.

This is another one that gives you the spaghetti and meatballs on the KOH prep.

Okay.

Section nine.

Immunologic and allergic.

The chronic itchy conditions.

Atopic dermatitis.

Eczema.

We mentioned the flexor surfaces.

The skin barrier is defective.

So it's very dry and sensitive to irritants.

The itch can be intense.

Contact dermatitis.

This is a hypersensitivity reaction.

There are two types.

Irritant, like getting bleach on your skin.

Or allergic, like poison IV or nickel.

The pattern is the key.

It appears exactly where the substance touched the skin.

Linear streaks for plants.

An earlobe rash for nickel earrings.

A rash around the belly button from the nickel in a jeans button.

Psoriasis.

A chronic inflammatory condition.

You see well demarcated erythematous plaques with a thick silvery scale.

Extensor surfaces like elbows and knees.

And you have to look at the nails.

You often see pitting, which are little divots in the nail plate.

And there's the auspice sign.

If you pick off the scale, you get these little pinpoint bleeding spots.

Sibiric dermatitis.

This is essentially dandruff.

It's an inflammatory reaction to yeast on the skin.

You get greasy yellow scales on the scalp, eyebrows, and in the nasolabial folds.

In babies, we call it cradle cap.

And finally, section 10.

Neoplastic eruptions.

We have to end on the most critical do not miss diagnosis.

Skin cancer.

Melanoma.

This is the killer.

It is a cancer of the melanocytes, the pigment producing cells.

We use the ABCDE checklist to screen moles.

Let's walk through that.

A is for asymmetry.

If you fold the mole in half, the two sides don't match.

B is for border.

Is the border irregular, ragged, notched, or blurred?

C is for color.

Is it all one uniform shade of brown, which is good?

Or is it a mix of black, blue, red, tan, and white, which is bad?

Variegation is a warning sign.

D is for diameter.

Is it larger than six millimeters, which is about the size of a pencil eraser?

E is for evolution.

Is it changing?

Is it growing, changing shape, changing color, or starting to bleed or itch?

Change is the most important sign.

What are the biggest risk factors we should be asking about?

Fair skin that burns easily.

A history of blistering sunburns, especially in childhood.

A family history of melanoma and having a high number of moles, usually over 50.

And the non -melanoma cancers.

Basal cell carcinoma, BCC, is the most common skin cancer by far.

It classically looks like a pearly, translucent papule, often with a rolled border and tiny blood vessels called telangiectatias.

It grows very slowly and rarely spreads, but it can invade local tissue, the so -called rodent ulcer.

And squamous cells.

Squamous cell carcinoma, SEC, looks different.

It's usually a red, indurated, or hard nodule with a thick, crusted scale.

It can be tender and can ulcerate.

It's very common on chronically sun -exposed areas, like the ears, the lower lip, and the bald scalp.

We have covered an incredible amount of ground today.

Wow.

From the basic grammar of mechule versus papule, to the life -threatening signs of mendicochemia and melanoma.

It's a lot to absorb.

It really is.

But if you take away one thing from this deep dive, let it be the process.

Don't just stare at a rationed guess.

Use the morphology to name what you see.

Use the arrangement to find the pattern.

Use the history to put it in context.

And then use your tools to confirm it.

It's about moving from that looks gross to that is a grouped vesicular eruption on an erythematous base in a dermatomal distribution.

Exactly.

When you can say that, you know it shingles.

You've cracked the code.

And remember, the skin is talking.

It's telling you about the patient's immune system, their exposures, their environment, and their internal health.

We just have to be good listeners and learn its language.

That's a perfect final thought.

The skin isn't just a surface.

It's a map.

A map to everything going on inside.

Thank you so much for breaking all of this down with us.

And to our listeners, thanks for diving deep into Chapter 28.

Hopefully, the next time you see a rash, you won't panic.

You'll get curious.

Thanks for having me.

This has been the Last Minute Lecture Team, signing off.