Chapter 48: Dermatologic Disorder Drug Therapy

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Welcome back to the Deep Dive.

I'm so glad you're here with us today because we are about to challenge a very common, and honestly,

a pretty dangerous assumption.

It is good to be back, and I think I know exactly which assumption you were talking about.

The idea that dermatology is just superficial, you know?

There's this cultural idea that skin issues are purely cosmetic.

It's pimples.

It's a rash.

It's a little sunburn.

It feels like the halalite version of medicine.

Oh, I know that reputation well.

It is the just put some cream on it mentality.

Yeah.

And frankly, for a nurse or any healthcare provider, that mindset is, well, it's dangerous.

Exactly.

Because today we are diving into Chapter 48, Dermatologic Disorders from Pharmacology, a patient -centered nursing process approach.

Right.

And when you actually peel back the layers, pun intended of this text, you realize we're just talking about lotions.

We are talking about drugs that can shut down your liver.

We're talking about medications so toxic to a fetus that there are federal registries just to prescribe them.

Yes.

And we're talking about skin failure that looks like a burn but is actually a drug reaction.

It's incredibly serious stuff.

That is the key insight right off the bat.

The skin is the largest organ in the body.

It is a massive complex system.

It's not just a wrapper.

Not at all.

And because it is on the outside, it is often a mirror for what is happening on the inside.

When we treat the skin pharmacologically, we are rarely just treating the surface.

They're pulling all these other levers.

Exactly.

We are pulling levers that affect the entire immune system, hormonal balance, and cellular regeneration.

It's systemic.

So here is the mission for this deep dive.

We are going to deconstruct Chapter 48.

We are going to move past that apply cream twice a day level of knowledge and get into the moenisms.

Right.

We need to understand why these drugs work, why they are dangerous, and how a nurse keeps a patient safe while using them.

And we are going to follow the structure of the text meticulously.

It's a logical progression.

Where are we starting?

We'll start with a necessary refresh of anatomy and physiology.

Because if you don't understand the layers, you won't understand absorption.

It's foundational.

Okay.

A and P first.

Then what?

Then we'll tackle the big ones.

Yeah.

Acne vulgaris and psoriasis.

I mean, those are two of the most common reasons people see a dermatologist.

From there, we'll move into what I call the specifics.

Things like warts, drug -induced dermatitis, hair loss.

And we will finish with a really, really heavy section on burns, both preventing them and the critical care required when they happen.

And of course, we will wrap it all up with the nursing process and clinical judgment.

Tying it all together for practice.

One quick housekeeping note before we start.

This is an educational deep dive into the provided source text.

We are exploring the pharmacology for nursing education.

Right.

We aren't doctors, and this isn't medical advice.

If you have a concerning mole or a rash, please go see a professional.

Always good advice.

Seriously.

Okay.

Let's get into the architecture.

The text opens by establishing the skin as the body's primary shield.

It lists three main functions.

Right.

Three main jobs.

First, this is the most obvious one, protection.

A barrier.

A barrier.

Exactly.

It keeps the outside world bacteria, chemicals, UV radiation out, and it keeps the inside world in.

Okay.

Protection.

What's number two?

Second is temperature regulation.

Think about it.

Vasodilation.

Vasoconstriction.

Sweating.

That's the skin acting as a radiator for your body.

Cooling you down, warming you up.

Makes sense.

And the third.

And third, and this is absolutely crucial for our burn discussion later,

is the prevention of fluid loss.

Right.

We take that for granted until it's gone.

You lose skin, you lose water.

Fast.

Incredibly fast.

It can lead to hypovolemic shock.

So now let's talk structure.

The text divides the skin into layers.

Two primary layers.

And they sit on top of a support structure.

You have the epidermis on the outside.

That's the part we see.

That's the part you see.

And the dermis underneath it, below all of that is the succutaneous tissue.

Okay.

So let's drill down into the epidermis.

The text breaks this down into four sub layers.

Why does a nurse need to know the sub layers of the skin?

It feels so granular.

It does, but it explains how skin regenerates and, more importantly for us, how drugs penetrate.

It's all about mechanism.

Okay.

So walk me through it.

Where do we start?

We start at the bottom.

The deepest layer of the epidermis is the basal layer or the stratum germinativum.

Germinativum.

Right.

It's like germination where things start.

Exactly.

This is the factory.

This is where new skin cells, the keratinocytes are born.

And then they migrate up.

They migrate up.

They move up through the next layer, the spinous layer, and then the granular layer.

And as they move up, they change.

How do they change?

They flatten out.

They lose their nucleus.

They fill up with this tough protein called keratin.

By the time they reach the surface, the cornified layer or the stratum corneum, they're essentially dead, flat sacks of protein.

And that cornified layer is the barrier we were just talking about.

It is the fortress wall.

It's what keeps water in and pathogens out.

When we design a topical drug, its very first challenge is how do I get through the stratum corneum?

So if a drug can't get past that layer, it's useless.

Pretty much.

Or it's designed to only work on that layer.

It all depends on the target.

Okay, so that's the epidermis.

Then we have the domus.

The dermis is the infrastructure.

It has its own layers, the papillary and the reticular.

But what's important is what's in it.

This is where you find fibroblasts.

Fibroblasts.

I know that word.

They build things.

They build things.

Specifically, they build collagen and elastic fibers.

Collagen for strength.

Elastin for stretch.

Precisely.

That's what gives skin its toughness and its resilience.

But the dermis also houses all the functional machinery.

Like what?

Blood vessels, nerve endings, sweat glands,

and super important for our talk on acne, the polospacious units.

Which are the hair follicles and the oil glands.

The hair follicles and their attached sebaceous glands.

Which brings us to the final layer, the subcutaneous tissue.

The foundation.

It's mostly adipose tissue fat.

It cushions, it insulates, and it contains the larger blood vessels and lymphatics that feed the skin above it.

Okay.

So before we get to the diseases, there is a vocabulary section in the text.

I feel like in dermatology, if you don't speak the language, you can't document anything.

Oh, you really can.

You can't just write, patient has a weird bump.

That would be malpractice.

I mean, honestly.

Documentation requires precision.

The text highlights four specific terms that differentiate lesions based on size and texture.

And this is critical for the assessment phase of the nursing process, right?

Absolutely.

This is day one assessments.

Let's run through them.

First one, macul.

What's a macul?

A picule is flat.

You cannot feel it if you run your finger over it.

It is non -palpable and it is small.

The cutoff is less than 10 millimeters.

Give me an example.

Think of a freckle or a flat age spot.

You can see it, but you can't feel it.

Okay.

Flat, small, can't feel it.

Got it.

Next, papule.

A papule is raised.

It is palpable.

You can feel it, but it is still small, less than 10 millimeters.

So like a mole.

A small raised mole is a perfect example.

Or a small wart, raised and small.

Okay.

So macule is flat, papule is raised.

Next up, vesicle.

A vesicle is a blister.

It is elevated, palpable, and filled with clear fluid.

And again, the size cutoff is less than 10 millimeters.

So like a chicken pox lesion.

A classic vesicle, yes.

And finally, the big one, plaque.

Plaques.

These are palpable lesions.

They can be depressed or elevated, but the defining feature is size.

They're greater than 10 millimeters.

So it's like a bigger, broader raised area.

Exactly.

When we talk about psoriasis later, plaques will be the operative word.

These large, scaly, raised lesions are classic plaques.

Okay.

We have our anatomy.

We have our vocabulary.

Let's talk about the most common skin disorder in the United States.

Acne vulgaris.

It is ubiquitous.

I mean, almost everyone deals with it at some point.

And it affects adolescents, adults.

It's distinct from the acne we see in neonates.

The text spends a good amount of time on the pathophysiology here.

I think there is a common misconception that acne is just dirty skin.

You know, you didn't wash your face.

You got a zit.

And the text explicitly and rightly debunks that.

That's a harmful myth.

Why is it harmful?

Because it leads to patients over washing, scrubbing their faces raw, which actually makes the inflammation worse.

So what's really going on?

Acne is a complex interplay of anatomy, hormones, and bacteria.

It starts in that polyspacious unit we mentioned, the hair follicle and the oil gland.

Oh, okay.

So walk us through the formation of a lesion, a single pimple.

How does it start?

It starts in the keratin plug.

The cells that line the inside of the follicle, they're supposed to shed off one by one.

But in acne, they get sticky.

They don't shed properly.

They clump together and form a blockage.

A microscopic plug.

And this traps everything behind it.

It traps sebum in the oil, and it traps bacteria inside the follicle.

The bacteria is propionobacterium acnes, right?

I think it's been renamed to cutie bacterium acnes.

Yes, you'll see both names.

The text uses P.

acnes.

Now you add the hormonal fuel to this fire.

Androgens.

Androgens, exactly.

During puberty, androgen production spikes.

This sends a signal to the sebaceous glands to go into overdrive and produce massive amounts of sebum.

So now you have a plug, and behind it, you have this growing pool of oil.

It's a feast for the bacteria.

It's an all -you -can -eat buffet.

Key acnes feeds on that sebum, it proliferates like crazy, and it releases these metabolic byproducts that are highly inflammatory.

And the inflammation is the redness and the pain.

The inflammation is what turns a simple clawed pore into a red angry pustule, or a deep painful cyst.

And the text distinguishes between open and closed comedones.

What's that?

A comedone is the non -inflammatory plug itself.

If the follicle is stretched open to the air, the lipids and melanin in the plug oxidize and turn dark.

That's a blackhead.

It's not dirt.

It's just oxidized oil.

Exactly.

If the pore is closed over by skin, the plug stays white or flesh -colored.

That's a whitehead.

So again, if it's not dirt, scrubbing it away won't work.

It will actually backfire.

The text is very clear on this.

Vigorous scrubbing or overwashing causes irritation.

It damages the skin barrier and inflames the skin further.

Okay, so that leads us right into management, starting with a non -pharmacologic approach.

If we aren't scrubbing, what are we doing?

Gentle cleansing.

Twice a day.

That's it.

Use a mild cleanser.

The goal is to remove excess surface oil without stripping the skin of all its natural lipids.

You want to support the skin barrier, not attack it.

What about diet?

The text weighs in on the whole pizza and chocolate debate.

It does.

It suggests a well -balanced diet, low in fat and sugar.

It specifically mentions avoiding excessive carbohydrates.

So while a single slice of pizza might not cause a breakout,

a persistently high glycemic diet might contribute to the overall inflammatory state of the body.

So it's more about the pattern than the single food.

I think that's a good way to put it.

Yeah.

Tosmatics.

Water -based.

That's the key.

If you have acne, you are already dealing with excess oil.

You do not want to be putting more oil on your face.

Look for products labeled non -comedogenic.

Which means they're tested to not clog pores.

Correct.

OK.

So that's the foundation.

Let's move to the pharmacology.

The text tiers this.

We start with mild to moderate acne using topical treatments.

The first line of defense is often benzoyl peroxide.

BP.

It's over the counter.

It's effective.

How does this actually work?

What's the mechanism?

Benzoyl peroxide is fascinating because it is effectively a chemical weapon against the bacteria.

Its mechanism is the release of free radical oxygen species.

Free radicals.

But wait, aren't those the bad guys?

Antioxidants fight free radicals?

Usually, yes.

But in this case, we're weaponizing them.

P.

acnes is an anaerobic bacterium.

Meaning it hates oxygen.

It thrives in an oxygen -free environment.

BP releases a flood of oxygen that oxidizes the bacterial proteins.

It essentially suffocates the bacteria with oxygen, if that makes sense.

It creates a hostile environment they can't survive in.

Exactly.

And because of that unique physical mechanism, bacterial resistance is very, very rare, which is a huge advantage.

How do you use it?

It comes in creams, gels, washes.

The text notes you can leave it on.

Or for sensitive skin, you can do short contact therapy.

Put it on for a few minutes and then wash it off.

That can reduce irritation.

But it's slow, right?

It's not an overnight fix.

No.

You have to manage patient expectations.

You have to tell them it takes four to six weeks to see a real resolution.

That requires patience.

Okay.

Next on the list of topicals are the retinoids.

Tretinoin, adipoline, tazeratine.

These are heavy hitters.

They are.

These are prescription strength.

Retinoids are vitamin A derivatives.

They don't just kill bacteria.

They fundamentally change how the skin grows and behaves.

So what's their mechanism?

They're not antibacterial like BP.

No.

They have two main actions.

First, they are chamedolytic.

They break up the keratin plugs we talked about.

They normalize that shedding process inside the follicle.

So they prevent the initial blockage.

They prevent the plug from ever forming.

But they also have powerful anti -inflammatory properties.

The text mentions they alter gene expression.

That sounds profound for a face cream.

It is profound.

They are small enough to get inside the skin cells into the nucleus and they bind to specific receptors there that control how genes are expressed.

They basically tell the skin cells, hey, stop sticking together, shed properly, turn over faster.

But ramping up cell turnover has a cost.

There's a reason people are sometimes afraid to start these.

Yes.

The initial retinization period.

Some people call it the retinoid uglies.

What does that look like?

Burning,

itching.

The medical term is pruritus and redness or erythema.

The skin can become very dry, sensitive, and flaky for the first few weeks.

And there are specific safety warnings here in the text.

Big ones.

Two major ones.

First, tazeratine is category X.

It is absolutely contraindicated in pregnancy.

Even topical vitamin A can be absorbed systemically and be teratogenic causing birth defects.

So pregnancy test is a good idea even before starting a topical in this case.

A very good idea.

The second warning is the sunburn alert.

Retinoids make your skin much more sensitive to the sun because they thin that outer cornified layer.

So sunscreen is non -negotiable.

Absolutely essential.

The text says clearly, do not use before or after extended sun exposure.

You will get a horrible sunburn.

What about topical antibiotics?

We mentioned BP, but what about actual antibiotics like clindamycin?

They are used, usually clindamycin or erythromycin.

They work just like you'd expect.

They accumulate in the follicle and reduce the amount of P -acnes.

But there's a huge warning flag here.

A huge one.

And this is major nursing consideration and patient education point.

You should never ever use them alone as monotherapy.

Why not?

Bacterial resistance.

It's a massive public health problem.

If you just use topical clindamycin by itself, the bacteria will quickly adapt and become resistant to it.

So you're breeding superbacteria on your face.

Essentially, yes.

The text strongly recommends combining them with benzoyl peroxide.

The BP helps prevent the development of resistance to the antibiotic.

That makes sense.

Okay, let's say the topicals aren't cutting it.

The acne is moderate to severe.

We move to systemic pharmacologic treatment.

We're talking about pills.

Right.

And the go -to oral antibiotics are the tetracyclines.

Doxycycline and minocycline are the most common, plus the original tetracycline itself.

We see these drugs used for Lyme disease, for pneumonia, but here they are for acne.

What are the rules for these?

They have some tricky ones.

They do.

Tetracyclines have a very specific set of contraindications.

The absolute biggest one.

You never ever give them to pregnant patients or young children, usually under the age of eight.

Because of the teeth.

Because of the teeth.

The drug is a chelator.

It binds to calcium.

In developing teeth, it gets incorporated into the enamel and causes permanent gray -brown discoloration and enamel hypoplasia, which means the enamel is weak.

And it affects bones too, right?

Yes.

It can affect fetal bone growth.

So pregnancy testing is absolutely relevant here too.

What about administration instructions?

I remember doxycycline has a weird rule about posture.

It does.

It's famous for it.

Doxycycline can be very caustic to the esophagus.

If the pill gets stuck halfway down, it can literally burn a whole cause esophageal ulceration.

Ouch.

So what's the instruction for the patient?

Take with a full glass of water and stay upright for at least 30 minutes after.

Do not take it and immediately lie down for bed.

And what about tetracycline itself?

Tetracycline is fussy about food and minerals.

It needs to be taken on an empty stomach.

One hour before or two hours after meals.

And absolutely no dairy, antacids, or iron supplements nearby.

Why?

Because the calcium in dairy or the minerals and antacids will bind to the drug in the gut and prevent it from being absorbed.

The dose becomes useless.

Okay.

Now we arrive at what you could call the final boss of acne treatment.

Severe nodulocystic acne.

The drug is isotretinoin.

Yes.

Formerly known by the brand name Accutane, this is the nuclear option for acne.

How does it work differently than the creams or the oral antibiotics?

It is a systemic retinoid and oral vitamin A derivative.

And it attacks every single aspect of acne pathophysiology.

All at once.

So what does it do?

It dramatically shrinks the sebaceous glands, which cuts down sebum formation by like 80%.

It stops the abnormal keratinization, so no more plugs.

It's a potent anti -inflammatory.

It effectively shuts down the entire acne -producing machinery of the skin.

A course is typically four to six months.

It sounds like a miracle cure.

For many people with severe scarring acne,

it is.

It can be life -changing.

But the side effect profile is extensive.

It's dose -dependent, right?

Very much so.

Almost 100 % of patients get chelitis severely chapped.

Cracking lips, dry skin, dry eyes, dry nose, leading to nosebleeds.

That's almost a given.

But those are the milder ones.

Those are the expected ones.

We also see things like dizziness, muscle aches, hair thinning, and extreme photosensitivity.

But the text flags two categories of very serious adverse effects that nurses most monitor for.

First one,

psychological.

Depression.

Depression and suicidal ideation.

There have been reports, and there's a black box warning about this, of patients on isotretinoin developing severe depression or having thoughts of self -harm.

So what does that mean for the nurse?

It means you have to screen for this.

At every single visit, you ask the patient and their family about mood changes.

How are you feeling?

Have you felt hopeless?

Have you had any thoughts of hurting yourself?

It's a mandatory conversation.

And the second major category is the reason for the IPL -DIG program.

Keratogenicity.

Isotretinoin is one of the most potent human teratogens known to medicine.

If a pregnant woman takes this drug,

the risk of severe life -altering birth defects is astronomically high.

So the FDA created this program, IPL -DIG.

This isn't just a sign here, consent form, is it?

No, it is a federally mandated risk management distribution program.

It locks down the entire supply chain.

The wholesaler, the pharmacist, the prescriber, and the patient must all be registered in the same central computer system.

The requirements are incredibly strict.

She has to commit to using two distinct effective forms of contraception, starting one month before therapy and continuing for one month after.

Two forms, not one.

Two forms.

For example, the pill and condoms.

She must have two negative pregnancy tests before she gets the first dose.

And then she must have a negative pregnancy test every single month before she could pick up her refill.

And if she doesn't?

Or if the test is a day late?

The pharmacy system will deny the claim.

The pharmacist physically cannot dispense the bottle until that negative test is registered in the system for that month.

Wow.

The text also mentions no blood donation.

Why is that?

Right.

Because if you donate blood while on isotretinoin, and that blood is transfused into a pregnant woman, you could cause birth defects in her baby.

So you cannot donate during treatment or for one full month after your last dose.

It really highlights how systemic this skin drug actually is.

It is the perfect example.

Absolutely.

And one final note on systemic acne treatment in the text.

Oral contraceptives.

Yes.

Certain combination estrogen progestin pills are FDA approved to treat acne in women, likely by regulating that hormonal component we discussed earlier.

Okay.

Let's pivot now to another major chronic skin condition.

Psoriasis.

Psoriasis is very different from acne.

Acne is bacterial and hormonal.

Psoriasis is autoimmune.

It is a chronic multi -system inflammatory disease.

What does it look like?

What's the classic presentation?

The classic presentation is well demarcated scaly erythematous plaques.

Erythematous meaning red.

They're often covered with these characteristic silvery scales.

And what is happening at the cellular level?

Why are those scales there?

Hyperproliferation.

The epidermal cells that carry tinnocytes are growing wildly uncontrollably fast.

A normal skin cycle from the basal layer to slobbing off takes about a month.

In a psoriatic plaque, it can happen in just three to four days.

So the cells are just piling up.

They're piling up on the surface because they can't mature and shed fast enough.

That pile up is the scale.

And you said multi -system.

What else does it affect?

Yes.

It's not just a skin disease.

About 25 to 30 % of patients with psoriasis will develop psoriatic arthritis.

The same inflammatory process that attacks the skin starts to attack the joints, causing pain, stiffness, and potentially permanent joint damage.

So how do we treat it?

The text starts with topicals again.

And from mild to moderate psoriasis, topical corticosteroids are the mainstay.

They are powerful anti -inflammatories, and they also slow down that rapid cell growth.

But here, the nuance is in the potency, right?

The text classifies them from class one down to class seven.

Exactly.

Potency is everything.

Class one is super potent.

Think clobetasal.

Class seven is low potency, like over -the -counter hydrocortisone.

And you have to match the direct to the body part?

You have to.

You would never put a class one super potent steroid on the face, the groin, or in the armpits.

The skin there is thin, and you'll get very high systemic absorption and local side effects.

You save the high potency stuff for thick, stubborn plaques on the elbows or knees.

What happens if you overuse them or use them for too long?

You can get skin atrophy.

The skin literally thins out, becomes fragile like tissue paper.

You can get striae, which are stretch marks.

And if you use a potent steroid for a long time and then stop abruptly, you can get a rebound effect where the psoriasis flares up worse than it was before.

Can a topical steroid affect the rest of the body?

Oh, absolutely.

If you apply a high potency steroid over a large surface area for a long time, you can absorb enough to cause systemic side effects.

You can suppress the adrenal glands.

You can cause Cushing's syndrome.

In children, it can even cause growth retardation.

So again, just a cream mindset is so dangerous.

It's completely wrong.

What other topicals do we have for psoriasis?

The text mentions vitamin D analogs like calcipotrine.

These work differently.

They work by promoting keratinocyte differentiation.

They tell the immature cells to grow up and mature properly instead of just multiplying.

Is there a catch with those?

The main one is if you use way too much, you can absorb enough to cause high calcium in the blood.

And a very specific interaction, the text points out.

UVA light inactivates calcipotrine.

So if a patient is also doing light therapy, they need to apply the cream after the light session, not before.

We also see tazeratine, the retinoid used here again.

Yep.

Same rules apply.

Works on cell differentiation, but is absolutely contraindicated in pregnancy.

And then there are calcineurin inhibitors, tacrolimus and pemacrolimus.

These are interesting.

They're immunosuppressants.

They block pro -inflammatory cytokines.

They're great for sensitive areas like the face or skin folds, because unlike steroids, they don't cause skin thinning.

Bet they're immunosuppressants, so risk.

Increased risk of local infections.

And the text has a warning about the potential for reactivation of viral infections like herpes or varicella.

There are some older treatments mentioned too, like coltar and anthralin.

They don't sound pleasant.

They're not.

They are effective but messy.

Coltar has a very strong unpleasant odor and it stains clothing and bedding.

Anthralin can stain skin and hair a brownish color.

They aren't the first choice, usually to the yuck factor, but they work.

Okay, let's talk about phototherapy.

Using light as a drug, the text mentions PUVA.

What is that?

PUVA stands for sorolin plus UVA light.

Sorolin is a photosensitizing drug.

You take it as a pill or sometimes as a soak, and it makes your skin hypersensitive to ultraviolet light.

And then you put them in a UVA light box.

Correct.

The combination of the drug and the light is very effective.

It's slowing down that rapid cell division in the skin.

That sounds counterintuitive.

Making skin sensitive to radiation on purpose.

It is a controlled burn, in a way.

It works.

But yes, it carries significant risks.

Short -term, nausea from the sorolin and the risk of a bad burn from the light.

Long -term, a significantly increased risk of skin cancer, including melanoma.

So when topicals and light therapy fail or aren't appropriate, we go to the systemic drugs.

And the traditional ones are intense.

First up, methotrexate.

Methotrexate is a folate anti -metabolite.

It was originally a chemotherapy drug.

In psoriasis, it works by slowing down DNA synthesis and thus slowing down the growth of those hyperproliferating epidermal cells.

But if it's a chemo drug, it must be toxic.

It is.

The text highlights its toxicity to three main organ systems.

The liver, primarily.

It can cause fibrosis and even cirrhosis over time.

It suppresses the bone marrow, which is myelosuppression, so you can get anemia and be at risk for infection.

And it can cause pulmonary fibrosis in the lungs.

So if you are the nurse caring for a patient on methotrexate, what are you monitoring constantly?

Liver function tests, LFTs, complete blood counts, CBCs, renal function, and, once again, pregnancy status.

Methotrexate is a powerful teratogen.

It can cause fetal death.

It's an abortifacient.

Next up is cyclosporine.

Another powerful immunosuppressant, most famously used in transplant patients to prevent organ rejection.

For psoriasis, it can bring about rapid relief for a severe flare.

But it's also very toxic.

Very hard on the kidneys.

Nephrotoxicity and hypertension are the main concerns.

It's not for long -term use.

And acetritin.

An oral retinoid, specifically for psoriasis.

And again, a retinoid, so it is strictly contraindicated in pregnancy.

This leads us to the modern era of psoriasis treatment, the biologics.

Or, as the text calls them, biologic response modifiers, BRMs.

These drugs changed everything.

I mean, they were a revolution.

Instead of carpet bombing the entire immune system, like methotrexate, these are like laser -guided missiles.

They target specific proteins, specific cytokines, that are causing the inflammation.

The biggest class mention is the TNF inhibitors.

Etanercept, infliximab, adalimumab.

Cuma necrosis factor, or TNF -alpha, is a master cytokine.

It's a key driver of the inflammatory cascade in psoriasis and psoriatic arthritis.

These drugs find it and block it.

The results can be stunning.

The psoriasis can clear up beautifully.

But there's always a but with these powerful drugs.

There is.

But TNF is also a key part of how your body fights certain infections.

Specifically, how it walls off latent tuberculosis, or TB.

So if you block TNF?

You can reactivate the TB.

Your body forms a granuloma, a little wall,

around sleeping TB bacteria in the lungs.

TNF is part of the glue that holds that wall together.

You give a TNF blocker, the wall can crumble, and the TB can wake up and become a full -blown disseminated infection.

So the safety protocol here is absolutely critical.

It is non -negotiable.

You must test the patient for TB and for hepatitis B before starting therapy.

A PPD skin test, or a blood test like a quantiferon gold.

That is a massive clinical pearl for any nurse.

TB tests before biologics.

Absolutely.

Also, they are contraindicated in patients with an active infection, in severe heart failure, and in those with demyelinating diseases like multiple sclerosis.

The text also mentions another class, the interleukin antagonists, like ustekinumab.

These block other cytokines like IL -12 and IL -23.

It's the same concept.

Very specific.

Targeted immune suppression to stop the psoriatic growth cascade.

Same general risks regarding infection apply.

Okay, let's shift gears.

We've covered the two big chronic diseases.

Let's hit what I was calling the grab bag section, starting with warts, verruca vulgaris.

Warts are caused by the human papillomavirus, HPV.

They are viral and they are contagious.

The treatment goal is basically to destroy the skin that is harboring the virus.

We have a few chemical weapons for this.

The first is salicylic acid.

Right.

The common over -the -counter option.

It's a keratolytic.

It promotes desquamation.

It softens and peels the skin off layer by layer, taking the virus with it.

The text notes a risk of salicylizum,

or salicylate toxicity, if you use it over a huge area.

But that's very rare with spot treatment of warts.

Then there's podophyllum resin.

This is a prescription physician -applied treatment, often for venereal warts.

It's cytotoxic.

It poisons the cells.

Yeah.

But it is teratogenic.

Absolutely no pregnancy use.

And if you apply it to a large area, it could be absorbed systemically and cause neuropathy.

It's potent stuff.

And my personal favorite for weird medical facts,

kentheridin.

Yes.

The blister beetle extract.

It's exactly what it sounds like.

It's a blistering agent.

A doctor paints it on the wart, covers it with tape.

Over the next day, it causes a blister to form underneath the wart.

And that lifts it off.

It lifts the virus -laden tissue right off the healthy skin below.

It can be painful, but it's quite effective.

The blister is later debrided.

And of course, there's cryotherapy.

Just freezing it off with liquid nitrogen.

Simple and effective.

Okay.

Moving to drug -induced dermatitis.

This section is scary because it can happen so fast and be so severe.

This is a hypersensitivity reaction.

A patient takes a common antibiotic for a UTI.

And a few hours or days later, suddenly they have a rash.

It can be a simple rash or hives, which are urticaria.

Or it can be life -threatening.

And we are talking about erythema multiform, Stevens -Johnson syndrome, or SJS, and toxic epidermal necrolysis, known as TEN.

These are medical emergencies.

They're on a spectrum of severity.

In SJS, you get blistering and erosion of the mucous membranes.

The mouth, the eyes, the genitals.

In TEN, the skin literally detaches.

The epidermis slows off in sheets.

The patient looks like a burn victim and is treated in a burn unit.

What are the main culprit drugs that can cause this?

The text points to the usual suspects.

Penicillins, sulfa antibiotics like Bactrim, and certain anticonvulsants like carbamazepine or lamontrigine.

If a patient on one of these drugs starts developing any kind of rash, especially with blistering or mucosal involvement, you stop the drug immediately and notify the provider.

Let's touch on contact dermatitis quickly.

The text breaks it into two types.

First is irritant contact dermatitis.

This is direct chemical or physical damage.

Like a nurse washing hands 50 times a day with harsh soap or getting bleach on the skin.

And the second type.

Allergic contact dermatitis.

This is a delayed type V hypersensitivity reaction.

It's immune mediated.

Classic examples are poison ivy, nickel in jewelry, or a latex allergy.

And the text has a specific do not for treating the itch from this.

Yes.

Do not put topical antipyridics, anti itch creams containing things like antihistamines or anesthetics on open wounds or broken skin.

It can lead to systemic absorption and toxicity.

So what should you use?

Stick to simple barrier creams like calamine lotion, which is zinc oxide or cool compresses.

And for the itch, oral antihistamines like diphenhydramine or benadryl are much safer.

A couple of other specific conditions are mentioned.

Impetigo.

You see this in kids a lot.

It's a bacterial infection, usually staph or strep, that causes these classic honey colored crusts.

And how do we treat that?

It's very contagious.

Treatment is usually a topical antibiotic like moperosin or red -up amulet.

But here's the nursing tip.

You have to soak and gently remove the crusts first.

If you just put the ointment on top of the crust, it will never get to the bacteria underneath.

And rosacea.

Rosacea is a chronic inflammatory condition causing flushing, visible blood vessels, and sometimes swelling or bumps on the face.

Treatment starts with avoiding triggers like spicy food, alcohol, or heat, and using sunblock religiously.

Pharmacologically, topical metronidazole and azelaic acid are common.

And hair loss.

Alopecia.

The text covers two main drugs.

First is minoxidil, brand name Rogaine.

It's a vasodilator.

And we don't really know for sure why it grows hair, but it does.

It's available over the counter.

What's the catch?

You have to keep using it forever.

If you stop, any hair you re -grew will fall out.

Hair loss resumes.

And the second drug is finasteride.

Finasteride, or Propecia, is an oral drug for male pattern baldness only.

It works by blocking the enzyme that converts testosterone to dihydrotestosterone, or DHT, which is the hormone that shrinks hair follicles.

And there is a huge safety flag here.

A huge one.

We've said teratogenic a lot today, but this one has a twist.

Finasteride is absolutely contraindicated in pregnancy because it can cause abnormalities in a developing male fetus.

But the twist is about handling it.

Exactly.

The warning is that pregnant women, or women who could become pregnant, should not even handle broken or crushed tablets.

The drug dust can be absorbed through the skin and still pose a risk to a male fetus.

That is a critical handling precaution every nurse and pharmacist needs to know.

Absolutely.

The text also gives a nod to a newer drug approved in 2023,

Ritalsatinib, for severe alopecia areata, which is an autoimmune form of hair loss.

Okay, we are in the home stretch now.

Let's talk about burns.

This is a massive topic in itself.

It is.

The chapter starts with prevention, which is sunscreen.

And the text breaks sunscreen down into two types, chemical and physical blockers.

Chemical blockers like oxybenzone or avobenzone act like a sponge.

They absorb UV radiation and convert it into a small amount of heat.

And physical blockers?

Physical blockers like titanium dioxide and zinc oxide act like a mirror.

They form a physical shield on the skin that scatters and reflects the UV radiation away.

And we need to worry about both UVA and UVB rays.

What's the difference again?

A good mnemonic is simple.

UVB is for burning.

UVB rays cause sunburn and are the primary cause of most skin cancers.

UVA is for aging.

UVA rays penetrate deeper, destroy collagen and lead to wrinkles and deep skin damage.

You need a broad spectrum sunscreen that protects against both.

What about SPF?

Is higher always better?

SPF 15 is the minimum to prevent burns.

But the American Academy of Dermatology recommends SPF 30 or higher to reduce the risk of skin cancer.

And the most important thing isn't the number.

It's reapplication.

You must reapply every two hours or more often if you're swimming or sweating.

Now if prevention fails or there is a thermal or chemical injury, we classify burns by depth.

Correct.

First degree is the most superficial.

It involves the epidermis only.

The skin is red, painful, dry, but no blisters like a typical sunburn.

Second degree?

Second degree is also called a partial thickness burn.

This goes into the dermis.

The hallmark here is blisters.

The skin will be pink or red, moist and very painful.

And third degree?

Full thickness.

This is the most severe.

It destroys the epidermis and dermis and goes into the subcutaneous tissue.

The skin can look black, white, charred or leathery.

And the really scary diagnostic clue.

There is often no pain in the center of the third degree burn.

Because the nerves are burned away.

The nerve endings in the dermis have been completely destroyed.

It's an ominous sign of a very deep injury.

In the emergency setting, for a patient with severe burns, the first priority isn't the skin cream.

It's the circulation.

Not even close.

It's ABCs first.

Airway, breathing, circulation.

With major burns, there's often inhalation injury.

But the immediate life threat is fluid loss.

When you lose a large area of skin, you lose your vapor barrier.

You leak massive amounts of fluid and protein and you go into hypovolemic shock.

The text mentions the Rule of Nines and the Parkland formula.

These are for fluid resuscitation, right?

Yes.

These are tools to quickly estimate the total body surface area of the burn and then calculate the massive amount of IV fluids these patients need, especially in the first 8 to 24 hours, to survive.

Once the patient is stabilized, then we can treat the wound itself.

And the text highlights specific topical anti -infectives for burns.

The main one is silver sulfateazine.

Yes, sylvadine.

For decades, this has been the gold standard for preventing infection in second and third degree burns.

It has broad coverage against bacteria and yeast.

What are the nursing considerations for it?

It's a sulfur drug, so you have to check for sulfa allergies.

It's contraindicated in near -term pregnancy and in neonates under 2 months old because of a risk of connectoris.

And a key side effect is that it can be absorbed and cause transient leukopenia, a drop in white blood cells.

And the alternative mentioned is mafenyde acetate.

Mafenyde is great because it penetrates through the escher, the thick dead tissue of the burn, which sylvadine doesn't do as well.

But it has a price.

And that price is pain.

A lot of pain.

It causes a severe burning sensation upon application.

You need to pre -medicate the patient for pain before dressing changes.

And biologically, it's a carbonic and hydrous inhibitor.

What does that mean for the patient?

It means it can throw off the body's acid -base balance and cause metabolic acidosis.

You have to monitor the patient's breathing rate and their arterial blood gases.

So you're monitoring ABGs because of a skin cream.

It all comes full circle.

Again, dermatology is systemic medicine.

Let's bring this all home with the nursing process.

We've covered a ton of drugs and conditions.

How do we synthesize this for a nursing student?

Okay, assessment is step one.

You need a detailed history of the lesions.

When did they start?

Do they itch?

You need to describe the lesions using the proper terms we learned.

Is it a papule, a vesicle, a plaque?

If there is purulent drainage, you anticipate an order for a culture.

And labs.

We've talked about labs a lot.

Baseline labs are absolutely non -negotiable for the systemic drugs.

Liver function, renal function, CBC for methotrexate,

lipid panels and LFTs for isotretinoin, and pregnancy tests.

I cannot stress this enough.

So many of these drugs, retinoids, methotrexate, tetracyclines, finasteride, are profoundly teratogenic.

What about the psychological assessment?

Crucial.

Skin conditions can destroy a person's body image and self -esteem.

They lead to anxiety, depression, social isolation.

And as we noted, some of the drugs themselves, like isotretinoin, have a direct link to depression.

You have to ask the patient how they're feeling.

Not just about their skin, but about their life.

For planning an intervention, it's all about safety and education.

Exactly.

Teach them how to apply the medications properly.

Thin layers.

On clean skin.

Use aseptic technique for burn dressings.

Teach them the specific warnings.

Don't go out in the sun with retinoids.

You absolutely cannot get pregnant on methotrexate.

Remember to stay upright after taking your doxycycline.

And managing expectations seems like a huge part of the intervention.

Patience.

That is the hardest part for so many patients.

Acne takes weeks to clear.

Hair takes months to grow back.

Burn rehabilitation can take years.

Nurses need to provide that continuous support and education through that long timeline so that patients don't give up on their treatment.

Finally, evaluation.

Straightforward.

Is the treatment working?

Are the lesions clearing?

Is the patient safe?

Are their labs stable?

Are they free of adverse effects?

And are they coping effectively with the psychological burden of their condition?

We really have covered the skin from the outside in.

From the sub layers of the epidermis, all the way to the complex immune modulation of biologics for psoriasis.

I think the big picture takeaway here is that the skin is a vital complex organ and treating it requires a deep, deep understanding of pharmacology because you are often balancing the potential for a cure against significant systemic risks.

It connects to everything.

The liver, the kidneys, the bone marrow, embryonic development, mental health.

It is the ultimate patient -centered puzzle.

There's so much to consider for each individual.

I want to leave you with a thought to mull over.

We spent this whole hour talking about how we use drugs to suppress things in the skin.

We're suppressing bacteria.

We're suppressing oil production.

We're suppressing the immune system.

As we get better and better at these targeted therapies like the biologics, it makes you wonder what else will we be able to treat through the skin?

Or maybe more interestingly,

what systemic diseases like cardiac issues or neurological issues might we eventually be able to diagnose just by analyzing the gene expression or the microbiome of a single simple skin patch?

That is a fascinating frontier.

The skin moving from being a mirror of disease to being the diagnostic window of the future.

Thank you for listening.

This has been a deep dive into Chapter 48.

A warm thank you from Last Minute Lecture Team.

See you next time.