Chapter 56: Dermatological Drugs – Skin Treatments & Wound Care

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Welcome to the Deep Dives.

Today, our mission is really a crash course in

dermatological pharmacology.

We're diving deep into chapter 56, focusing just on topical drugs.

And it's not just about listing meds.

Not at all.

We're exploring this fundamental challenge.

How do you get potent drugs into the skin,

the body's largest organ, for local action?

While keeping them out of the bloodstream as much as possible.

That's the key tension.

Exactly.

Local effect versus systemic absorption.

Right.

And to really get that, you've got to appreciate the skin itself.

I mean, it's an amazing structure.

Protection, sensation, regulating temperature, and crucially, that protective barrier function.

It keeps this weakly acidic surface.

The pH is usually between 4 .5 and 5 .5.

Which sounds technical, but it's actually quite smart.

Oh, totally.

That slight acidity, it's a natural defense, really discourages lots of nasty microorganisms from growing.

Okay.

So let's talk architecture.

The book mentions two main layers, right?

First, there's the epidermis, a vascular, so no blood vessels.

Correct.

That's the outermost thinner layer.

And within that, the real powerhouse for protection is the stratum corneum.

Ah, the horny layer.

Sounds tough.

It is.

Built from keratin, water repellent.

It's the main barrier we're trying to get drugs through.

Okay.

And beneath that?

That's the dermis.

Much, much thicker, like 40 times thicker.

And unlike the epidermis, it's packed with blood vessels, nerves, glands,

the works.

So that's the danger zone for systemic absorption.

Precisely.

The drug needs to get through the epidermis, but ideally, stop before it hits those deep dermal blood vessels in large amounts.

Which brings us right back to how these drugs are delivered.

The core idea seems to be the package is the potency, almost.

That's a great way to put it.

The formulation, the vehicle, it's huge.

It determines how nice it feels, sure.

But more importantly, how effective it is, how deep it penetrates.

So give us some examples, like cream versus ointment.

Okay, so cream is water -based.

It usually feels lighter, easier to remove.

Good for moist areas, maybe larger surfaces.

And ointment, though, that's greasy.

It's occlusive, meaning it forms the sealed layer over the skin.

Like trapping things in.

Exactly.

It attracts moisture, which is great for dry, scaly stuff.

And that occlusion, it seriously pushes the drug penetration,

makes it more potent, effectively.

And gels.

Gels are another common one.

Their formulation often promotes even better penetration than creams, kind of a middle ground sometimes.

The goal is always local action, minimal systemic uptake.

Okay, groundwork laid.

Now what happens when that barrier is breached?

Let's talk infections.

Bacterial ones first.

Things like impetigo, folliculitis.

Cellulitis, yeah.

Usually caused by the usual suspects.

Striptococcus pyogenes, Staphylococcus aureus.

So what do we use?

Well, we often start with well -known agents.

Bucetracin, for instance.

It's a polypeptide, messes with bacterial cell wall building.

Bacteriostatic or bactericidal?

Can be either.

Depends on the bug and concentration.

You often see it mixed with neomycin and polymixin B.

Ah, Neosporin and those triple antibiotic ointments.

Exactly.

Generally pretty safe, but you always watch for local reactions like a rash.

Allergies can happen.

But the big worry these days is resistance.

MRSA specifically.

What's in the toolkit for that?

Yeah, MRSA is a huge challenge.

And that's where Mupurosin, brand name Bactroban, becomes really important.

Prescription only.

Used for impetigo, right?

But also - Also, and this is key, for treating nasal colonization with MRSA.

Trying to stop the spread, basically.

It's a really high leverage intervention.

Side effects.

Usually pretty mild.

Maybe some local burning or itching.

Nothing too dramatic, typically.

Okay, shifting gears dramatically.

Burns.

A completely different ball game.

Why is topical therapy so essential, even if the patient's getting IV antibiotics?

Ah, good question.

Because a serious burn destroys the local blood supply in that damaged tissue.

So the IV drugs just can't get there.

Exactly.

Even potent systemic antibiotics can't reach the site in concentrations high enough to work effectively.

So we have to go topical.

Drugs like silver sulfidizine or flamazine.

For preventing and treating infection in second and third degree burns.

Makes sense.

But doesn't that create a new problem?

It absolutely does.

It's a paradox.

You need the topical because the systemic stuff can't get in.

But the skin barrier is totally gone.

Right.

So the risk of the topical drug getting absorbed systemically goes way up.

So the drug choice is critical.

Extremely.

Silver sulfidizine works on the cell membrane and wall, but you have to be super vigilant about potential systemic effects.

And crucially, it's contraindicated if the patient has a known sulfalogy, phonemide allergy.

Very important.

Okay.

From bacterial invaders to something more complex.

Yeah.

Acne.

Not just an infection.

Yeah.

Hormones, genetics, and that specific bug,

propionobacterium acnes.

Right.

Acne vulgaris.

It's multifactorial.

So our treatments often hit it from different angles.

Benzoyl peroxide is a classic example.

How does that one work?

It releases active oxygen.

P.

acnes hates oxygen.

It's anaerobic.

So it creates a hostile environment.

Plus it's keratolytic.

It softens and loosens that outer skin layer, helping to unplug pores.

But you need to tell patients, this takes time.

Like 8 to 12 weeks for real improvement.

And side effects.

Peeling.

Mild peeling and redness are expected, especially at first.

But if you see blistering, significant swelling that suggests an allergy and they need to stop and report it right away.

Then we get into the vitamin A derivatives, the retinoids.

Yes.

Topical tretinoin is powerful stuff.

It basically speeds up skin cell turnover, causes peeling.

Good for acne, but also sun damage.

Yeah.

Interestingly, it seems to help repair UV damage by boosting caudrine production.

But the big nursing point here,

photosensitivity.

Mimi.

Makes the skin very sensitive to sunlight.

So apply it in the evening and sunscreen during the day is absolutely non -negotiable.

Start with lower strengths too.

Okay.

This leads us to probably the biggest warning in the chapter.

Yeah.

Oral isotretinoin.

Accutane.

Given the risks, is it still justified?

It is, but only for severe recalcitrant cystic acne, the kind that hasn't responded to anything else.

But the risk.

It's huge.

Teratogenicity.

It's a proven human keratogen.

Causes severe birth anomalies.

This means incredibly strict risk management programs are mandatory.

Like Canada's PPP pregnancy prevention program.

Requiring counseling.

Contraception.

Absolutely.

Documented negative pregnancy tests.

Ongoing contraception for anyone who could potentially become pregnant.

It's that serious.

And there's more, isn't there?

Mood changes.

Yes.

There are case reports linking isotretinoin used to depression and anxiety.

It's vital patients know this and report any mood changes immediately.

Patient education here is just paramount.

Absolutely highlights the need for communication.

Okay.

Let's pivot to another chronic condition.

Psoriasis.

Right.

Psoriasis.

That chronic condition with the thick scaly plaques.

It's caused by keratinocytes skin cells growing abnormally fast.

The topicals aim to slow that down.

Exactly.

Calcipotrial is one.

It's a synthetic vitamin D3 analog.

It helps regulate the growth and reproduction of those overactive keratinocytes.

And are there retinoids for psoriasis too?

Right.

With similar risks.

Good connection.

Yes.

Tazeratine is a receptor -selective retinoid used for psoriasis.

It helps normalize how the skin cells differentiate.

And just like isotretinoin.

Pregnancy risk.

Definitely.

It's not recommended during pregnancy.

Requires that negative pregnancy test before starting.

The risk is tied to the retinoid mechanism itself, not just whether it's oral or topical.

Okay.

Let's quickly cover some other common skin issues.

Fungi.

Ah, yes.

Fungi, like Candida, causing yeast infections and dermatophytes, which cause tinea, or ringworm,

athleks foot, jock itch.

They like warm, moist places.

They do.

Luckily, we have good OPC options.

Clutrimazole, you know, canistin is great.

Treats both dermatophytes and yeast.

And importantly, it's considered safe during pregnancy.

Good to know.

And myconazole.

Similar profile.

Monastatomycotine.

Also OTC.

Treats both types of infections effectively.

Widely used.

What about viruses, like herpes outbreaks, topical or systemic?

Well, systemic therapy is usually better for managing the whole viral condition long -term.

But for acute outbreaks, like a cold, sore flare -up, topicals are used.

A cycle of your zoverax is the main one.

How does it work?

It messes with the enzymes the virus needs to replicate its DNA.

Stops it from multiplying locally.

Application sounds intense, though.

It is.

Four to six times a day.

For up to ten days.

That's a huge commitment for adherence and really critical.

You must use a finger caught or glove for application.

To avoid spreading it.

Exactly.

Spreading it to other parts of your body or to other people.

Very important instruction.

Four to six times daily.

Wow.

Okay, last group in the section.

Parasites.

Licensed scabies.

Ectoparasites.

Yeah, treatments often face resistance problems because we've used neurotoxic pesticides for so long, but there's a newer interesting option.

Dometicone, 50%.

NIDA.

How's it different?

It's not neurotoxic.

It works physically.

It basically suffocates the lice and their eggs by blocking their breathing spiracles.

That smothers them.

Pretty much.

And because it's a physical mechanism, not chemical, resistance doesn't develop.

Apply to dry hair, leave it 30 minutes, comb out.

Sometimes physics wins.

Fascinating.

Okay, let's talk about some of the most widely used topicals.

Anesthetics and the big one, anti -inflammatories.

Right.

Topical anesthetics are fairly straightforward.

They numb the skin block, nerve impulses, good for insect bites, minor procedures, maybe before an injection.

Like EMLA cream.

Yeah, the lidocaine -prelicaine combo.

Very common.

But remember, it needs time to work, usually about an hour.

So you have to plan ahead for procedures.

Okay, now the heavy hitters.

Topical corticosteroids.

Yeah.

Anti -inflammatory, anti -itch,

vasoconstrictive.

They do a lot.

But the key seems to be potency.

Potency is everything with topical steroids.

And it goes right back to that core principle we started with.

The vehicle matters.

How so?

Ointments are the most occlusive, right?

So they drive the steroid in the most effectively.

They're the most potent.

Then usually gels, then creams.

And finally, lotions are the least potent.

Same drug, different vehicle, different strength.

That's crucial to understand.

And side effects.

Oh, yeah.

Local reactions are common with long -term or high potency use.

Skin thinning, fragility, stretch marks, acne -like eruptions, hypopigmentation.

And because they suppress the immune system locally?

You get an increased risk of secondary infections.

Fungal, bacterial overgrowth in the treated area.

You have to watch for that.

And they can stop working effectively over time.

Yes.

That's tachyphylaxis.

A rapid decrease in effectiveness with repeated use.

It's a real issue with chronic steroid application.

And a huge safety point.

Never combine oral and potent topical steroids.

Absolutely critical.

The risk of systemic toxicity, adrenal suppression.

Yeah.

It's just too high.

Avoid combining them unless specifically directed under close supervision.

Okay.

We also have a couple of other interesting topicals mentioned.

Hair growth.

Right.

Minoxidil, Rogaine.

It's actually a vasodilator.

Started as a blood pressure med.

Topically, it stimulates hair growth for some people.

Systemic risks if absorbed.

Yes.

If enough gets absorbed, you could see tachycardia, fluid retention, weight gain, things related to its blood pressure effects.

And an interesting tip.

Heat, like from a blow dryer, can apparently reduce its effectiveness.

Good practical point.

And finally, anti -cancer topicals.

Yeah.

Specifically, Floresil or eFUDEX.

It's an anti -metabolite.

Used for pre -cancerous lesions like actinic keratosis or superficial basal cell carcinomas.

How does it work?

It basically targets and destroys rapidly growing cells like those abnormal skin cells.

But patients need serious education here.

Because?

Because it causes a significant local reaction.

Redness, erosion, crusting, pain.

It looks quite dramatic as it works.

Plus, major photosensitivity, sun avoidance is key.

Okay.

That covers a lot of drugs.

Let's bring it back to the clinic.

The nursing process.

Given everything we've discussed about absorption varying with age, skin condition, what are the absolute assessment priorities?

Assessment is just fundamental here.

First up, allergies.

Always check.

Especially if they have a known allergy to a systemic antibiotic that often carries over to the topical form.

Makes sense.

What else?

Age is critical.

Children, older adults, their skin is thinner, more fragile, more permeable.

That means a much higher risk of the drug getting into the bloodstream.

You have to be more cautious.

Maybe use lower potencies or apply less frequently.

And skin condition itself.

Absolutely.

Is the skin broken, inflamed, hydrated?

All these affect how much drug gets absorbed.

Also, a really important point for diverse populations.

In patients with darker skin tones, redness erythema might not be obvious visually.

So how do you assess inflammation?

You have to palpate.

Feel for warmth.

Warmth often indicates inflammation in darker skin when redness isn't apparent.

It's a key assessment skill.

Okay.

Assessment done.

Now, implementation.

Applying the medication.

What are the non -negotiables?

Rule number one,

always cleanse the area first.

Gently remove any old medication, crusts, debris.

You want the new dose applied to clean skin.

And the most important personal protective equipment.

Gloves.

Always wear gloves.

This isn't just standard precautions for the patient.

It's to protect you, the caregiver.

You don't want potent corticosteroids or antivirals absorbing into your own skin day after day.

Critical point.

And the application technique itself.

Less is more.

Apply a very thin layer.

Just enough to cover the affected area.

Only the medication directly touching the skin does any good.

Piling it on just increases waste and the risk of side effects or systemic absorption.

Got it.

Thin layer, wear gloves,

and shake lotions.

Yes.

Definitely shake lotions or solutions well before applying to make sure the drug is evenly distributed.

And obviously patient education.

Hugely important.

Covering adherence, especially for things like a psych lover needing multiple daily doses.

Explaining expected side effects versus allergic reactions.

Reinforcing those photosensitivity warnings for retinoids and floresil.

And of course, the absolute criticality of the pregnancy prevention programs for isotretinoin and tazeratine.

So how do we know if it's working?

Evaluation.

When do you call the provider?

You monitor for the therapeutic response you expect.

Is the redness going down?

Less itching.

Signs of healing.

Lesions shrinking.

That's what you want to see.

And if you don't see it.

If there's no improvement within say 48 to 72 hours or if things actually get worse, more pain, swelling, drainage, new irritation, or especially if the patient develops systemic symptoms like a fever, then you absolutely need to notify the prescriber right away.

Great summary of the clinical side.

So that was quite a deep dive.

Really zeroing in on that core tension.

Getting drugs to work locally in the skin while minimizing systemic risks.

Yeah, we hit some key areas.

The necessity of topicals like silver sulfateazine for burns because systemic drugs can't reach.

The complexity and serious risks of retinoids like isotretinoin.

And that crucial link between the vehicle ointment, cream, lotion, and the potency of corticosteroids.

Absolutely.

And the underlying message is that you really need to understand not just the drug but the formulation.

How it interacts with the skin and all those nursing considerations.

Assessment, application, education.

That's what makes topical therapy safe and effective.

Couldn't agree more.

So as you digest all this, here's a final thought to chew on building on what we discussed.

We know topical corticosteroid potency varies hugely based on the vehicle.

Ointment is strongest, lotion weakest.

We also talked about tachyphylaxis, the drug losing effectiveness over time.

So imagine you have a patient with chronic

psoriasis experiencing tachyphylaxis to their current steroid cream.

How might a clinician ethically manage that without just jumping to a stronger steroid molecule, potentially increasing long -term risks?

Could manipulating the vehicle maybe switching from a cream to a more occlusive ointment base of the same drug be a potential strategy to regain efficacy before escalating the drug itself?

Oh, that's a good one.

Using formulation science to manage tolerance.

Interesting angle.

Something for you to consider as you continue your studies.

Thanks for joining us for this deep dive.

From our team to yours, this has been the Last Minute Lecture Team signing off.