I - Inflammatory Skin Conditions

What is Seborrheic Dermatitis?

Subacute/Chronic inflammatory disorder

epidermal skin layer → increased proliferation

Where is seborrheic dermatitis commonly seen?

In areas of greatest sebaceous gland activity → scalp, face, chest

Presents commonly as a chronic, red, scaly, and itchy rash

What are the clinical features of infantile seborrheic dermatitis?

Occurs in first 3 months of life

Greasy scales/crust on bright red base

Common sites: scalp (cradle cap), behind ears, neck, skin folds

Self-limited → clears by 8–12 months

Rarely recurs before puberty

What are the clinical features of adult seborrheic dermatitis?

Occurs around fourth and seventh decade of life

Scalp → greasy scaling patches/plaques, thick crusting

Face → flaky/yellow scales on red, itchy skin

Ears → scaling, fissures, swelling possible

Also affects chest (V-area), back, skin folds

Seasonal pattern → better in warm weather, worse in cold

What are the treatment goals of seborrheic dermatitis?

Reduce inflammation and epidermal turnover rate of scalp/affected skin

Minimize or eliminate erythema/scaling

Minimize itch

What are the primary treatments for seborrheic dermatitis?

They work to control the disease rather than curing

Medicated shampoos

Topical corticosteroid

Examples of medicated shampoos used to treat seborrheic dermatitis?

Pyrithione zinc → OTC

Selenium sulfide → OTC

• rinse thoroughly → prevents hair discoloration (esp. light/blonde hair)

Ketoconazole → Rx

How can OTC Pyrithione zinc and Selenium sulfide be used for seborrheic dermatitis?

Work shampoo into the scalp, leave lather on the hair and affected areas for 3-5mins

Daily for 1-2 weeks → then 2-3 times a week for 4 weeks → OTC products

Once controlled, apply weekly to prevent relapse

Can follow up with cosmetic shampoo/conditioner to control odor

How can Rx Ketoconazole be used for seborrheic dermatitis?

Work shampoo into the scalp, leave lather on the hair and affected areas for 3-5mins

2 times a week for 4 weeks

Once controlled, apply weekly to prevent relapse

Can follow up with cosmetic shampoo/conditioner to control odor

How can topical corticosteroids be used to treat seborrheic dermatitis?

Used for increased inflammation

Hydrocortisone ointment can be used 2x daily

Limit use up to 7 days, then consult PCP

What are salicylic acid and sulfur used for in seborrheic dermatitis?

Keratolytic agents → help loosen and remove keratin scales

Slow onset of action → weeks to months

Limited effectiveness compared to first-line treatments

Help reduce scaling by decreasing skin pH

How is cradle cap/seborrheic dermatitis managed?

Self-limiting condition

First-line → massage scalp with baby oil to loosen scales

Use non-medicated shampoo to remove flakes → gentle baby shampoo

If no improvement → refer to pediatrician

What is Diaper Dermatitis?

Diaper Rash

A skin rash that occurs in the diaper area

Causes → occlusion, moisture, contact with urine/feces, shift in skin pH friction

Appears as bright red shiny, wet looking patches/lesions on skin

Onset is very fast, but healing is slow

What can influence diaper rash?

Infants urinate up to ~20x/day → then decreases to ~8×/day by 8 months

Breast-fed infants have lower risk

• Breast-fed stool = less alkaline, less irritating

Transition to solid foods can trigger diaper rash

What possible complications can result from diaper dermatitis?

Secondary infections → bacterial or fungal

Genital damage

Skin ulceration

What causes fungal diaper dermatitis and what does it look like?

Usually Candida albicans

Yeast infection often shows satellite lesions → clusters

Papules/pustules at margins of diaper dermatitis or in the skin folds

Non-pharmacologic counseling diaper rash?

Keep the patient dry

Change diaper at least 6x a day

Clean area with plain water / bland soft cloth or wipe

Make sure skin is dry before re-diapering → air dry

Disposable diaper decrease rates of severe diaper dermatitis

What are protectants used for in diaper rash treatment?

Non-prescription options (FDA-approved ingredients)

Act as a physical barrier → block irritants, reduce/absorb moisture

Most commonly used → zinc oxide

What are the top pharmacist recommended products for diaper rash?

Desitin Diaper Rash Cream → zinc oxide 40%, cod liver oil, white petrolatum, lanolin, talc

A+D Original Ointment → white petrolatum, lanolin

Boudreaux’s Butt Paste → zinc oxide 16%, mineral oil, white petrolatum

What are the key components of a triple butt paste for diaper rash?

Main component → Protectants/Emollients → A+D, white petrolatum (Vaseline), zinc oxide (Desitin®)

Antifungals → clotrimazole (OTC), nystatin (Rx)

Antacid → Maalox liquid, loose stools → decreases pH

Antibacterial → bacitracin ointment, questionable efficacy

Anti-inflammatory → hydrocortisone, short term use

How do you treat a candida/fungal diaper rash?

Treated with barrier creams + antifungal

Antifungals → clotrimazole (OTC), nystatin (Rx)

What are bacterial causes of diaper rash and how are they treated?

Perianal streptococcus → bright red rash around anus → requires oral antibiotics

Staph infection → crusted or oozing lesions → bacitracin or mupirocin (Rx), often still needs oral antibiotics

If unclear or not improving → refer to pediatrician

What are the key take-home points for managing diaper dermatitis?

Keep area clean and dry

Re-apply topical treatment after every diaper change

Combination “mixes” may include multiple barrier creams (protectants/emollients)

Know what’s in the mix →Antifungal, Topical corticosteroid, Antacid liquid

What is the typical treatment duration and follow-up plan for diaper rash?

Usually treated short-term (a few days) with OTC products

If no improvement after 7 days → refer to medical provider

If improving by 7 days → continue treatment for ~3 more days

What are the contraindications for self treatment of diaper rash?

Pesions present for > 7 days

Secondary infections → bacterial, fungal, viral

Presence of rash outside diaper region

Presence of broken skin → ulcers, blisters, peeling skin

Oozing, blood, vesicles, or pus at lesion sites

What prevents diaper rash?

Frequent diaper changes

Keeping area dry

Using protectants regularly → especially after bowel movement to prevent rash

What are the two types of contact dermatits?

Irritant contact dermatitis → 80-90% of all cases

Allergic contact dermatitis → 10-20% of all cases

Overall, contact dermatitis occurs in 1-10% of the population

Irritant contact dermatitis?

Caused by exposure to strong irritants → occupational acids, alkalis, fluorides

Primary irritants → cause direct skin damage

Presents with immediate severe irritation and blistering after exposure

Allergic contact dermatitis?

Caused by allergens

Ex; Plants: Toxicodendron, Metals: nickel, cobalt, chromium, Rubber and adhesives, Cosmetics, Topical anesthetics, Topical antibiotics, Topical diphenhydramine

Irritant vs Allergic contact dermatitis delay to reaction?

Irritant → minutes to hours

Allergen → days, much slower

Irritant vs Allergic contact dermatitis causative substances?

Irritant → H2O, urine, flour, detergents, hand sanitizers, soap, alkalis, acids, solvents, salts, surfactants, oxidizers

Allergen → Low molecular weight & lipid-soluble substances, fragrances, nickel, latex, benzocaine, neomycin, leather

What is the first and second line treatments in contact dermatitis?

1st → Corticosteroids

2nd → Fragrances free moistures / emollients

What are the possible mechanisms involved in the treatment of contact dermatitis?

Anti-inflammatory effects

Immunosuppressive effects

Antiproliferative effects

Vasoconstrictive effects

How corticosteroids ranked in potency?

From class 1 to class 7

Class 1 → most potent

Class 7 → least potent

Low potency corticosteroids?

Class 6/7

Safe for infants, children, longer duration, or intertriginous areas

Medium potency corticosteroids?

Class 4/5

Safe for short durations in infants and children → face, axillae, genitals ok in adults

High potency corticosteroids?

Class 2/3

May be used with close supervision in children for short (<2 weeks) duration

Ultra high potency corticosteroids?

Class 1

No occlusion, maximum duration 2-4 weeks

Do not use in infants, children, on face, axillae, or groin

How do corticosteroids effect the HPA axis?

Exogenous steroids cause negative feedback on the HPA axis

Leads to decreased endogenous cortisol production over time

Typically seen with high/ultra-high potency topical steroids

Risk increases with use on >20% body surface area for >4 weeks

What factors should be considered when selecting a topical corticosteroid?

Potency

Vehicle type → ointment > gel > cream > lotion

Frequency of application

Area being treated (size and location)

How does the treatment area affect the choice of corticosteroid formulation?

Large areas → ointments may be impractical (too greasy/viscous)

Hairy/scalp areas → prefer foam, shampoo, or aerosol

Less suitable → ointments or creams for scalp/hair-bearing skin

How is topical corticosteroid potency chosen when treating dermatitis?

For dermatitis, potency depends on skin thickness and location

Thick skin (palms, soles, scalp) → high potency steroids

Moderate skin (arms, legs, abdomen) → medium potency steroids

Thin/sensitive skin (face, eyelids, anogenital area) → low potency steroids

What counseling points are important for topical corticosteroid use in dermatitis?

Use a small amount → a little goes a long way

Apply only to affected dermatitis areas

Wash hands before and after application

What are the side effects of topical corticosteroids?

Acneiform lesions

Striae → thinning of skin

Pigmentation changes

Folliculitis

Fungal infections, delayed wound healing

Possible perioral dermatitis if applied close to the mouth

The most potent the more quickly these symptoms can present !!!!

OTC Hydrocortisone?

Is the only OTC topical corticosteroid available

Available as → Hydrocortisone 0.5–1%

Can be effective for small-area contact dermatitis (may need stronger Rx steroid for larger areas)

Apply to affected area 3–4 times daily

When are systemic corticosteroids used in contact dermatitis?

Used when ≥20% body surface area is affected

Indicates more severe/widespread contact dermatitis

What systemic corticosteroid is used for contact dermatitis?

Prednisone → 0.5–1 mg/kg daily for ~10 days

Less 2–3 week courses usually do not require tapering

Dermatology often still uses tapers to reduce flares

What is poison ivy?

A type of allergic contact dermatitis

How do you treat poison ivy?

Topical hydrocortisone → 3-4x daily

Oral hydrocortisone → prednisone can be used as well

Oozing → astringents → domeboro, witch hazel, or calamine

Topical diphenhydramine?

NEVER THE ANSWER !!!!!

Non-pharmacologic options for allergen contact dermatitis?

Know the allergen and avoid it

Wear protective clothing when potentially being exposed to allergen

Non-pharm options urushiol oil specific?

Do not burn the plants → increases exposure

Immediately after exposure → remove clothes and wash separately with laundry detergent

Wash things that may have had oil transfer to them

Clip/trim nails to avoid transfer of urushiol

Wear gloves when washing contaminated objects

Barrier products for poison ivy?

Zanfel

Tecnu

Tecnu extreme

Exclusions for self treatment for allergen/irritant dermatitis?

Involvement of >20% BSA

Swelling of the body/extremities

Swollen eyes/eyelids shut

Discomfort in genitalia from itching, redness, swelling, or irritation

Involvement and/or itching or mucous membrane of mouth, eyes, nose, or anus

Signs of infection

What is the treatment for a contact dermatitis flare?

inflammation/pruritus → Corticosteroids

Oozing →Aluminum acetate, witch hazel, calamine, dressings

Itch relief/sleep→ 1st gen antihistamines

Atopic Dermatitis?

Eczema

Chronic inflammatory pruritic skin disease

Caused by → genetics, environment, skin barrier defects, immune system

What are the pattern and characteristics of atopic dermatitis?

Chronic, relapsing course

Often improves in childhood by puberty

Some develop atopic triad → asthma, allergic rhinitis, eczema

• associated with increase IgE and other atopic conditions

How does immune dysfunction contribute to atopic dermatitis?

Imbalance of TH1 and TH2

TH2 overactivity → increase IL-5, IL-13 → more inflammation and IgE

TH1 normally helps → decrease IgE and inflammation

Why is keeping the skin barrier intact important in atopic dermatitis?

It helps to limit the access of infection, dust, allergens, etc.. that can trigger inflammation

What are the main goals of nonpharmacologic treatment for atopic dermatitis?

Avoid triggers

Reduce itching and scratching

Maintain skin hydration

Prevent infection

Restore skin barrier function

What are recommended nonpharmacologic treatments for atopic dermatitis?

Fragrance-free moisturizers / emollients used regularly

Mild cleansers

Ex; ceramides (CeraVe), white petrolatum, Eucerin, Vanicream, Cetaphil

Non-pharmacologic suggestions for atopic dermatitis?

Avoid excessive bathing

Apply moisturizers immediately after bathing

Use humidifier in dry seasons/low humidity environments

Avoid known irritants

Minimize scratching

Wet wraps

Bleach baths

What is the treatment for a atopic dermatitis flare?

Inflammation → Emollients then topical corticosteroids, → Eucrisa → topical calcineurin inhibitors

Pruritis/Controlling allergies → 1st or 2nd generation oral antihistamines

Eucrisa / Crisaborole ?

Used for atopic dermatitis

MOA → PDE-4 inhibitor → prevents cAMP breakdown → decreases pro-inflammatory cytokines and increases anti-inflammatory mediators

Dosing → topical used 2x daily

2% ointment

Side effects → itching, hypersensitivity reactions

Pimecrolimus/Elidel and Tacrolimus/Protopic?

Used for atopic dermatitis

Calcineurin inhibitors

MOA → inhibits calcineurin from initiating T cell activation → decreases itching/inflammation

What Pimecrolimus/Elidel and Tacrolimus/Protopic used as?

An alterative option to long-term use of corticosteroids → but much more $$$

No skin atrophy/striae and can be applied to face and children

What are the side effects/black box warning of calcineurin inhibitors?

Pimecrolimus/Elidel and Tacrolimus/Protopic can cause → burning, stinging, and immunosuppression

Long term use has been linked to basal cell and squamous cell carcinomas as well as lymphomas

What are alternative treatments for moderate–severe atopic dermatitis?

JAK inhibitors (oral/topical):

• Cibinqo (abrocitinib) – oral

• Rinvoq (upadacitinib) – oral

• Opzelura (ruxolitinib) – topical

Interleukin antagonists (injectables):

• Dupixent (dupilumab) – blocks IL-4 & IL-13

• Adbry (tralokinumab) – blocks IL-13

Atopic vs Contact Dermatiitis?

Contact → Topical or oral corticosteroids, avoid allergen

Atopic → Maintain skin barrier, can progress to topical steroids, calcineurin inhibitors, eucrisa, complex immunologic agents

Psoriasis?

Increased proliferation of epidermis due to inappropriate migration of T cells/cytokines leading to plaque formation

Chronic inflammatory multi-system disease that waxes/wanes over time

Can be associated with other disease → Chron’s, Ulcerative colitis, MS, obesity, lymphoma

What are the characteristic lesions of plaque psoriasis?

Thick raised plaques (most common form, ~80–90% of cases)

Silvery-white scales

Well-demarcated deep red (erythematous) lesions

What are the therapeutic goals of psoriasis?

Chronic disease → control symptoms

Maximize adherence to therapies

Minimize drug toxicity

Improve cosmetic appearance of the skin

Preserve quality of life

Minimize joint symptoms when present

How is psoriasis classified by severity?

Based on quality of life scores and psoriasis area severity indices

PASI improvement of 75% → treatment is considered effective

Mild → <3% BSA

Moderate → 3–10% BSA

Severe → >10% BSA

What is the treatment algorithm for mild to moderate psoriasis?

Start with topical agents and moisturizers

If inadequate → add phototherapy

If still inadequate → add systemic agents

If controlled → step down to lowest effective doses and continue maintenance

What is the treatment algorithm for moderate to severe psoriasis?

Start → systemic therapy and topical agents or phototherapy

If inadequate → switch to more potent systemic therapy or rotate ≥2 systemic agents

If still inadequate → biologic (complex therapy)

If controlled → step down to lowest effective dose + continue moisturizers

What are the general principles of topical therapy in psoriasis?

Vehicle matters (cream, ointment, etc.)

Can be used short-term or long-term

Can be combined with phototherapy or systemic therapy

Choose regimen based on patient adherence and ease of use

What are the goals and key points of topical corticosteroids in psoriasis treatment?

Goals → decrease erythema, scaling, and pruritus

Often use higher potency earlier than in other skin conditions

Guidelines recommend starting with potency level 2–5

Main role → reduce inflammation and plaque symptoms

What are key dosing considerations for topical corticosteroids in psoriasis?

Occlusion (plastic wrap / wet wraps) increases potency

Apply BID to TID

Ointments are more potent than creams

Vehicle choice depends on plaque location and skin area

Type of hydrocortisone cream for lesions on hands/feet?

High potency

Vehicle → Ointments, emollients, gels

Ex; Betamethasone, clobetasol, triamcinolone

Type of hydrocortisone cream for lesions on trunks/extremities?

Potency → Med-High

Vehicle → Ointments, creams, emollients

Ex; Fluocinonide cream, triamcinolone

Type of hydrocortisone cream for lesions on scalp?

Potency → Med-High

Vehicle → Solutions, oil, sprays, foams

Ex; Clobetasol solution/foam, Derma Smoothe-FS

Type of hydrocortisone cream for lesions on Face or Axillae?

Potency → Low-Med

Vehicle → Creams, lotions

Ex; Desonide, Hydrocortisone

Type of hydrocortisone cream for lesions on ear canals?

Potency → Low

Vehicle → Lotions, creams, solution, oils

Ex; Desonide lotion, fluocinolone oil

Counseling for topical steroids?

A lil bit goes a long way

Only apply to affected area

Wash hands before/after use

Use higher potency steroids no longer than 2-3 weeks for flares unless under supervision of provider

Higher potency → side effects can pop up earlier

What are vitamin D analogs and how are they used in psoriasis treatment?

First-line topical therapy → often combined with topical corticosteroids or used to provide steroid-sparing effect

Ex; Calcipotriene

MOA: regulates skin cell growth and differentiation

Dosing: thin layer applied BID

$$$$

Possible adverse effects of Vitamin D analogs?

Burning, itching, skin irritation

Erythema, dry skin

Exacerbation of psoriasis

Hypercalcemia → rare

Other steroid sparing topical therapies for psoriasis?

Tazarotene (Tazorac): topical retinoid → increases cell turnover → used common in acne

Calcineurin inhibitors → used for maintenance after 2–4 weeks of steroids or in sensitive areas (face, groin, armpits, nails)

• Typically limited use: ~8–12 weeks for calcineurin inhibitors

Phototherapy in psoriasis ?

UVA radiation

Causes DNA damage → decreases skin cell proliferation

Can be delivered via light boxes or controlled sun exposure

Typical regimen: ~15 minutes, no sunscreen, ~3 times per week (summer)

Possible adverse effects of phototherapy?

Increased risk of skin cancer

Cataracts

Nausea

Skin burning

What is coal tar and how is it used in psoriasis treatment?

3rd/4th line therapy

MOA → inhibits skin cell reproduction

Forms → shampoos, bath preparations

Often used with phototherapy

Adverse effects → unpleasant odor, staining, messy to use

When is systemic therapy first-line in psoriasis?

When psoriatic arthritis → joint involvement is present

Widespread skin involvement/lesions

Moderate to severe disease (>3% BSA)

Examples of systemic therapies for psoriasis?

Methotrexate

Cyclosporine

Acitretin

Methotrexate?

MOA → Folate antagonist leading to decreased cell replication

Dosing → 10-25mg once weekly

Titrate upwards based on response by 2.5mg/week

Max dose → 30mg/week

Methotrexate adverse effects?

GI toxicity → anorexia, nausea

Liver toxicity → fibrosis/cirrhosis

Neutropenia, thrombocytopenia, anemia

MANY DDIs

Cyclosporine?

MOA → Immunosuppressant via reversible inhibition of lymphocytes

Works very fast

Cyclosporine dosing?

PEDs → 3-5mg/kg daily

Adults → 150mg-300mg BID

Cyclosporine requirements?

Bloodwork and monitoring requirements → CBC, BMP, Trigs, Uric acid, BP

MANY DDIs

Acitretin?

Aka Soriatane

MOA → unknown, thought to decrease cell life proliferation/differentiation

Avoid alcohol

Known teratogen → pregnancy may be considered 3 years after last does

Acitretin adverse effects?

Hyperlipidemia

Liver toxicity

Bone/muscle pain

Pseudotumor cerebri → increase in intracranial pressure without tumor → headache, vision changes, papilledema

Eye irritation

Contraindicated in pregnancy (teratogenic)