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L 21 Dermatology Disorders - Noninfectious, Inflammatory: Comprehensive Study Notes

Classification scheme for dermatologic disorders

  • Papulosquamous and eczematous dermatoses
  • Urticarias and erythemas
  • Autoimmune connective tissue diseases
  • Autoimmune bullous diseases
  • Bacterial
  • Viral
  • Fungal
  • Malignant
  • Protozoal
  • Benign
  • Infectious
  • Non-infectious inflammatory
  • Neoplastic
  • Dermatologic disorders
  • Other
  • Metabolic and toxic insults/trauma
  • Genodermatoses and developmental anomalies

Atopic Dermatitis

  • Epidemiology
    • The most common chronic, relapsing skin disease seen in infancy and childhood
    • Approximately 9.6\times 10^6 U.S. children under the age of 18 have AD, and \tfrac{1}{3} have moderate to severe disease
    • The prevalence of childhood AD has increased from 8\% to 15\% since 1997
    • An estimated 16.5\times 10^6 U.S. adults (7.3\%) have AD, with nearly 40\% affected with moderate to severe disease
    • Children may have disease remission in adolescence that recurs during adulthood
    • 1\text{ in } 4 adults report adult-onset of symptoms
  • Pathogenesis
    • Multifactorial: skin barrier abnormalities, altered immune response, and reduced antimicrobial activity of the skin (interacting factors)
    • Loss-of-function mutations in the FLG gene (filaggrin) in some people; filaggrin is a major protein in the stratum corneum essential for outer epidermal hydration
    • Leaky skin barrier → increased water loss and entry of pathogens/allergens
    • About 70\% of patients have a family history of atopic disease (allergic rhinitis, asthma, eczema)
  • Clinical manifestations
    • Severe xerosis (dry skin); fine scaling and roughness
    • Intense pruritus, especially at night
    • Erythema, erosions, oozing, crusting; cutaneous reactivity
    • Scratching → inflammation → eczematous lesions
  • Triggers for flare-ups
    • Foods (food allergy common in children)
    • Aeroallergens (dust mites, pet dander)
    • Infection
    • Temperature/humidity extremes
    • Irritants (soaps, detergents with fragrance)
    • Tight-fitting clothing/abrasive fabrics (e.g., wool)
    • Stress
  • Location by age
    • Infants: face, scalp, cheeks, extensor surfaces; diaper area usually spared
    • Older children: antecubital and popliteal folds, head, posterior neck, dorsum of feet and hands
    • Adolescents/Adults: face, back, wrists, hands, dorsal feet; limb flexural and extensor surfaces may be involved
  • Diagnosis and severity assessment
    • Diagnosis based on clinical features
    • Severity determined by extent of lesions, intensity of pruritus, and impact on quality of life (sleep, activities)
    • Treatment goals: reduce severity and number of flares
  • Nonpharmacologic management
    • Skin hydration and trigger avoidance
    • Emollients/thick creams (low water content) applied at least twice daily
    • Hydration after bathing or hand washing
    • Wet wraps can be helpful
  • Pharmacotherapy 1) Topical corticosteroids
    • Therapy for acute flares and relapse prevention
    • Use ointment rather than cream/lotion
    • Start with the least-potent class that is effective; increase potency with age and disease severity
    • Low potency for face and skin folds; monitor for skin atrophy (most common adverse effect)
      2) Topical immunomodulators
    • Tacrolimus (PROTOPIC), pimecrolimus (ELIDEL)
    • Approved for children older than 2 years; can be used on face
    • Possible link with cancer; no definitive causal link
      3) Crisaborole (EUCRISA)
    • Topical PDE4 inhibitor; approved 2016; safe, somewhat effective; more expensive than topical corticosteroids
      4) Dupilumab (DUPIXENT)
    • Dual IL-4 and IL-13 signaling inhibitor; biologic; addresses pro-inflammatory response
    • Approved for pediatric patients 6 months and older with moderate-severe AD not adequately controlled with topical therapies or when those therapies are not advisable
      5) JAK inhibitors
    • Various agents under investigation/approval; used in refractory cases
  • Guidelines and practice parameters (AAAI/ACAAI JTFPP 2023)
    • Clinicians should address diagnosis accuracy, triggers, and shared decision making before new therapy
    • Topical treatments: moisturizers, corticosteroids, calcineurin inhibitors, PDE inhibitors; consider bleach baths for infection control
    • Emphasis on education, triggers avoidance, adherence, and stepwise therapy based on severity
    • Maintenance and proactive strategies; consideration of systemic therapies for severe disease when appropriate
  • Nonpharmacologic guidelines (2023 JTFPP summary)
    • Moisturizers: bland, fragrance-free; at least once daily; more effective with regular use
    • Bleach baths: used as an adjunct in certain patients to reduce bacterial colonization (low certainty evidence)
    • Proactive maintenance therapy: treat flare-prone areas with intermittent calcineurin inhibitors or mid-potency steroids to reduce relapse
  • Complications & prognosis
    • Complications: susceptibility to bacterial/viral/fungal skin infections; bleach baths to prevent superinfection; antibiotics as needed
    • Prognosis: most severe in infancy/young children; about 80\% of children outgrow AD by adolescence or adulthood, though xerosis and hypopigmentation may persist; familial history, early onset, severe disease, and comorbid allergic disease predict poorer long-term remission
  • Additional notes
    • Atopic march: infants with AD may develop food allergies, allergic rhinitis, and asthma later in childhood
    • The role of filaggrin gene FLG mutations and barrier integrity in disease susceptibility

Contact Dermatitis

  • Definition and types
    • Acute or chronic skin inflammation due to environmental exposures
    • Affects all ages; subdivided into irritant and allergic contact dermatitis
    • Irritant contact dermatitis: nonimmunologic, chemical/physical alteration of epidermis, occurs only at contact site, burning/stinging pain
    • Allergic contact dermatitis: delayed-type hypersensitivity, extends beyond contact area, requires sensitization
  • Pathogenesis
    • Irritant: direct chemical/physical irritation; high concentration leads to immediate symptoms
    • Allergic contact dermatitis (ACD): sensitization to chemical, subsequent reaction upon re-exposure; T-cell mediated response
  • Clinical manifestations
    • Acute ACD: well-demarcated plaques with erythema, edema, vesicles; erosions with serous crusts; linear/irregular patterns
    • Chronic ACD: lichenified, scaly plaques from ongoing exposure
  • Common triggers
    • Nickel, poison ivy (urushiol), rubber, clothing, cosmetics, fragrances, topicals, workplace exposures
  • Patch testing
    • TRUE Test or similar: 35 allergens + 1 control; patches applied to back; home wear until removal
    • Reading times: first read at 48 hours; additional reading at 96 hours
    • Pre-test instructions: avoid topical corticosteroids at patch site for 1 week; avoid systemic/long-acting steroids for 1–2 weeks
    • Post-test: avoid showering until patch removal; avoid sweating/heavy lifting until evaluation
  • Patterns and examples
    • Common patterns include allergens in: rubber, nickel, clothing, cosmetics, dyes, metal objects; illustrative patterns show multiple potential sources
  • Diagnosis
    • Based on history, exam, and patch test results
  • Treatment
    • Nonpharmacologic: avoid irritants/allergens, cold compresses, colloidal oatmeal baths, patient education with allergen avoidance resources
    • Pharmacotherapy: topical corticosteroids; oral or IM corticosteroids for severe cases; oral antihistamines for pruritus; epinephrine for anaphylaxis in severe reactions; biologics such as anti-IgE (omalizumab) for selected cases
  • Prognosis
    • Allergic contact dermatitis typically resolves in 2$-$4 weeks if re-exposure to the allergen is prevented

Seborrheic Dermatitis

  • Definition and epidemiology
    • Chronic inflammatory disease with sebaceous gland activity and folds; prevalence 3$-$5\%; more common in immunocompromised patients; affects all ages; males > females; peak incidence in the 5^{th}–6^{th} decades
    • In infants (cradle cap) onset in first 3 months of life
    • Extensive disease can be a sign of HIV; often coexists with psoriasis
  • Pathogenesis
    • Chronic inflammation and sebaceous gland overactivity; genetic and environmental factors
    • Possible relation to abnormal immune response to yeasts Pityrosporum ovale and Malassezia furfur
  • Clinical manifestations
    • Erythematous plaques with greasy, loose scale; generally symmetrical
    • Common locations: scalp, eyebrows, beard area, ears, nasolabial folds, anterior chest, umbilicus, intertriginous areas (less scale)
  • Pharmacotherapy
    • Adults: scalp shampoos with zinc pyrithione or selenium; ketoconazole shampoo 1% or 2% used twice weekly; facial disease with mild, intermittent topical corticosteroids near eyes; ketoconazole 2% cream for persistent areas; intertriginous areas with low-potency corticosteroids; adjuncts include selenium lotion and ketoconazole/clotrimazole gels/creams
    • Infants: mild scalp shampoo; mineral oil or petroleum to loosen scales (cleansed afterward); ketoconazole 1% cream for extensive disease; short course low-potency steroids to suppress inflammation

Psoriasis

  • General features
    • Common, benign chronic inflammatory skin disease with genetic predisposition and environmental triggers
    • Affects ≈ 2\% of world population; equal sex distribution; can present at any age; several variants; plaque psoriasis is most common; guttate psoriasis often post-streptococcal infection
    • Psychosocial impact can be substantial
  • Pathogenesis
    • Complex, chronic immune-mediated disease; skin findings from keratinocyte hyperproliferation and abnormal differentiation, inflammatory cell infiltrates, and vascular dilation
  • Clinical manifestations
    • Silvery scales on bright red, well-demarcated plaques; symmetrical distribution; plaques may be large (up to 20\text{ cm})
    • Nail involvement common: pitting, onycholysis
    • Koebner phenomenon: new lesions at trauma sites
    • Auspitz sign: pinpoint bleeding after scale removal
    • Common sites: scalp, extensor elbows/knees, gluteal cleft, palms, soles; possible psoriatic arthritis (oligoarthritis of small joints of hands/feet)
  • Variants
    • Plaque psoriasis (most common)
    • Guttate psoriasis (often after streptococcal pharyngitis, more in children/young adults)
    • Inverse psoriasis (flexural areas)
  • Treatment (by disease severity)
    • Mild disease: topical or intralesional corticosteroids; topical vitamin D (calcipotriene); anthralin; topical retinoids; coal tar; broadband/narrowband UV-B; phototherapy with sensitizers (P-UVA); calcineurin inhibitors
    • Moderate to severe disease: systemic therapies (methotrexate and other immune-modulators); systemic retinoids; biologics (etanercept, adalimumab, infliximab, certolizumab pegol, ustekinumab, secukinumab); apremilast (OTETZLA)
  • Prognosis
    • Chronic disease with flares; many patients require long-term therapy; potential for psoriatic arthritis

Urticaria

  • Definition and overview
    • Involves hives, angioedema, or both; wheals are intensely pruritic erythematous plaques; may have angioedema
    • About 20\% of people will have one episode in their lifetime
  • Pathogenesis
    • Mediated by cutaneous mast cells and basophils in the superficial dermis
    • Release of mediators (notably histamine) causes itching and vasodilation leading to wheals; deeper release can cause angioedema
  • Types
    • Acute urticaria: < 6\text{ weeks}; etiologies include infections, IgE-mediated allergic reactions, inhaled allergens, insect stings, foods, drugs, contact allergens
    • Chronic urticaria: > 6\text{ weeks}; etiologies include idiopathic causes, chronic spontaneous urticaria, autoantibodies against mast cell IgE receptors, and inducible factors (solar, cold, cholinergic, dermatographism); systemic disorders can be associated
  • Clinical manifestations
    • Flushing, itching, burning with transient, migratory pink/red wheals; central pallor; lesions appear and resolve within 24 hours
  • Management
    • Nonpharmacologic: avoid identified triggers
    • Pharmacotherapy: antihistamines (H1/H2 inhibitors), systemic steroids for selected cases, epinephrine for angioedema/anaphylaxis, biologics targeting IgE (omalizumab)

Erythema Multiforme

  • Pathogenesis
    • Delayed-type hypersensitivity (type IV); cell-mediated immune response against epidermal antigens
    • Precipitants include infections (HSV, M. pneumoniae, GAS, EBV), drugs, malignancy, autoimmune disease, immunizations
  • Clinical manifestations
    • Abrupt onset of lesions 3–14 days after precipitant; new lesions may appear for up to 10 days
    • Fever, malaise, mucosal involvement in EM major
    • Hallmark: target lesions (dusky center or blister with dark red inflammatory zone and pale edematous ring)
    • EM minor lacks mucosal involvement; major involves mucosa
    • Lesions on extensor surfaces, face, neck, palms, soles; may have mucous membrane involvement
  • Diagnosis and treatment
    • Diagnosis based on history and clinical presentation; skin biopsy if uncertain
    • Treatment: oatmeal baths, emollients; relieve pruritus with antihistamines and topical steroids; severe EM may require systemic steroids; recurrent EM due to HSV may require antiviral prophylaxis
  • Prognosis
    • Typically resolves within ~2 weeks; recurrences are common

Erythema Nodosum

  • Pathogenesis
    • Delayed-type hypersensitivity reaction; inflammation of subcutaneous fat (painful nodules)
    • More common in women in their 20s–40s (W>M 10:1)
  • Known precipitants
    • Infections (strep most common in children), Mycoplasma, EBV, TB, syphilis; drugs (oral contraceptives, antibiotics); systemic diseases (inflammatory bowel disease, sarcoidosis); pregnancy
  • Clinical manifestations
    • Exquisitely tender nodules on legs, usually pretibial bilaterally; prodrome of fever, malaise, arthralgia
    • Lesions primarily on anterior legs; can occur on arms, trunk, face
    • Easier to palpate than to visualize
  • Diagnosis
    • Labs (CBC, ESR, CXR, PPD, ASO) if underlying systemic disease suspected; skin biopsy can confirm EN
  • Treatment and prognosis
    • Nonpharmacologic: bed rest, leg elevation, compression
    • Pharmacologic: analgesia with NSAIDs
    • Prognosis: spontaneous resolution after about 6\text{ weeks}; recurrences may occur

Patch Testing (allergic contact dermatitis evaluation)

  • Test methodology
    • TRUE Test and other panels consist of 35 allergens + 1 control; pre-impregnated patches placed on the back
    • After patch application, patient returns home; a map labeling allergen locations is provided
    • Return visit at 48 hours for patch removal and initial reading; 96-hour reading for additional results
  • Patient instructions
    • Before application: avoid topical corticosteroids at patch site for 1 week; avoid systemic/long-acting corticosteroids for 1–2 weeks
    • After application: do not shower until patch removal; avoid excessive sweating and heavy lifting
  • Reading and interpretation
    • Readings assess: erythema, edema, vesicles, papules, and distribution of reactions; patterns help identify implicated allergens

Patterns of Allergic Contact Dermatitis

  • Common sources/categories observed in patterns
    • Nickel-containing items: jewelry, coins, keys, zippers
    • Rubber/latex products: gloves, elastic components
    • Clothing and fabrics with dyes or finishing agents
    • Personal care products, cosmetics, and topical medications
    • Household items: undergarments, underclothing, CPAP masks, makeup applicators
    • Metals and hardware: eyeglasses, undergarment fasteners, watches
  • Practical takeaway
    • Exterior sources across daily life; multiple exposures often involved; patch testing helps identify specific offenders for avoidance

Clinical considerations across infectious/inflammatory spectrum

  • Seborrheic dermatitis often coexists with psoriasis and may reflect an altered skin microbiome with yeast species Pityrosporum ovalis and Malassezia furfur
  • Psoriasis may present with nail changes and may be linked to psoriatic arthritis; Koebner phenomenon and Auspitz sign are classic clues
  • Atopic dermatitis is tied to a broader atopic phenotype and may follow an atopic march with allergic rhinitis and asthma
  • Urticaria can be acute or chronic; management includes antihistamines, steroids, epinephrine for anaphylaxis, and biologics like omalizumab in select cases
  • Erythema multiforme is often triggered by HSV or drugs and presents with targetoid lesions; EM major can involve mucosa
  • Erythema nodosum is a panniculitis-like reaction with pretibial nodules and systemic symptoms; management focuses on symptomatic care and treating triggers

Key connectives to prior/principles and real-world relevance

  • Skin barrier integrity and immune dysregulation recur across atopic dermatitis and psoriasis as central themes; barrier repair and immunomodulation are common strategies
  • Inflammation and infection interplay: bleach baths for AD and seborrheic/skin infections; antimicrobial strategies are used to prevent superinfection
  • Patch testing as a practical tool to identify contact allergens, enabling targeted avoidance and often leading to symptom improvement
  • Multimodal management (topical, systemic, biologic) reflects the need to tailor therapy to disease severity and patient-specific factors, including age, comorbidities, and tolerance for risk/side effects

Formulas and numerical references used in this content

  • Atopic Dermatitis epidemiology and prevalence
    • Population counts and prevalence: 9.6\times 10^6 children; 1/3 with moderate to severe disease
    • Childhood prevalence change: 8\% \to 15\% since 1997
    • Adult prevalence: 16.5\times 10^6 adults; 7.3\%
    • Family history: 70\%
    • Adult-onset proportion: \tfrac{1}{4} of adults
  • Psoriasis prevalence
    • Global prevalence: 2\% of the population
  • Prognostic timeframes
    • Erythema multiforme resolution window: typically within 2\text{ weeks}; recurrences common
    • Erythema nodosum resolution: about 6\text{ weeks}
  • Patch testing panels
    • Allergen count: 35 allergens + 1 control; reading at 48h and 96h

Notes suitable for exam review

  • Be able to differentiate irritant vs allergic contact dermatitis by mechanism, trigger patterns, and patch testing outcomes
  • Recognize hallmark signs: Koebner phenomenon in psoriasis, Auspitz sign, target lesions in erythema multiforme, pretibial nodules in erythema nodosum, and nemesis of flares in atopic dermatitis
  • Understand age-related patterns in atopic dermatitis and the concept of atopic march
  • Recall major systemic therapies for psoriasis and atopic dermatitis, including biologics (dupilumab for AD; etanercept, adalimumab, infliximab, ustekinumab, secukinumab for psoriasis) and the role of JAK inhibitors and crisaborole
  • Patch testing logistics are essential for diagnosing allergic contact dermatitis; ensure familiarity with TRUE Test protocol and patient preparation/aftercare

If you’d like, I can convert this into a printable one-page summary or create focused flashcards for each disease with the most exam-relevant points.