Section 14.1: Inflammatory & Autoimmune Skin Conditions

Why This Matters for the PANCE

The PANCE blueprint allocates 4-5% to the Dermatologic System, where inflammatory and autoimmune conditions represent the majority of questions. You must be able to identify atopic dermatitis, psoriasis, and acne vulgaris from clinical vignettes, map out their distinct pathophysiologic pathways, and select appropriate pharmacotherapy.

Atopic Dermatitis (Eczema)

Atopic dermatitis is a chronic, relapsing, pruritic inflammatory skin disease linked to immune dysregulation and epidermal barrier dysfunction.

• Pathophysiology: Often driven by loss-of-function mutations in the filaggrin gene, impairing stratum corneum integrity. This leads to transepidermal water loss and allergen permeability. The immune response is helper T-cell type 2 (Th2) mediated, yielding IgE hyperproduction. It is part of the atopic triad (eczema, asthma, allergic rhinitis).
• Clinical Presentation: Presents as severe pruritus ('the itch that rashes'). Chronic scratching causes lichenification (thickened skin with exaggerated markings). Distribution varies by age:
  • Infants: Red, scaly, weeping plaques on cheeks, scalp, and extensor surfaces. The diaper area is spared.
  • Children/Adults: Symmetrical scaly plaques on flexural folds (antecubital/popliteal fossae, wrists, neck).
• Diagnostic Workup: Primarily a clinical diagnosis based on history and flexural distribution. Skin biopsy is rarely required but would show spongiosis.
• Clinical Management:
  • Non-pharmacologic: Frequent application of thick, unscented emollients (ointments or creams) immediately after lukewarm bathing. Avoid harsh soaps and triggers.
  • Topical Corticosteroids (TCS): The mainstay for acute flares. Low-potency steroids (e.g., desonide 0.05% or hydrocortisone 2.5%) are mandatory for thin-skinned areas (face, neck, skin folds) to prevent skin atrophy and striae. Medium-to-high potency steroids (e.g., triamcinolone acetonide 0.1% or clobetasol propionate 0.05%) are reserved for thick plaques on the trunk or extremities.
  • Steroid-Sparing Agents: Topical calcineurin inhibitors (e.g., tacrolimus) are preferred for sensitive areas or long-term maintenance to avoid epidermal thinning.

Psoriasis Vulgaris

Psoriasis is a chronic, systemic, immune-mediated inflammatory skin condition characterized by rapid epidermal hyperproliferation.

• Pathophysiology: T-cell hyperactivation (Th1 and Th17 cells) triggers an inflammatory cascade involving TNF-alpha, IL-17, and IL-23. This drives keratinocyte hyperproliferation, shortening epidermal turnover time from 28 days to 3–5 days, leading to scaly plaque formation.
• Clinical Presentation:
  • Plaque Psoriasis: Symmetrical, well-demarcated erythematous plaques with thick, silvery scales on extensor surfaces (elbows, knees), the scalp, and the lumbosacral region.
  • Guttate Psoriasis: Sudden eruption of multiple small, tear-drop shaped erythematous papules with fine scale on the trunk and limbs, classically preceded by a Group A beta-hemolytic Streptococcus pharyngitis infection by 1-3 weeks.
• Key Exam Signs:
  • Auspitz Sign: Pinpoint bleeding when a scale is scraped off, exposing engorged capillaries in the dermal papillae.
  • Koebner Phenomenon: New plaques appearing at sites of local physical trauma (scratches, surgical incisions).
  • Nail Changes: Pitting, 'oil-drop' discoloration, and onycholysis.
• Clinical Management:
  • Mild-to-Moderate (<10% BSA): High-potency topical corticosteroids (e.g., clobetasol 0.05%) combined with topical vitamin D analogs (e.g., calcipotriene) or topical retinoids.
  • Moderate-to-Severe (>10% BSA or Joint Involvement): Requires phototherapy (narrowband UVB) or systemic agents like oral methotrexate, cyclosporine, or acitretin. Biologic therapies targeting TNF-alpha (e.g., adalimumab), IL-17 (e.g., secukinumab), or IL-23 (e.g., ustekinumab) are highly effective. Note: Systemic corticosteroids are contraindicated due to the risk of triggering life-threatening pustular psoriasis upon withdrawal.

Acne Vulgaris

Acne vulgaris is a chronic inflammatory disease of the pilosebaceous unit.

• Pathophysiology: Involves follicular hyperkeratinization, androgen-stimulated sebum overproduction, colonization by Cutibacterium acnes, and subsequent inflammation.
• Clinical Presentation:
  • Comedonal: Closed comedones (whiteheads) and open comedones (blackheads).
  • Inflammatory: Erythematous papules and pustules.
  • Nodulocystic: Large, painful nodules and cysts (>5 mm) that lead to scarring.
• Clinical Management:
  • Mild (Comedonal): Topical retinoids (e.g., tretinoin, adapalene) are first-line. Add benzoyl peroxide for mild inflammatory lesions.
  • Moderate (Papulopustular): Topical retinoid plus benzoyl peroxide plus a topical antibiotic (e.g., clindamycin 1%). If refractory, add an oral antibiotic (e.g., doxycycline). PANCE Pearl: Never use topical or oral antibiotics as monotherapy due to resistance; always pair them with benzoyl peroxide.
  • Severe (Nodulocystic): Oral isotretinoin.
• Isotretinoin Safety (iPLEDGE Program): Due to extreme teratogenicity, female patients must obtain two negative pregnancy tests before starting, commit to using two forms of effective contraception starting 1 month before and ending 1 month after therapy, and undergo monthly pregnancy testing. Monitor lipid panel and LFTs regularly. Key side effects include dry skin, severe cheilitis, hypertriglyceridemia, hepatotoxicity, and psychiatric symptoms.

Psoriasis, Eczema, and Acne Comparison Table

Classic PANCE Traps and Clinical Pearls

• Avoid Systemic Steroids in Psoriasis: Oral prednisone for plaque psoriasis can precipitate life-threatening pustular psoriasis rebound upon discontinuation.
• Differentiate from Rosacea: Rosacea lacks comedones, helping distinguish it from acne.
• Topical Steroid Selection: Avoid high-potency steroids on thin skin (face, neck, groin) to prevent irreversible skin atrophy.

Lichen Planus

Lichen planus is a chronic, cell-mediated autoimmune mucocutaneous disease affecting middle-aged adults.

• Classic Presentation: The "6 P's" — Pruritic, Purple, Polygonal, Planar Papules and Plaques. Lesions often have fine white streaks (Wickham striae).
• Distribution: Wrists, forearms, ankles, lower legs, and oral mucosa (reticular white streaks on the buccal mucosa). Mucosal involvement is painful.
• Associations: Hepatitis C infection, certain medications (thiazides, beta-blockers, ACE inhibitors, NSAIDs).
• Management: Topical corticosteroids are first-line. Systemic corticosteroids, phototherapy, or oral retinoids for severe or widespread disease. Screen for hepatitis C.

Pemphigus Vulgaris and Bullous Pemphigoid

These are autoimmune blistering disorders — distinguish them carefully.

• PANCE Trap: Pemphigus vulgaris is life-threatening (extensive skin and mucosal loss → fluid loss, infection risk). It requires immediate systemic corticosteroids and immunosuppression. Bullous pemphigoid is more benign and responds well to treatment.