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Category	High-Yield Facts
Risk Factors	Personal or family history of atopy (the "atopic triad": eczema, asthma, allergic rhinitis); filaggrin gene mutations; onset usually in infancy (before age 5, often by 6 months); urban residence, higher socioeconomic status ("hygiene hypothesis")
Etiology	Combination of an impaired skin barrier (structural protein defects) and a dysregulated, skewed immune response, with secondary microbial colonization
Patient Presentation	An infant or child brought in for a chronic, relapsing, intensely itchy rash — "the itch that rashes." Parents describe constant scratching, poor sleep, and dry skin. In adults, presentation may be a flexural rash or chronic hand dermatitis
Classic Physical Exam	Infants: erythematous, oozing, crusted patches on the cheeks and extensor surfaces (sparing the diaper area). Children/adults: lichenified, dry, scaly plaques in flexural areas (antecubital and popliteal fossae). Associated stigmata: Dennie-Morgan lines (infraorbital folds), allergic shiners, Hertoghe sign (lateral eyebrow thinning), keratosis pilaris, xerosis, white dermographism
Key Diagnostic Results	Diagnosis is clinical (Hanifin and Rajka criteria). Elevated serum IgE and peripheral eosinophilia may be seen but are neither sensitive nor specific and are not required for diagnosis
Management	Stepwise: emollients and trigger avoidance (foundation of all care) → topical corticosteroids or topical calcineurin inhibitors for flares → phototherapy → systemic agents (dupilumab, JAK inhibitors, cyclosporine) for severe/refractory disease
Keywords	"Itch that rashes" (not a "rash that itches"), flexural involvement, xerosis, lichenification, atopic march, Dennie-Morgan lines, white dermographism, eczema herpeticum

01 Pathophysiology

Atopic dermatitis is best understood as a disease of two interacting failures: a defective epidermal barrier and a dysregulated immune response. The single most heavily tested mechanistic concept is the filaggrin gene mutation. Filaggrin is a structural protein essential for aggregating keratin filaments and forming the cornified envelope of the stratum corneum. Loss-of-function mutations in the filaggrin gene lead to a defective, "leaky" skin barrier, which causes increased transepidermal water loss, resulting in the clinically obvious xerosis (dry skin) that is nearly universal in these patients.

This barrier defect matters because it does more than just dry the skin — it also allows increased penetration of environmental allergens, irritants, and microbial antigens into the epidermis and dermis. Once inside, these antigens are taken up by Langerhans cells and presented to naive T cells, driving a T-helper 2 (Th2)-predominant immune response in the acute phase. Th2 cytokines — particularly interleukin-4 and interleukin-13 — are the key mediators tested on exams, because they are the specific targets of dupilumab (a monoclonal antibody against the IL-4 receptor alpha subunit shared by both cytokines). This Th2 skew also drives B-cell class switching to IgE production, which explains the elevated serum IgE frequently found in these patients, even though IgE elevation is not required for diagnosis.

The intense pruritus that defines this disease is driven directly by these same inflammatory cytokines (IL-4, IL-13, and IL-31) acting on cutaneous sensory nerve fibers. This produces the classic "itch-scratch cycle": pruritus leads to scratching, scratching causes further mechanical disruption of an already-defective barrier, and this disruption triggers more inflammation and more itch. Chronic scratching over time produces lichenification (thickened, leathery skin with accentuated skin markings), which is why the clinical morphology shifts from acute, oozing, weeping lesions in infancy to dry, thickened, lichenified plaques in chronic or adult disease.

Finally, the disrupted barrier and altered local immunity favor Staphylococcus aureus colonization, found on the skin of the majority of these patients even in areas that appear uninvolved. This colonization is not incidental — staphylococcal superantigens further amplify the local inflammatory response, which is why secondary bacterial infection is a common complication and why some patients benefit from measures that reduce bacterial burden, such as dilute bleach baths.

02 Classification and Clinical Manifestation

Phase	Typical Age	Distribution	Morphology
Infantile phase	Birth to 2 years	Face (cheeks, forehead), scalp, extensor surfaces of extremities; classically spares the diaper area (moisture protects the barrier there)	Acute: erythematous, edematous, oozing and crusted papules and plaques
Childhood phase	2 years to puberty	Flexural surfaces — antecubital and popliteal fossae, wrists, ankles, neck	Subacute to chronic: dry, scaly, lichenified plaques; excoriations common
Adult phase	Adolescence/adulthood	Flexural areas persist; also hands, eyelids, and can localize to face/neck ("head and neck dermatitis")	Chronic lichenification, hyperpigmentation, hand dermatitis is common in this group

A related concept the exam likes to test is the "atopic march": atopic dermatitis in infancy tends to precede, and is a risk factor for, the later development of food allergy, allergic rhinitis, and asthma — in roughly that chronological order.

03 Diagnostic Workup

Test	Purpose	Typical Findings
Clinical criteria (Hanifin and Rajka / UK Working Party)	Best initial and definitive test — this is a clinical diagnosis	Pruritus plus a chronic/relapsing course, typical morphology and distribution by age, personal or family history of atopy
Serum total IgE	Supportive only, not diagnostic	Often elevated but neither sensitive nor specific; do not order to "confirm" the diagnosis
Skin biopsy	Reserved for atypical presentations or to exclude mimics	Spongiotic dermatitis — a nonspecific finding shared with other eczematous conditions
Patch testing	Used when allergic contact dermatitis is a suspected co-existing trigger or mimic, not for routine workup of atopic dermatitis itself	Identifies specific contact allergens
Skin culture / viral swab (Tzanck or PCR)	Ordered acutely if superinfection is suspected	Staphylococcus aureus in bacterial superinfection; herpes simplex virus in suspected eczema herpeticum

The critical exam point here is that atopic dermatitis has no confirmatory laboratory or histologic gold standard — it is diagnosed clinically based on morphology, distribution, chronicity, and personal or family atopic history. Ordering an IgE level as the "next step" to confirm the diagnosis is a classic distractor answer; the correct next step is almost always clinical assessment and, in an established patient with a sudden worsening, evaluation for secondary infection. The one scenario where biopsy or culture genuinely changes management is when the presentation is atypical (asymmetric, poorly responsive to therapy, or suggestive of an infectious or malignant mimic such as cutaneous T-cell lymphoma in an older adult).

04 Management and Treatment

Line of Therapy	Agents	Role
Foundational (all patients, all severities)	Emollients/moisturizers applied liberally and frequently, especially after bathing; lukewarm (not hot) baths; fragrance-free products; trigger avoidance	Restores barrier function, reduces flare frequency, reduces need for other agents
Mild-to-moderate flares	Low-to-mid potency topical corticosteroids (e.g., hydrocortisone, triamcinolone) for the face/flexures and body respectively	First-line anti-inflammatory therapy for acute flares
Steroid-sparing / sensitive areas	Topical calcineurin inhibitors (tacrolimus, pimecrolimus)	Used on the face, eyelids, and skin folds to avoid steroid-induced atrophy
Moderate-to-severe, refractory disease	Phototherapy (narrowband UVB); systemic immunosuppression with cyclosporine; biologics (dupilumab); JAK inhibitors (upadacitinib, abrocitinib)	Escalation when topical therapy fails to control disease
Secondary infection	Dilute bleach baths, topical or oral antistaphylococcal antibiotics; IV acyclovir for eczema herpeticum	Treats superinfection, an important complication requiring recognition

Acute management of a flare centers on anti-inflammatory control: a topical corticosteroid of appropriate potency for the affected body site, applied for a limited course, combined with aggressive emollient use. Long-term management is about maintenance — continuous emollient use, trigger identification and avoidance (harsh soaps, wool fabrics, extremes of temperature, sometimes specific food or environmental allergens), and stepping down to the lowest effective therapy once controlled, sometimes using proactive intermittent topical anti-inflammatory application ("weekend therapy") to prevent relapse in previously affected areas.

A key contraindication and dosing point that is heavily tested: prolonged, high-potency topical corticosteroid use on the face, eyelids, or skin folds risks cutaneous atrophy, telangiectasia, and periorificial dermatitis — this is precisely why topical calcineurin inhibitors exist as an alternative for those sites. Topical calcineurin inhibitors themselves carry a boxed warning regarding a theoretical malignancy risk, though this is not considered clinically significant with appropriate use.

The single most important "next best step" scenario on this topic is the patient with well-controlled atopic dermatitis who develops sudden, painful, monomorphic, "punched-out" vesicles or erosions, sometimes with fever — this is eczema herpeticum, a dermatologic emergency caused by disseminated herpes simplex virus infection through the disrupted skin barrier. The correct next step is prompt initiation of systemic (typically intravenous) acyclovir, not simply escalating topical steroids, which would worsen a viral infection.

05 Differential Diagnosis and Distractors

Differential	Why It's Similar	Key Discriminator
Allergic contact dermatitis	Also pruritic, eczematous, can be chronic and relapsing	Distribution corresponds to a specific contact exposure (jewelry, cosmetics, plants) rather than classic flexural pattern; positive patch testing; no personal/family atopy required
Seborrheic dermatitis	Common in infants ("cradle cap"), can overlap in distribution on the face and scalp	Greasy, yellow, scaly plaques concentrated on scalp, eyebrows, nasolabial folds; less intensely pruritic; not associated with atopic history
Psoriasis	Chronic, scaly, relapsing plaques	Well-demarcated plaques with thick silvery scale, favors extensor surfaces (elbows, knees) and scalp/nails; Auspitz sign; less intensely pruritic than atopic dermatitis
Scabies	Intense pruritus, especially at night; can affect infants and involve flexural areas	Burrows, involvement of finger web spaces and genitals; close contacts also affected; identifiable mites/eggs on scraping
Nummular (discoid) eczema	Eczematous, pruritic, chronic	Coin-shaped, well-demarcated round plaques rather than diffuse flexural involvement; often on extremities in adults, not necessarily linked to atopic history
Tinea corporis	Scaly, sometimes pruritic patch	Annular lesion with a well-defined, often raised, scaly border and central clearing; positive potassium hydroxide preparation showing hyphae
Cutaneous T-cell lymphoma (mycosis fungoides)	Chronic, pruritic, scaly patches/plaques, can mimic eczema for years	Adult onset, poor response to standard eczema therapy, biopsy shows atypical lymphocytes (Pautrier microabscesses)

06 Traps and High-Yield Pearls

The most common way students miss questions on this topic is by over-ordering tests — reflexively selecting "check serum IgE" or "skin biopsy" as the next step when the vignette already gives a classic clinical picture (infant with itchy, oozing facial patches sparing the diaper area, or a child with flexural lichenified plaques and a family history of asthma). The exam is testing whether you recognize that atopic dermatitis is a clinical diagnosis, and that reaching for labs when the clinical picture is already classic is both unnecessary and the wrong answer. The second major trap is a vignette describing a patient with known, previously stable atopic dermatitis who now develops rapidly worsening, monomorphic vesicular or punched-out lesions with systemic symptoms — failing to recognize eczema herpeticum and instead choosing to simply increase topical steroids is one of the highest-yield "gotchas" in dermatology, because steroids in that setting would worsen the underlying viral infection. Finally, watch for questions distinguishing atopic dermatitis from its mimics purely by distribution and age pattern (flexural in children/adults versus extensor/facial in infants, versus extensor surfaces in psoriasis, versus a specific contact site in allergic contact dermatitis) — the core competency being tested throughout this topic is your ability to use morphology, distribution, and age to drive a clinical diagnosis and to recognize the one true diagnostic emergency (eczema herpeticum) within an otherwise benign, chronic disease.

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