Inflammatory dermatoses

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Spongiotic Dermatitis - Soggy Skin Saga

  • Core Process: Intraepidermal intercellular edema (spongiosis), giving a "soggy" appearance to the epidermis.
  • Histopathology:
    • Widened intercellular spaces, highlighting desmosomal attachments (intercellular bridges).
    • Superficial perivascular inflammatory infiltrate, typically with lymphocytes and often eosinophils.
    • Later stages show acanthosis (epidermal hyperplasia) and parakeratosis.
  • Clinical Correlation: The characteristic finding in all forms of eczematous dermatitis (e.g., allergic contact, atopic, nummular).

⭐ In acute allergic contact dermatitis, a spongiotic reaction with a prominent eosinophilic infiltrate is a classic diagnostic feature.

Histopathology of Spongiotic Dermatitis

Psoriasiform Dermatitis - Silvery Scale Story

  • Patho: T-cell mediated process driving keratinocyte hyperproliferation.
  • Histo: Classic findings include:
    • Acanthosis: Regular, downward elongation of rete ridges.
    • Parakeratosis: Retained nuclei in the stratum corneum.
    • Munro's microabscesses: Neutrophils in the stratum corneum.
    • Suprapapillary plate thinning over dilated, tortuous capillaries.
  • Clinical: Well-demarcated erythematous plaques with silvery scales, often on extensor surfaces. Associated with nail pitting and psoriatic arthritis.

Psoriasis histology with key features labeled

Auspitz Sign: Pinpoint bleeding when a scale is scraped off, resulting from the exposure of superficial dermal papillae vessels.

Interface Dermatitis - Borderline Battleground

  • Pathogenesis: T-cell mediated cytotoxic inflammation targeting basal keratinocytes at the dermoepidermal junction (DEJ).
  • Histologic Hallmarks:
    • Basal Vacuolization: Clearing or "bubble" formation in the basal layer.
    • Lichenoid Infiltrate: Dense, band-like lymphocytic infiltrate hugging/obscuring the DEJ.
    • Dyskeratosis: Apoptotic keratinocytes (Civatte/colloid bodies).

Histopathology of Inflammatory Dermatoses

  • Two Main Patterns:
    • Cell-Poor (Vacuolar): Sparse infiltrate, prominent vacuolation. Ex: Lupus, Dermatomyositis.
    • Cell-Rich (Lichenoid): Dense infiltrate obscuring the DEJ. Ex: Lichen Planus, GVHD, Drug Eruptions.

⭐ In Lichen Planus, the dense infiltrate attacks the DEJ, creating a characteristic "sawtooth" pattern of the rete ridges.

📌 Mnemonic (Lichenoid causes): Lichen Planus, Erythema Multiforme, GVHD, Drugs (LEGDs).

Vesiculobullous Dermatoses - Blistering Battles

  • Pemphigus Vulgaris

    • Pathophysiology: Type II HSR. IgG autoantibodies against desmogleins (Dsg1, Dsg3) in desmosomes.
    • Level of Split: Intraepidermal (acantholysis).
    • Clinical: Flaccid, easily ruptured bullae; painful oral mucosal erosions are common.
    • Histology: Tombstoning of basal cells. Immunofluorescence shows net-like pattern.
    • 📌 Mnemonic: Vulgaris is Vulgar/severe (often fatal if untreated), involves Vestibule (mouth).
  • Bullous Pemphigoid

    • Pathophysiology: IgG autoantibodies against hemidesmosomes (BPAG1/BP230, BPAG2/BP180).
    • Level of Split: Subepidermal.
    • Clinical: Tense, firm bullae; pruritic. Oral mucosa is usually spared.
    • Histology: Linear IgG and C3 deposits at the dermo-epidermal junction.
  • Dermatitis Herpetiformis

    • Pathophysiology: IgA antibodies cross-react with reticulin in dermal papillae.
    • Clinical: Intensely pruritic vesicles on extensor surfaces. Strong association with Celiac disease.
    • Histology: Microabscesses with neutrophils at tips of dermal papillae.

Nikolsky Sign: A key clinical differentiator. Positive in Pemphigus Vulgaris (gentle rubbing separates epidermis), but negative in Bullous Pemphigoid.

Skin split levels in bullous diseases

High‑Yield Points - ⚡ Biggest Takeaways

  • Psoriasis is marked by acanthosis, parakeratosis, and Munro's microabscesses; associated with HLA-C.
  • Atopic Dermatitis (Eczema) histologically shows spongiosis and is linked to the atopic triad.
  • Lichen Planus features a sawtooth lymphocytic infiltrate and is associated with Hepatitis C.
  • Pemphigus Vulgaris has intraepidermal bullae from anti-desmoglein antibodies; Nikolsky sign is positive.
  • Bullous Pemphigoid has subepidermal bullae from anti-hemidesmosome antibodies; Nikolsky sign is negative.
  • Erythema Multiforme presents with target lesions, commonly triggered by herpes simplex virus (HSV).

Practice Questions: Inflammatory dermatoses

Test your understanding with these related questions

A 72-year-old nursing home resident is complaining of pruritis. She is noted to have multiple, tense blisters on her trunk as well as the flexor surfaces of her extremities. The blisters have an erythematous base. You are unable to extend the blisters when you apply lateral traction. You suspect an autoimmune bullous dermatosis. Which of the following is the cause of the likely condition?

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Flashcards: Inflammatory dermatoses

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Which inflammatory dermatitis has a "saw-tooth" appearance histologically?_____

TAP TO REVEAL ANSWER

Which inflammatory dermatitis has a "saw-tooth" appearance histologically?_____

Lichen planus

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