Inflammatory dermatoses.

Dr. Abd Rehman

Objectives

• • • Define dermatoses.

Name some common acute and chronic inflammatory dermatoses Describe the morphologic changes seen in 1. Urticaria 2. Eczemas 3. Erythema multiforme 4. Lichen planus

Definition - Dermatosis

Nonspecific term used to denote any cutaneous abnormality or eruption.

• Types of inflammatory dermatoses • Acute lesions of the skin lasting from days to weeks and infiltrated by mononuclear cells self-limited / chronic phase • • • Chronic may begin with an acute stage.

exhibit their most characteristic features over many months to years The skin surface in some chronic inflammatory dermatoses is roughened as a result of excessive or abnormal scale formation and shedding (desquamation).

Name some common acute and chronic inflammatory dermatose

s

• • • Acute Urticaria, Acute Eczematous Dermatitis Erythema Multiforme • • • Chronic Psoriasis Lichen Planus Lichen Simplex Chronicus

Urticaria

• • • • Pathogenesis localized mast cell degranulation dermal microvascular hyperpermeability. erythematous, edematous, and pruritic plaques termed wheals.

Pathogenesis of urticaria

• •

IgE-dependent urticaria

Exposure antigens including pollens, foods, drugs, and insect venom. antigen-induced release of vasoactive mediators from mast cell granules via sensitization with specific immunoglobulin E (IgE) antibodies •

IgE-independent urticaria

directly incite mast cell degranulation, such as opiates and certain antibiotics

Histologic features of urticaria

• • • very sparse superficial perivenular infiltrate of mononuclear cells Superficial dermal edema results in more widely spaced collagen bundles. Degranulation of mast cells, that normally reside around superficial dermal venules Urticaria. Histologically, there is superficial dermal edema and dilated lymphatic and blood-filled vascular spaces.

Clinical Features -Urticaria

• • • • ages of 20 and 40 years. develop and fade within hours (usually <24 hours), but episodes may persist for days or even months. small, pruritic papules to large edematous plaques with erythema resulting from superficial vascular dilation. any area exposed to pressure, such as the trunk, distal extremities, and ears.

Acute Eczematous Dermatitis

• 'eczema‘ (Greek word) for 'boiling', which reflects that the skin can become so acutely inflamed that fluid weeps out or vesicles appear. • • =dermatitis ACUTE  CHRONIC • red, papulovesicular, oozing, and crusted lesions at an early stage. • With persistence, these lesions develop into raised, scaling plaques.

• • • • most common form, contact dermatitis EXOGENOUS - poison ivy ENDOGENOUS- ingested food or drug Most of these forms resolve completely

• Stages of eczema development. A, Initial dermal edema and perivascular infiltration by inflammatory cells is followed within 24 to 48 hours by epidermal spongiosis and microvesicle formation (B). C, Abnormal scale, including parakeratosis, follows, along with progressive epidermal hyperplasia (D) and hyperkeratosis (E) as the lesion enters into a more chronic stage.

Pathogenesis of allergic contact Dermatitis - poison ivy

Histology-Acute Eczematous Dermatitis

• • • • • • • Spongiosis-the accumulation of edema fluid within the epidermis "spongiotic dermatitis." Intercellular bridges are stretched Keratinocytes get seperated superficial perivascular lymphocytic infiltrate, papillary dermal edema, mast cell degranulation. Eosinophils prominent in drug - induced

• • Eczematous dermatitis. A, In an acute allergic contact dermatitis, numerous vesicles appear at the site of antigen exposure (in this case, laundry detergent that persisted in clothing). B, Histologically, intercellular edema produces widened intercellular spaces within the epidermis, eventually resulting in small, fluid-filled intraepidermal vesicles.

Eczematous dermatitis

• B, Note the patterned erythema and scale associated with nickel contact dermatitis resulting from this woman's necklace.

Clinical Features- Eczematous Dermatiti s

• • Pruritic, edematous, oozing plaques, often containing vesicles and bullae. (Acute) • persistent antigen stimulation • scratching or rubbing of the lesion . • • • (chronicity) acanthosis Hyperkeratosis Susceptibility is often inherited

Etiology

ERYTHEMA MULTIFORME Targetoid lesion

red macule or papule with a pale vesicular or eroded center hypersensitivity multiform" lesions infections drugs.

herpes simplex, mycoplasmas Histoplasma sulfonamides, penicillin, salicylates macules, papules, vesicles, and bullae

Pathogenesis - erythema multiforme

• inciting drug or microbe • cytotoxic T cells • cross-reactive antigens of the basal cell layer of skin • damage

Histology - erythema multiforme

• A, Lesions show a central zone of dusky pink-gray discoloration =epidermal necrosis or early blister formation, surrounded by a pink-red rim, -target appearance of erythema multiforme minor. • • B, Early lesions show alignment of lymphocytes along the dermoepidermal junction with injury to basal epidermal cells as a result of the cytotoxic injury.

This is an interface dermatitis (there is destruction of cells at the epidermal-dermal interface),

Severity of lesion

Early lesions superficial perivascular, lymphocytic infiltrate +dermal edema margination of lymphocytes along dermoepidermal junction +degenerating keratinocytes discrete, confluent zones of basal epidermal necrosis +blister formation toxic epidermal necrosis, the necrosis extends through the full thickness of the epidermis

Clinical Features types

Minor Erythema multiforme Major/Stevens Johnson syndrome/ toxic epidermal necrolysis herpesvirus Idiopathic reactions to drugs antibiotics or NSAIDS

CHRONIC INFLAMMATORY DERMATOSES Lichen Planus • • • • "Pruritic, purple, polygonal, planar papules, and plaques“ "p's” self-limited resolves spontaneously 1 to 2 years after onset.

Oral lesions may persist for years. • • Pathogenesis Expression of altered antigens at the level of the basal cell layer and the dermoepidermal junction may elicit a CD8+ T cell-mediated cytotoxic immune response. The altered antigens could be due to viral infection or perhaps drug treatment

• Histology -Lichen Planus interface dermatitis dense, continuous infiltrate of lymphocytes along the dermoepidermal junction • as a response to damage, the basal cells show a resemblance in size and contour to more mature cells of the stratum spinosum (squamatization).

• This pattern of inflammation causes the dermoepidermal interface to assume an angulated, zigzag contour ("sawtoothing").

• Anucleate, necrotic basal cells are seen in the inflamed papillary dermis -colloid bodies or Civatte bodies. • changes of chronicity: epidermal hyperplasia, hypergranulosis, and hyperkeratosis.

Lichen planus

A, band of lymphocytes along the dermoepidermal junction, rete ridges have acquired a pointed, or "sawtooth," architecture. interface dermatitis, but the infiltrate is more bandlike (lichenoid) and hyperkeratosis and hypergranulosis are definite signs of chronicity. B, Multiple flat-topped papules with white, lacey or netlike markings (Wickham striae) are characteristic.

Lichen planus

Papules  plaques Hyperpigmentation may result from melanin loss into the dermis from the damaged basal cell layer. • • • Multiple lesions are symmetrically distributed, wrists and elbows, glans penis oral mucosa