Acute Inflammatory Dermatoses PDF

Acute inflammatory dermatoses last days to weeks characterized by inflammation, edema, and sometimes epidermal, vascular, or subcutaneous injury some may persist, transitioning to a chronic phase; others are selflimited Acute inflammatory dermatoses-1-Urticaria Clinical features: common disorder 2...

Acute inflammatory dermatoses last days to weeks characterized by inflammation, edema, and sometimes epidermal, vascular, or subcutaneous injury some may persist, transitioning to a chronic phase; others are selflimited Acute inflammatory dermatoses-1-Urticaria Clinical features: common disorder 20-40 years of age lesions usually develop and fade within hours episodes can persist for days or even months small, pruritic papules to large, edematous, erythematous plaques localized or generalized most cases respond to antihistamines, but may require treatment with leukotriene antagonists, monoclonal antibodies or immunosuppressive drugs Acute inflammatory dermatoses-1-Urticaria Pathogenesis: Type 1 hypersensitivity rxn Antigens include viruses, pollens, foods, drugs, and insect venom IgE-independent urticaria can result from exposure to substances that directly incite mast cell degranulation, such as opiates and certain antibiotics In the vast majority of cases, no clinical cause is discovered even with extensive investigation Acute inflammatory dermatoses-1-Urticaria Morphology: Often subtle Sparse superficial infiltrate of mononuclear cells, rare neutrophils, and sometimes eosinophils Superficial dermal edema Acute inflammatory dermatoses-2-Acute eczematous dermatoses «Eczema» is a clinical term that embraces a number of conditions with varied underlying etiologies. «spongiotic dermatitis» is a histopathologic term that encompass all «eczematous dermatoses» Acute inflammatory dermatoses-2-Acute eczematous dermatoses Clinical features: new lesions take the form of erythematous papules, often with overlying vesicles with persistence, these lesions coalesce into raised, scaling plaques nature and degree of these changes vary among the clinical subtypes Acute inflammatory dermatoses-2-Acute eczematous dermatoses Allergic contact dermatitis: topical exposure to an allergen and is caused by «delayed hypersensitivity reactions». Atopic dermatitis: formerly attributed to allergen exposure, now thought to often stem from defects in keratinocyte barrier function, defined as skin with increased permeability to substances to which it is exposed, such as potential antigens Drug-related eczematous dermatitis: hypersensitivity reaction to a drug Photoeczematous dermatitis: appears as an abnormal reaction to UV or visible light Primary irritant dermatitis: exposure to substances that chemically, physically, or mechanically damage the skin Acute inflammatory dermatoses-2-Acute eczematous dermatoses While atopic dermatitis reflects a genetic predisposition and can persist for years or decades, other forms of eczematous dermatitis resolve completely when the offending stimulus is removed or exposure is limited, stressing the importance of investigating the underlying cause. Acute inflammatory dermatoses-2-Acute eczematous dermatoses Susceptibility to atopic dermatitis is often inherited Usually appears in early childhood and remits spontaneously as patients mature into adults. Children with atopic dermatitis often have asthma and allergic rhinitis. Acute inflammatory dermatoses-2-Acute eczematous dermatoses Pathogenesis: Allergic contact dermatitis is triggered by exposure to an environmental contact-sensitizing agent, that chemically reacts with self-proteins, creating neoantigens that can be recognized by the T cell arm of the adaptive immune system. The self-proteins are processed by epidermal Langerhans cells, which migrate to draining lymph nodes and present the antigen to naïve T cells. This sensitization event leads to memory; on reexposure to the antigen, the activated memory CD4+ T lymphocytes migrate to the affected skin sites during the course of normal circulation. There they release cytokines that recruit additional inflammatory cells and also mediate epidermal damage, as in any «delayed-type hypersensitivity» reaction. Acute inflammatory dermatoses-2-Acute eczematous dermatoses Morphology: Spongiosis: edema splays apart keratinocytes, intercellular bridges are stretched and become more prominent superficial perivascular lymphocytic infiltrate, dermal edema eosinophils may be present in general the histologic features are similar regardless of cause, emphasizing the need for careful clinical correlation. Acute inflammatory dermatoses-3-Erythema multiforme Clinical features: uncommon, usually self-limited wide array of lesions, including macules, papules, vesicles, and bullae (hence the term «multiforme»). well-developed lesions have a characteristic “targetoid” appearance Acute inflammatory dermatoses-3-Erythema multiforme has a broad range of severity forms associated with infection (most often herpesvirus) are less severe Erythema multiforme caused by medications may progress to more serious eruptions, such as Stevens-Johnson syndrome or toxic epidermal necrolysis. These forms can be life-threatening, as they may cause sloughing of large portions of the epidermis, resulting in fluid loss and infections complications similar to those seen in burn-injured patients. Acute inflammatory dermatoses-3-Erythema multiforme Pathogenesis: appears to be a hypersensitivity response to certain infections and drugs Infections: herpes simplex, mycoplasma, and some fungi Drugs: sulfonamides, penicillin, salicylates, hydantoins, and anti-malarials Characterized by epithelial injury mediated by skin-homing CD8+ cytotoxic T lymphocytes. The cytotoxic T cell attack is focused on the basal cells of cutaneous and mucosal epithelia, presumably due to recognition of still unknown antigens. Certain human lymphocyte antigen (HLA) haplotypes are associated with the disease. Acute inflammatory dermatoses-3-Erythema multiforme Morphology: Early lesions: superficial perivascular lymphocytic infiltrate lymphocytes along the dermoepidermal junction «interface dermatitis» apoptotic keratinocytes dermal edema Acute inflammatory dermatoses-3-Erythema multiforme With time; discrete, confluent zones of basal epidermal necrosis appear, with concomitant blister formation Acute inflammatory dermatoses-3-Erythema multiforme More severe forms: Steven’s Johnson Syndrome (10% of the skin is involved) and toxic epidermal necrolysis (30% of skin is involved) necrosis extends through the full thickness of the epidermis PART II CHRONIC INFLAMMATORY DERMATOSES Chronic inflammatory dermatoses Chronic inflammatory dermatoses are persistent skin conditions that exhibit their most characteristic features over many months to years, although they may begin with an acute stage. The skin surface in some chronic inflammatory dermatoses is roughened as a result of excessive or abnormal scale formation and shedding. Chronic inflammatory dermatoses-1-Psoriasis Clinical features: common chronic inflammatory dermatosis 1% to 2% of individuals in USA associated with an increased risk for heart attack and stroke, a relationship that may be related to a chronic inflammatory state also associated in up to 10% of patients with arthritis Chronic inflammatory dermatoses-1-Psoriasis well-demarcated, pink to salmon– colored plaque covered by loosely adherent silverwhite scale elbows, knees, scalp, lumbosacral areas, intergluteal cleft, glans penis, and vulva. nail changes occur in 30% of cases. mostly limited in distribution, but it can be widespread and severe. clinical subtypes are defined by pattern of involvement and severity. Chronic inflammatory dermatoses-1-Psoriasis lesions can be induced in susceptible individuals by local trauma (Koebner phenomenon) Genome-wide association studies have linked an increased risk for psoriasis to polymorphisms in HLA loci and genes affecting antigen presentation, TNF signaling, and skin barrier function. Chronic inflammatory dermatoses-1-Psoriasis Pathogenesis: a T cell-mediated inflammatory disease, presumed to be autoimmune in origin, although the antigens are not well described. Both genetic (HLA types and other susceptibility loci) and environmental factors contribute to the risk. It is unclear whether the inciting antigens are self-antigens, environmental antigens, or some combination of the two. Chronic inflammatory dermatoses-1-Psoriasis Sensitized populations of T cells home to the dermis, including CD4+ TH17 and TH1 cells and CD8+ T cells, and accumulate in the epidermis. These cells secrete cytokines and growth factors that induce keratinocyte hyperproliferation, resulting in the characteristic lesions. Chronic inflammatory dermatoses-1-Psoriasis Morphology: marked epidermal thickening (acanthosis), with regular downward elongation of the rete ridges increased epidermal cell turnover and lack of maturation results in loss of the stratum granulosum and extensive parakeratosis Chronic inflammatory dermatoses-1-Psoriasis Kogoj microabscess: neutrophils within epidermis Munro microabscess: neutrophilic aggregates in stratum corneum Chronic inflammatory dermatoses-1-Psoriasis thinning of the epidermal cell layer overlying the tips of dermal papillae dilated and tortuous blood vessels within the papillae. these vessels bleed readily when the scale is removed, giving rise to multiple punctate bleeding points (Auspitz sign) Chronic inflammatory dermatoses-2-Lichen Planus Clinical Features: “Pruritic, purple, polygonal, planar papules, and plaques” these papules are highlighted by white dots or lines termed Wickham striae. middle-aged adults multiple lesions, usually symmetrically distributed Hyperpigmentation Chronic inflammatory dermatoses-2-Lichen Planus extremities, wrists and elbows, vulva and glans penis. 70% of cases also involve the oral mucosa, where the lesions manifest as white papules with a reticulate or netlike appearance lesions usually resolve spontaneously within 1 to 2 years, but the oral lesions may persist Chronic inflammatory dermatoses-2-Lichen Planus Pathogenesis: may result from a CD8+ T cell–mediated cytotoxic response against antigens in the basal cell layer and the dermoepidermal junction that are produced by unknown mechanisms, perhaps as a consequence of a viral infection or drug exposure. Chronic inflammatory dermatoses-2-Lichen Planus Morphology: prototypical interface dermatitis the inflammation and damage are concentrated at the interface of the squamous epithelium and papillary dermis. lymphocytes are intimately associated with basal keratinocytes Civatte (colloid) bodies: Anucleate, necrotic basal cells Chronic inflammatory dermatoses-2-Lichen Planus well-developed changes of chronicity: acanthosis, hypergranulosis, hyperkeratosis dermoepidermal interface has a zigzag contour=sawtoothing basal cells looks like more mature cells of the stratum spinosum= squamatization Chronic inflammatory dermatoses-3-Lichen simplex chronicus Clinical Features: lesions often are raised, erythematous, and scaly and can be mistaken for keratinocytic neoplasms manifests as roughening of the skin, which takes on an appearance reminiscent of lichen on a tree. is a response to local repetitive trauma, usually from rubbing or scratching nodular forms exist that are referred to as prurigo nodularis Chronic inflammatory dermatoses-3-Lichen simplex chronicus Pathogenesis: not understood, but the trauma probably induces epithelial hyperplasia and eventual dermal scarring. Lichen simplex chronicus can be superimposed on and mask another (often pruritic) dermatosis. It is therefore important to rule out an underlying cause while recognizing that the lesion may be entirely trauma-related. Chronic inflammatory dermatoses-3-Lichen simplex chronicus Morphology: acanthosis, hyperkeratosis, and hypergranulosis elongation of the rete ridges, fibrosis of the papillary dermis, and a dermal chronic inflammatory infiltrate these lesions are similar in appearance to normal volar (palms and soles) skin, in which skin thickening serves as an adaptation to repetitive mechanical stress. Summary: • Many specific inflammatory dermatoses exist and can be mediated by IgE antibodies (urticaria), antigen-specific T cells (eczema, erythema multiforme, and psoriasis), or trauma (lichen simplex chronicus). • Underlying genetic susceptibility plays a role in atopic dermatitis and psoriasis. • Clinical correlation is essential to diagnose specific skin diseases, since many have overlapping, nonspecific histologic features.