Pathology – Lecture 3: Acute Inflammatory Dermatoses
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Terminology
o Macule – circumscribed lesion of up to 5mm in diameter characterized by flatness and
usually distinguished from surrounding skin by coloration
o Patch – circumscribed lesion of more than 5mm in diameter characterized by flatness and
usually distinguished from surrounding skin by coloration
o Papule – elevated dome-shaped or flat-topped lesions 5mm or less across
o Nodule – elevated lesion with spherical contour greater than 5mm across
o Plaque – elevated flat-topped lesion, usually greater than 5mm across (may be caused by
coalescent papules)
o Vesicle – fluid filled raised lesion 5mm across or less
o Bulla – fluid filled raised lesion more than 5mm across
o Blister – common term used for vesicle or bulla
o Pustule – discrete, pus filled, raised lesion
o Wheal – itchy, transient, elevated lesion with variable blanching and erythema formed as
the result of dermal edema
o Secondary Skin Lesions
 Scale – dry, horny, plate-like excrescence, usually the result of imperfect
cornification
 Crust – collection of dried serum and cellular debris (like a scab)
 Erosion – slightly depressed areas of skin in which part/all of the epidermis is lost
 Don’t penetrate beyond the dermoepidermal jxn and thus heal w/o scarring
 Ulcer – focal loss of epidermis and dermis; heal w/ scarring
 Fissure – linear loss of epidermis and dermis w/ sharply defined, nearly vertical
walls
 Atrophy – depression in the skin due to thinning of the epidermis or dermis
 Scar – abnormal formation of CT implying dermal damage
 Initially think and pink but become white and atrophic
Urticaria (Hives)
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Characterized by localized mast cell degranulation and resultant dermal microvascular
hyperpermeability culminanting in edematous plaques called wheals
Most often occurs in children and young adults
Lesions develop and fade in hours and episodes may last for days to months
Sites include any area exposed to pressure such as the trunk, distal extremities, and ears
Pathogenesis
o IgE-mediated
 Type I hypersensitivity rxns = most cases (food allergies, anaphylaxis)
 Circulating Ags interact w/ cell membrane-bound IgE to release histamine
o Immune complexes
 Type III hypersensitivity rxns (via blood, plasma, Ig, drugs, insect stings)
 IgG or IgM + antigen deposition in vessel walls  activate complement  urticaria
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 C5a and C3a – potent releasers of histamine from mast cells
 Seen in dz like serum sickness and SLE
o Non-immunologic release of histamine
 Caused by aspirin/NSAIDs
o Unknown mechanism
 Various infections
Histamine
o Major mediator of urticaria
o Causes endothelial cell contraction  vascular leak b/t cells  tissue edema and wheals
o Produces the “Triple response” of Lewis when injected into skin:
 Vasodilation (local erythema)
 Axons reflex (peripheral flare)
 Wheal
Atopic Dermatitis
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Pathogenesis
o Hyperactivity of Th2 cells and downregulation of Th1 cells
  inflammatory rxns in various organ systems
   IgE production in response to environmental antigens (atopy)
Clinical Presentation
o Atopy
 Immune aberration in genetically predisposed populations
  Th2 activity   IL-3, 4, 5, 13  eosinophilia and mast cell growth
 Type I hypersensitivity manifestations
o Pruritis
 Classic lesion if AD
o Eczema
o Altered vascular reactivity
Morphology
o Gross variation
 Acute flares w/ inflamed, red, blistered and weepy patches
 B/t flares, skin may be normal or suffer from chronic eczema
o Microscopic
 Spongiosis – hallmark of AD = “spongiotic dermatitis”
 Edema seeps into intercellular spaces of epidermis, interrupting the
desmosomes
 Inflammatory infiltrate
 Papillary dermal edema and mast cell degranulation
Etiology
o Genetic factors (family hx of atopy in 70-90% of pts)
o Environmental Factors
 Contact irritants
 Inhalants
 Food allergy
Allergic Contact Dermatitis
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Skin rash, usu. pruritic caused by a type IV hypersensitivity rxn to a substance that touches the skin
Clinical
o Acute ACD – w/in 24-72 hrs after exposure
 Skin is erythematous and edematous
 Bullae that weep clear serum as they break, forming yellow crusts
 Very pruritic
o Chronic ACD – related to low concentrations of weak allergens
 Dry, scaly (lichenified) erythematous pruritic plaques
 Etiology
o Rhus dermatitis
 Poison ivy, oak, and sumac
 Caused by urushiol
o Nickel
 Leading cause of ACD in the world
 Earrings or necklaces are assoc.
o Rubber latex
o p-Phenylenediamine (PPD)
 Component of hair dye products and henna tattoos
o Textiles
o Preservative chemicals
 Diagnosis
o Patch testing
 Uses a panel of small amts of diluted chemicals applied to skin and left in place for
48 hrs to detect a rxn
o Skin biopsy
 Helps exclude other disorders
 Pathogenesis
o Type IV (delayed, cell-mediated) hypersensitivity
 Induction phase
 Langerhans cells detect and pick up the protein-allergen complex and present
them to naïve T cells (sensitizing them)
 Elicitation phase
 Occurs on re-exposure and the sensitized cells encounters the Ag
  release of inflammatory cytokines
Erythema Multiforme
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Uncommon, self-limited disorder that appears to be a hypersensitivity reaction to certain drugs
(sulfonamides, penicillin, barbiturates, salicylates, hydantoins, antimalarials) and infections
(herpes simplex, mycoplasmal infxns, histoplasmosis, coccidiomycosis, typhoid, leprosy) as well as
malignancies (carcinomas and lymphomas) and collagen vascular diseases (lupus erythematous,
dermatomyositis, periarteritis nodosa)
Patients have a “multiform” of lesions – macules, papules, vesicles, bullae as well as the
characteristic target lesion (red macule or papule with a pale, vesicular, or eroded center)
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Spectrum of severity
o Erythema multiforme minor – localized eruption of skin w/ no mucosal involvement or
involvement of only oral mucosa
o Erythema multiforme major – prominent cutaneous and mucosal involvement
o Stevens-Johnson Syndrome – extensive and symptomatic febrile form of this disease that
is seen often in children; extensive mucosal and cutaneous epithelial necrosis
o Toxic Epidermal Necrolysis – another variant that results in diffuse necrosis and sloughing
of cutaneous and mucosal epithelial structure; high mortality
Clinical Features
o Prodromal Sxs
 Suggest a viral syndrome – fever, malaise, myalgias, arthralgias, HA, sore throat,
cough, N/V/D
o Oral Lesions
o Other Mucosa – red conjunctivae, chemosis, and lacrimation; genital ulcerations
o Skin Lesions
 Target lesions
 Typical targets – round, well-defined borders w/ concentric palpable,
edematous rings paler than the centre disc
 Raised atypical targets – palpable erythematous lesions w/ rounded shape
but poorly defined borders and dark central area; may become nectrotic;
seen in EM major or SJS
 Flat atypical targets – not palpable and form ill-defined erythematous areas
w/ tendency to central blister formation; most common in SJS
 Erythematous or purpuric macules w/ or w/o blister formation – most
common in SJS
Lab Studies
o Morphology
 Dermal edema and perivascular inflammatory infiltrate w/ macs and lymphocytes
(CD4 > CD8)
Etiology
o Infections and medications
 Herpes simplex virus  EM minor (due to IFN- production)
 VZV, CMV, EBV
 Mycoplasma spp.
 Drugs