non neoplastic study guide Flashcards
urticaria
localized mast cell degranulation that results in dermal microvascular hyper permeability
Pruritic, edematous plaques
Wheals, aka hives
o Mast cell dependent IgE dependent – localized type I hypersensitivity reaction
Triggered by binding of antigen to IgE antibodies attached to mast cells
o Mast cell dependent IgE independent – exposure to substances that induce mast cell
degranulation
o Mast cell independent IgE independent – triggered by local factors that increase
vascular permeability
o Small pruritic papules that may coalesce
o Very subtle histology
Eczema
Consists of several different categories depending on the initiating event
o All types are T cell mediated inflammatory reactions
o Erythematous, papulovesicular, oozing, crusted lesions
If persistent develop reactive acanthosis and hyperkeratosis
Raised, scaly plaques
poison ivy/poison oak is the classic example
histology shows spongiosis- intercellular edema
Psoriasis
chronic autoimmune inflammatory dermatosis Approximately 15% of patients have associated arthritis o Koebner phenomenon – psoriatic lesions can be induced in susceptible individuals by local trauma
- Well-demarcated, pink-tan plaque
- Covered by a loosely adherent sliver-white scale
- Nail changes are common
- Histology shows marked acanthosis with regular elongation of the rete ridges
- The granular layer is thinned or absent
- Overlying parakeratotic scale
-
Auspitz sign – appearance of multiple, pinpoint blood spots when the scale is lifted/removed from the plaque
- Due to the presence of dilated, tortuous blood vessels within the dermis
- Munro microabscess – collection of neutrophils within the upper layers of the epidermis
lichen Plans
- self-limited disorder that usually resolves spontaneously within 1-2 years
- Koebner phenomenon may be seen
- Purple, polygonal, pruritic, papules (4 Ps)
- Papules may coalesce to form plaques
- Wickham striae – white dots or lines present on the papules/plaques
- Oral lesions are common – white lacy areas of the oral mucosa
-
Dense lymphoid infiltrate along the dermoepidermal junction (DEJ)
- Civatte/colloid bodies – anucleate, necrotic basal epithelial cells
Erythema nodosom
a form of panniculitis (inflammatory recation of the subcutaneous adipose tissue)
- Extremely tender plaques and nodules
- Most commonly on the lower legs
- Erythema multiforme – self-limited hypersensitivity reaction
- Reaction to drugs and infections (herpes)
- Characteristic targetoid lesions in a symmetric distribution
- Perivascular lymphocytic infiltrate and lymphocytic infiltrate along the DEJ (interface dermatitis)
- Stevens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN) – severe drug hypersensitivity reactions
- Painful rash followed by eruption of multiple blisters that rapidly ulcerate
- TEN – diffuse necrosis and sloughing of cutaneous and mucosal surfaces
Erythema multiforme
self-limited hypersensitivity reaction
- Reaction to drugs and infections (herpes)
- Characteristic targetoid lesions in a symmetric distribution
- Perivascular lymphocytic infiltrate and lymphocytic infiltrate along the DEJ (interface dermatitis)
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Steven-Johnson syndrome
(SJS)/Toxic Epidermal Necrolysis (TEN) – severe drug hypersensitivity reactions
- Painful rash followed by eruption of multiple blisters that rapidly ulcerate
- TEN – diffuse necrosis and sloughing of cutaneous and mucosal surfaces
Pemphigus vulgaris
- caused by IgG autoantibodies against desmogleins 1 and 3
- Result in dissolution of intercellular attachments within the epidermis and mucosal epithelium
- Oral ulcers may present long before skin involvement occurs
- Superficial vesicles and bullae that rupture easily (positive Nikolsky sign)
- Leave behind shallow erosions
- Immunofluorescence (IF) shows a net-like pattern of intercellular IgG deposits
- Blister formation occurs in a suprabasal location
- There is a single layer of intact basal cells at the base of the blister
- “row of tombstones”
- There is a single layer of intact basal cells at the base of the blister
bullous pemphigoid
- caused by autoantibodies against hemidesmosomes
- Oral lesions may be seen in approximately 10-15% of patients
- Usually appear after the presence of cutaneous lesions
- Tense bullae that do not rupture easily
- Heal without scarring
- IF shows a linear pattern of complement deposition along the DEJ
- Subepidermal blister
- Oral lesions may be seen in approximately 10-15% of patients
dermatitis herpetiformis
- extremely pruritic urticaria along with grouped vesicles
- May occur in association with celiac disease
-
IgA antibodies cross react with reticulin
- Resulting in a subepidermal blister
- Bilateral, symmetric, grouped blisters that preferentially involve extensor surfaces, elbow, knees, upper back, and buttocks
- IF shows granular IgA deposits localized to the tips of dermal papillae
Acanthosis nigricans
- thickened, hyperpigmented skin
- Commonly in flexural areas
Fibroepithelial polyps
- aka acrochordons or skin tags
- Soft, flesh-colored, pedunculated lesions
- Fibrovascular cores covered by benign squamous epithelium
Epidermal inclusion cysts
– unilocular squamous lined cysts filled with loose keratin debris
Verrucae and types
- commonly known as warts
- Caused by HPV
- Generally self-limited
- Spontaneous regression within 6 months to 2 years
- Verruca vulgaris – most common type; can occur anywhere
-
Verruca plana – flat wart
- Common on the face or dorsal surface of the hands
- Verruca plantaris – seen on the soles of the feet
- Verruca palmaris – seen on the palms of the hands
-
Condyloma acuminatum – seen in the anogenital tract
- Associated with HPV types 6 and 11
- Undulant epidermal hyperplasia
- Koilocytosis – pale halo surrounding nucleus of cells infected with HPV
mulluscum contagiosum
- self-limited viral disease of the skin caused by a poxvirus
Pruritic umbilicated papules
