Dermatopathology part 3 Flashcards
Dermatofibroma
looks like melanoma.
Benign fibrous histiocytoma
occurs on the leg.
slow growing
flesh colored to pigmented papule
displays dimple sign. Depresses when squeezed
can be pruritic and patinets may complain that it bleeds when they shave their legs
it is fibrous reaction to some past trauma to the skin
can leave it alone or remove it with punch biopsy or cryotherapy
dermatofibroma histology
benign prolferation of fibroblasts with collagen
higher manification shows whirling (aka pinwheel or storiform) fibroblasts with collagen bundles
may be overlying hyperkeratosis and hyperpigmentation, giving them a reddish brown color
mycosis fungoides (cutaneous T cell lymphoma) age group, location on body, and stages
T cell lymphoma that presents in skin and may evolve into a generalized lymphoma
usually >40 years old
trunk
Three stages: Patch > plaque > nodule
Mycosis fungoids Histology
T helper cells form bands in superficial dermis
invade epidermis as single cells or clusters
nodular lesions grow deeply into dermis and spread systemically
Mastocytosis Urticaria pigmentosa
Usually in children
> 50% of mastocytosis cases
usually multiple mastocytomas. Round to oval, red-brown papules and plaques pruritic and may blister, apprea shortly after birth
Systemic mastocytosis
usually adults 10% of cases
skin lesions similar to urticaria pigmentosa plus multi organ mast cell infiltration: bone marrow, liver, spleen and lymph nodes
Mastocytosis signs and symptoms
Darier sign: Wheal (dermal edema and erythema) when sin lesion is rubbed
Dermatographism: hive occurs when normal skin is troked with a pointed instrument
Systemic disease trigreed by foods, drugs, ETOH
Signs and Sx due to release of histamine, heparin, other mast cell contents.
Mastocytoma Histology
Metachromatic granules within dendritic mast cells
monomorphous dermal infiltrate
no epidermotropism
Fried egg cells: central nuclei with rigid rim of peripheral cytoplasm
giemsa stain helps visualize mast cell granules
Ichthyosis
disorder which impair epidermal maturation
Congential but also acquired
Ichthyoses histology
all forms have build up of compacted stratum corneum with loss of basket weave pattern
strtum granulosum normal to slightly thickened: lamellar, x linked, congenital ichthyosiform erythoderma
Stratume granulosum thin or absent: ichtyosis vulgaris
URticaria (hives) description, location
wheals (pruritic apules to edematous plaques)
from mast cell degranulation and subsequent microvascular hyperpermeability
develop and disappear within hours but episodes may last for day to week.
Located commonly on trunk extremities, ears
Urticaria pathogenesis
antigen induced mast cell degranulation through sensitization with specific IgE antibodies
follows exposure to multiple antigens: pollens, foods, drugs, insect venom
Urticaria HIstology
subtle histologic changes
superficial dermal perivenular infiltrate, neutrophils early then mononuclear cells
collagen bundles more widely spaced due to dermal edema
dilated lymphatics from absorption of edema fluid
usually no epidermal changes
Acute eczematous dermatits aka spongiotic dermatitis
dermatitis with underlying edema. Several subcategories.
Contact dermatitis types
inflamatory reaction cased by an exogenous chemical
two forms: irritant and allergic
Contact dermatitis: irritant
produced by a substance that has direct toxic effects on the skin (acid)
not an immunologic condition
rash begins shortly after expsoure
allergic contact dermatitis
cell medited delayed type hypersensitivity reaction
sensitization of skin occurs 1-2 weeks after 1st exposure
reexposure causes dermatitis in hours to days
common allergens: poison ivy, mangos, iodine, nickel, rubber, cosmetics
contact dermatitis clinical features
erythematous papules and vesicles with oozing > crusting and scaling
very pruritic
contact dermatitis diagnosis
clinically based on H&P
patch testing to identify allergn if the dianogiss is in doubt, rash not responsive, the rash recurs
contact dermatitis TX
avoid the allergen/irritant
apply cool watercompresses
antihistamines for itch
apply topical steroids
systemic steroids for severe cases
Atopic dermatitis eczema
chronic, waxing and waning extremely pruritic, condition beginning in 1st year of life
look for family history of allergies, asthma, and eczema
condition is worse in winter due to decreased humidity
etiology unknown
Atopic dermatitis eczema clinical presentation and location
papules, vesicles, oozing, and crusting
distribution is age dependent: babies get it on face, diaper and extensor surface of extremtities. Children and adults get it on neck, face, axillae, antecubital and popliteal fossas
despite oozing, skin is very dry
Atopic dermatitis TX
antihistmaine
moisturizer
topical steroids
bleach baths and sunlight may help
Lichenification
epidermal thickening characetrized by visible and palpable skin thickening with accentuated skin lines. Chronic atopic dermamtiits
nummular dermatitis
“coin-shaped”
itchy red plaque with vesicles and distinct borders
more likely in young
same treatment for atopic dermatitis
show up on foot
asteatotic dermatitis
“winter itch”
old people in winter
dry cracked skin that becomes itchy
TX: avoid excessive bathing
use room humdiifers
moisturizers
topical stroids if inflamed
Erythema multiforme
immune mediated hypersensitivty reaction reuslting in epidermal cell injury
epidermal cell are attacked by CD8 cytotoxic T cells; target Ag unknown
not rare but uncommon
erythematous macules and papules, vesicles and bullae (multiforme) on extremities that are strikingly symmetric. Target lesions are diaggnositc
lesions may become pruritic and painful
Erytema multiforme causes
triggers: idiopathic, medication, HSV infection, mycoplasma pneumonia
meds
erythema from HSV can recur, can use acyclovir as prophylaxis or at first sign of HSV infection for recurrent erythema mutifrome
antihistmaines and analgesics for symptomatic relief
usually self limited
Erythema mulitform histo
Early: superficial perivascular lymphochytic infiltrate, dermal edema, accumulation of lymphocytes along dermoepidermal junction assciated with degenerating and necrotic keratinocytes
later: lymphocytes migrate into epidermis, epidermal necrosis occurs with blister formation. Target lesion has central necrosis surrounded by perivenular inflammation
Stevens johnson syndrome
more sever than erythema mutliforme
children > adults
invovement of of mucous membranes including mouth and conjunctivae
systemic manifestations may include fever, difficulty eating, renal failure, and sepsis
causes are usually sulfa drugs and anticonvulsants
Stevens johnson TX
supportive
stop medication
may need to treat in burn unit Maintain hydration, prevent secondary infection, provide pain relief
15% mortality
toxic epidermal necrolysis
more sever than stevens johnson
dermatologic emergency
detachment of large areas of epidermis
mortality rate is 30%
treatment is the same as stevens johnson: stop medication and treat in burn unit.
