Dermatopathology part 3

Question 1

Dermatofibroma

Answer 1

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

Question 2

dermatofibroma histology

Answer 2

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

Question 3

mycosis fungoides (cutaneous T cell lymphoma) age group, location on body, and stages

Answer 3

T cell lymphoma that presents in skin and may evolve into a generalized lymphoma

usually >40 years old

trunk

Three stages: Patch > plaque > nodule

Question 4

Mycosis fungoids Histology

Answer 4

T helper cells form bands in superficial dermis

invade epidermis as single cells or clusters

nodular lesions grow deeply into dermis and spread systemically

Question 5

Mastocytosis Urticaria pigmentosa

Answer 5

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

Question 6

Systemic mastocytosis

Answer 6

usually adults 10% of cases

skin lesions similar to urticaria pigmentosa plus multi organ mast cell infiltration: bone marrow, liver, spleen and lymph nodes

Question 7

Mastocytosis signs and symptoms

Answer 7

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.

Question 8

Mastocytoma Histology

Answer 8

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

Question 9

Ichthyosis

Answer 9

disorder which impair epidermal maturation

Congential but also acquired

Question 10

Ichthyoses histology

Answer 10

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

Question 11

URticaria (hives) description, location

Answer 11

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

Question 12

Urticaria pathogenesis

Answer 12

antigen induced mast cell degranulation through sensitization with specific IgE antibodies

follows exposure to multiple antigens: pollens, foods, drugs, insect venom

Question 13

Urticaria HIstology

Answer 13

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

Question 14

Acute eczematous dermatits aka spongiotic dermatitis

Answer 14

dermatitis with underlying edema. Several subcategories.

Question 15

Contact dermatitis types

Answer 15

inflamatory reaction cased by an exogenous chemical

two forms: irritant and allergic

Question 16

Contact dermatitis: irritant

Answer 16

produced by a substance that has direct toxic effects on the skin (acid)

not an immunologic condition

rash begins shortly after expsoure

Question 17

allergic contact dermatitis

Answer 17

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

Question 18

contact dermatitis clinical features

Answer 18

erythematous papules and vesicles with oozing > crusting and scaling

very pruritic

Question 19

contact dermatitis diagnosis

Answer 19

clinically based on H&P

patch testing to identify allergn if the dianogiss is in doubt, rash not responsive, the rash recurs

Question 20

contact dermatitis TX

Answer 20

avoid the allergen/irritant

apply cool watercompresses

antihistamines for itch

apply topical steroids

systemic steroids for severe cases

Question 21

Atopic dermatitis eczema

Answer 21

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

Question 22

Atopic dermatitis eczema clinical presentation and location

Answer 22

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

Question 23

Atopic dermatitis TX

Answer 23

antihistmaine

moisturizer

topical steroids

bleach baths and sunlight may help

Question 24

Lichenification

Answer 24

epidermal thickening characetrized by visible and palpable skin thickening with accentuated skin lines. Chronic atopic dermamtiits

Question 25

nummular dermatitis

Answer 25

“coin-shaped”

itchy red plaque with vesicles and distinct borders

more likely in young

same treatment for atopic dermatitis

show up on foot

Question 26

asteatotic dermatitis

Answer 26

“winter itch”

old people in winter

dry cracked skin that becomes itchy

TX: avoid excessive bathing

use room humdiifers

moisturizers

topical stroids if inflamed

Question 27

Erythema multiforme

Answer 27

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

Question 28

Erytema multiforme causes

Answer 28

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

Question 29

Erythema mulitform histo

Answer 29

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

Question 30

Stevens johnson syndrome

Answer 30

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

Question 31

Stevens johnson TX

Answer 31

supportive

stop medication

may need to treat in burn unit Maintain hydration, prevent secondary infection, provide pain relief

15% mortality

Question 32

toxic epidermal necrolysis

Answer 32

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.