Non Neoplastic Skin Diseases (Slides)

8/3/2019 Non Neoplastic Skin Diseases (Slides)

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Nonneoplastic Skin Diseases


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Skin

The skin is composed of an epidermal layer (e) from which specialized adnexa (hair follicles, h; sweat glands, g; and sebaceousglands, s) descend into the underlying dermis (d).

This projection of the epidermal layer (e) and underlying superficial dermis demonstrates the progressive upward maturation ofbasal cells (b) into cornified squamous epithelial cells of the stratum corneum (sc). Melanin-containing dendritic melanocytes (m)

(and rare Merkel cells containing neurosecretory granules) and midepidermal dendritic Langerhans cells (lc) are also present. Theunderlying dermis contains small vessels (v), fibroblasts (f), perivascular mast cells (mc), and dendrocytes (dc), potentiallyimportant in dermal immunity and repair.


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Epidermis


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Epidermis


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Desmosomes &

Hemidesmosomes

K l d f h i i d d h d i k d di bli i


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Knowledge of the proteins composing desmosomes and hemodesmosomes is key to understanding blistering

disorders. Desmogleins 1 and 3 (Dsg1, Dsg3) are functionally interchangeable components of desmosomes,

but have different distributions within the epidermis (left panel).

In pemphigus vulgaris, autoantibodies against Dsg1 and Dsg3 cause blisters in the deep suprabasal

epidermis, whereas in pemphigus foliaceus, the autoantibodies are against Dsg1 alone, leading to superficial,

subcorneal blisters.

In bullous phemphigoid, autoantibodies bind BPAG2, a component of the hemidesomes, leading to blister

formation at the level of the lamina lucida of the basement membrane.Dermatitis herpetiformis is caused by lgA autoantibodies to the fibrils that anchor hemidesmosomes to the

dermis.

The various forms of epidermolysis bullosa are caused by genetic defects in genes encoding proteins that

either form or stabilize desmosomes or hemidesmosomes. 6/4, 6/4 integrin.


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Langerhans cells, S100 stain


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Dermis &

subcutis


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Dermis & Subcutis

How easy it is to differentiate between the papillary and reticular layer of the dermis. Immediately beneath the epidermis

you should see a layer which at low magnification appears rather evenly stained. At high magnification the stain should

resolve into a fine network of collagen fibres, which blend with equally fine elastic fibres. Cells are more numerous in the

papillary layer and you should see more nuclei in this area than in the deeper reticular layer. Also, the papillary layer

contains the capillary network which supplies the epidermis, The reticular layer contains coarse collagen and elastic fibres

and the larger vessels which feed into the capillary network of the papillary layer..


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Hair FollicleThe hair follicle is divided into 4 parts: bulb, suprabulbar area,

isthmus, and infundibulum.


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Hair Follicles


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Transverse section of hair follicle


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Sebaceous glands are usually embedded in the dermis. Although they empty intothe hair canal of the hair follicle, this point will only be visible for a few of them because of the

thinness of the sections. It should however be possible to follow the fate of the secretory cells.

Deep in the sebaceous glands cells are smaller with intact nuclei. Cell size increases with the

accumulation of sebum as the cells are gradually displaced towards the opening of the gland

into the hair follicle. The nuclei condense, become darker and irregularly shaped.


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Sweat glands

unusually thick, haematoxylin stained section of

the skin

Th t t b l d th i iti l t f th d t ll f l t f


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The secretory tubulus and the initial segment of the duct usually form a cluster of

round or irregularly shaped profiles, which stain darker than the surrounding

connective tissue. The different cell types in the secretory epithelium of merocrine

sweat glands are only visible in well preserved glands. The red rim around the

secretory tubulus is formed by the cytoplasm of myoepithelial cells. Their small, dark

nuclei may be visible close to the periphery of the tubulus.


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WartEpidermal acanthosis with hyperkeratosis, parakeratosis, and papillomatosis


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Wartkoilocytosis and keratohyaline granules (arrows)


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Warts

Verruca vulgaris


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Verruca

vulgarisStriking papillomatosis with

pointed mounds resembling

church spires.


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Warts

Verruca plana


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Verruca planahyperkeratosis of loose lamellar type, acanthosis without papillomatosis or

parakeratosis. Numerous vacuolated cells, the horny layer had a pronounced

basketweave resulting from the vacuolization of the horny cells


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Warts

Verruca plantaris


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Venereal Warts

Condyloma acuminatum


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Epidermodysplasia verruciformis

E id d l i if i


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Epidermodysplasia verruciformisEpidermis shows large keratinocytes with blue-green cytoplasm and perinuclear

pallor.

Molluscum Contagiosum


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Molluscum Contagiosum


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Molluscum ContagiosumLobulated endophytic epidermal hyperplasia (that produces a circumscribed

intradermal pseudotumor).


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Molluscum

bodieslarge, ellipsoid,homogeneous, cytoplasmic

inclusions in cells of the

stratum granulosum and the

stratum corneum


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Impetigo

contagiosa


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Impetigo bullosa


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Impetigo bullosaaccumulation of fluid and neutrophils beneath the stratum corneum, with variable

acantholysis.

Tinea


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Tinea

Tinea


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Tinea


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Tinea

(PAS staining)


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Tinea Versicolor


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Ichthyosis

Urticaria


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UrticariaA, Erythematous, edematous, often circular plaques are characteristic.

B, There is superficial dermal edema, manifested by spaces between collagen

bundles, and dilated lymphatic and blood-filled vascular spaces; the

epithelium is normal.

Stages of eczema development


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Stages of eczema developmentA, Initial dermal edema and perivascular infiltration by inflammatory cells is followed

within 24 to 48 hours by epidermal spongiosis and microvesicle formation (B). C,

Abnormal scale, including parakeratosis, follows, along with progressive acanthosis (D)

and hyperkeratosis (E) as the lesion becomes chronic.

Allergic contact dermatitis


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Allergic contact dermatitisSpongiosis with intraepidermal vesicles perivascular lymphocytic and

eosinophilic infiltrate seen throughout the dermis and subcutaneous fat. Few

vessels showing lymphocytic infiltration of the wall


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Erythema multiforme


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Stevens-Johnson syndrome

ryt ema


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ryt emamultiforme

In early lesions, there is vacuolization

of the basal layer, with lymphocytes in

the dermoepidermal junction and a

sparse superficial perivascular

lymphoid infiltrate. Look for individual

necrotic keratinocytes in prickle cell

layer.

Erythema


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Erythema

multiformeWhen the lesion is more advanced,

one can see a subepidermal bullaedue to dermal edema and to

necrosis of the basal layer of the

epidermis.

Dyskeratosis is evidenced.


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Erythema

multiformewell developed subepidermal

bullae.

Dermatomyositis


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Dermatomyositishyperkeratotic stratum corneum, epidermal atrophy, hydropic degeneration

of the basal cell layer, papillary dermal edema, dermal mild perivascular

lymphocytic infiltration and increased mucin deposition

P i i


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Psoriasis

In psoriasis, there is marked acanthosis, with regular downward


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p , , g

elongation of the rete ridges (sometimes described as appearing

like test tubes in a rack).

Note also parakeratosis and diminished granular cell layer.


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There is thinning of the portion

of the epidermal cell layer that

overlies the tips of dermal

papillae (suprapapillary plates)

and dilated, tortuous blood

vessels within these papillae.Note also neutrophils aggregates

in stratum corneum and

superficial epidermis


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Pityriasis rubra pilaris


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Lichen simplex chronicus

S b h i D titi


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Seborrheic Dermatitis


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Typically, mounds of parakeratosis containing neutrophils and serum, often

present at the ostia of hair follicles (so-calledfollicular lipping).


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Seborrheic

dermatitis


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Lichen Planus


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Lichen Planus

Note bandlike chronic


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Note bandlike chronic

inflammatory infiltrate along

the dermoepidermal junction,

Sawtoothing of rete ridges,hyperkeratosis and

hypergranulosis


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Blistering (Bullous) DiseasesSchematic representation of histologic levels of blister formation.

A, In a subcorneal blister the stratum corneum forms the roof of the bulla (as

in pemphigus foliaceus).

B, In a suprabasal blister a portion of the epidermis, including the stratum

corneum, forms the roof (as in pemphigus vulgaris).

C, In a subepidermal blister the entire epidermis separates from the dermis

(as in bullous pemphigoid).

Knowledge of the proteins composing desmosomes and hemodesmosomes is key to understanding blisteringdisorders. Desmogleins 1 and 3 (Dsg1, Dsg3) are functionally interchangeable components of desmosomes,

but have different distributions within the epidermis (left panel)


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but have different distributions within the epidermis (left panel).

In pemphigus vulgaris, autoantibodies against Dsg1 and Dsg3 cause blisters in the deep suprabasal

epidermis, whereas in pemphigus foliaceus, the autoantibodies are against Dsg1 alone, leading to superficial,

subcorneal blisters.

In bullous phemphigoid, autoantibodies bind BPAG2, a component of the hemidesomes, leading to blister

formation at the level of the lamina lucida of the basement membrane.

Dermatitis herpetiformis is caused by lgA autoantibodies to the fibrils that anchor hemidesmosomes to the

dermis.

The various forms of epidermolysis bullosa are caused by genetic defects in genes encoding proteins that

either form or stabilize desmosomes or hemidesmosomes. 6/4, 6/4 integrin.


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Pemphigus Vulgarissuperficial vesicles and bullae that

rupture easily, leaving shallow erosions

covered with dried serum and crust

Pemphigus vulgaris

(1) Suprabasal intraepidermal bullae


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(1) Suprabasal, intraepidermal bullae

(2) Superficial perivascular inflammatory infiltrate

(3) "Tombstoning" of basal keratinocytes

(4) Normal stratum corneum with basketweave appearance

(5) Acantholysis


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Pemphigusvulgaris


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Pemphigus

vegetans

Pemphigus vegetans


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Histopathological examination showing acanthosis, papillomatosis, suprabasal

acantholysis, intraepidermal microabcesses filled with eosinophils, and an

inflammatory infiltrate composed of lymphocytes and numerous eosinophils in the

upper dermis


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Pemphigus foliaceus


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Pemphigus foliaceusAcantholysis occurs in subcorneal areas

(only the granular cell layer is affected).


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Direct

immunofluorescence of

pemphigus.

A, In pemphigus vulgaris

there is deposition of

immunoglobulin along the

plasma membranes of

epidermal keratinocytes in

a reticular or fishnet-likepattern. Also note the early

suprabasal separation due

to loss of cell-to-cell

adhesion (acantholysis).

B, In pemphigus foliaceus

the immunoglobulindeposits are more

superficial.

Pemphigus erythematosus


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Pemphigus erythematosus

Blisters selectively involve the malar area ofthe face in a lupus erythematosuslike fashion.

Acantholysis occurs in subcorneal areas


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Paraneoplastic

pemphigus(A) Oral erosion (arrow)

and (B) eroded papules

on the neck of a patient

with paraneoplastic

pemphigus caused by

Castleman disease.

(C, D) Chest radiographs

show a right posterior

mediastinal mass

(arrows).

Paraneoplastic pemphigus


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Suprabasal acantholysis

band-like chronic inflammatory

cell infiltrate


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Bullous

Pemphigoid

pruritic tense bullae, filled with

clear fluid, on normal or red

patches of skin.

Bullous Pemphigoid


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Bullous PemphigoidSubepidermal blister. Numerous eosinophils in the edematous dermis.


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Bullous

Pemphigoid

Linear IgG and C3 antibodies to hemidesmosomes at lamina


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g

lucida of basement membrane. the pattern has been likened to

ribbon candy.


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Epidermolysis bullosa acquisita


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Bullous lupus

erythematosus


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Epidermolysisbullosa

f d l b ll


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Types of Epidermolysis bullosa

EB simplex


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EB simplexintact stratum corneum and upper epidermis, with vesicle formation in the lower

epidermis at the basal layer caused by degeneration of individual epidermal cells

Heme Synthesis


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and porphyrin metabolism

porphyria cutanea tardaacute intermittent porphyria

congenital erythropoietic porphyria


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Porphyria cutanea tardaSun exposed areas develop blistering

(vesicles and bullae), erosions and

ulcerations, fragile skin, pigmentary

changes, and scarring.

Porphyria cutanea tarda


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There is a cleft in a subepidermal plane. There is focal serum and few inflammatory

cells within the cleft. The dermal papillae are rigid (festooning). A significant

inflammatory infiltrate is not noted in the dermis.

Note dermal papillae protrusion into bulla with festooned pattern.


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Also roof of blister has eosinophilic, PAS+ linear globules (caterpillar bodies)

Porphyria cutanea tarda


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IgG beneath the basement membrane zone and

around dermal blood vessels


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Dermatitis herpetiformisLesions consist of intact and eroded (usually scratched) erythematous blisters, often

grouped.

Dermatitis herpetiformis


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Dermatitis herpetiformisSubepidermal blister with papillary neutrophilic microabscesses

Dermatitis herpetiformis


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Dermatitis herpetiformisgranular IgA deposits in the dermal papillae

Li I A


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Linear IgA

dermatosis

Scleroderma


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Scleroderma


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Scleroderma

Lichen Sclerosus


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thinned epidermis with superficial dermal collagen homogenization and a

mid-dermal lymphocytic infiltrate

Erythema nodosum


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y

E th d


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Erythema nodosum

(Septal panniculitis)

Erythema nodosum


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Erythema nodosum


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Erythema

induratum


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Erythema induratum

(lobular panniculitis)

Lipodermatosclerosis


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Predominantly septal

with membranocyctic fat necrosischaracterized by cystic cavitis lined by

crenulated hayaline membrane.There are variable mild perivascular lymphocytic

infiltrate.


Acne Vulgaris


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Acne Vulgaris


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Stages of acne(A) Normal follicle(B) open comedo

(blackhead)

(C) closed comedo

(whitehead)

(D)papule

(E) pustule.

Acne Vulgaris


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(closed comedon)

Acne vulgaris


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Acne vulgaris

(opencomedon)

Acne Rosacea


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Acne Rosacea

Papulopustular rosacea

(A) Mild. (B) Moderate. (C)

Severe.

Papulopustular rosacea


Severe.

Rhinophyma


Severe.

Rosacea


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(1) Telangiectases

(2) Inflammation in & around the hair follicles

Rosacea


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note telangiectases

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Non Neoplastic Skin Diseases (Slides)