non neoplastic skin diseases (slides)
TRANSCRIPT
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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
basket- weave 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 dermatitis
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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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.
Lipodermatosclerosis
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
(A) Mild. (B) Moderate. (C)
Severe.
Rhinophyma
(A) Mild. (B) Moderate. (C)
Severe.
Rosacea
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(1) Telangiectases
(2) Inflammation in & around the hair follicles
Rosacea
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note telangiectases