Pathology of Common Skin Diseases With Clinical Correlates

7/28/2019 Pathology of Common Skin Diseases With Clinical Correlates

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A) Tumors Arising From Keratinocytes

Basal Cell Carcinoma

Right: pigmented BCC, sometimesmelanin in tumor cellsLeft: translucent, pearly appearance:

dermal nests of basaloid cellssurrounded by rim of mucin

Smooth surface: epidermis usuallyintact

Left: Ulcerated BCC, in moreadvanced lesionsRight: another example of pearlyappearance

Is the commonest of all malignancies in North America Can be locally destructive but has an extremely low likelihood of metastasis. Pathologists can diagnose the nests of basaloid cells even on small fragmented biopsies

Left: Demonstrates smooth pearly surface of BCC and also telangiectasesCenter: Demonstrates peripheral palisading of tumor cells beside tumor cellsRight: again demonstrates peripheral palisading

From Robbins


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Actinic Keratosis

Seborrheic Keratosis

Left: Excessive scale formation in this lesion has produced a "cutaneous horn."

Center: sharply demarcated columns of compact hyperkeratosis and parakeratosis: results in sharpdemarcation, roughness and scale grosslyRight: Progression to full-thickness nuclear atypia, with or without the presence of superficial epidermalmaturation, heralds the development of early squamous cell carcinoma in situ. These extremely common sun-induced premalignant lesions within the epidermis sometimes

progress Confinement of proliferation to epidermis: results in lack of nodularity or induration, usually

papules or macules Subtle enlargement and pleomorphism of keratinocytes Dermal inflammatory cells: gives rise to red planar papule or plaque

Right: sharply demarcated epidermal thickening with a domed superficial aspect and horizontal deepaspect Note cysts containing keratin (white plugs), results in comedo-like plugsLeft: the pathology (right image) gives rise to a stuck on appearance , that has a warty like texture. Melanin within tumor keratinocytes gives rise to brown colour The prevalence unsightly idiopathic benign tumors increases with age (uniformly present when >60)


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Wart

B)Tumors Arising from Melanocytes

Melanocyte Nevus

A Multiple papules with rough pebble-like surfacesB (Low Power) Papillomatosis (undulation of the epidermis) producing verrucous or pebble-like surface (A)C (High Power) course keratohyaline granules and perinuclear vacuolationD This shows in situ hybridization showing viral DNA within epidermal cells (FYI) Also not shown is blood in stratum corneum, resulting in red or black dots on paring Hyperkeratosis (B) and parakeratosis (not shown)produces scale


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Melanoma

Nested pale slightly pigmented cells, hencelesion is usually brown in pigmentation

Tumor cells a the dermo-epidermal junctionand/ or in the dermis hence can be a macule,papule or polyp

Small size, symmetry and circumscriptionresults the same characteristics grossly

Nested and singly dispersed cells with pale, slightly pigmented cytoplasm at the dermo-epidermal andin the dermis, produces the varied brown pigmentation.

Large size: D iameter often 6mm or greater Asymmetry from side to side: Asymmetry in gross Singly dispersed tumor cells in the epidermis at the edge of the lesion: B order irregular Upward spread of tumor cells above the basal layer of the epidermis, sometimes with melanin in

stratum corneum: sometimes black in Color Sometimes melanin in the deep dermis: sometimes areas of blue Colour Sometimes dermal inflammation or vascular proliferation: sometimes areas of red Colour (bottom

right image) Sometimes fibrosis: sometimes areas of white Colour (bottom left image)


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Hemangioma

Intact epidermis: results in a smooth surface of lesion

Dermal profliferation of cells with round andangulated nuclei (packed dermis) produces anodule as in image B.

Image C: Note the characteristic overlyingepidermal hyperplasia and the tendency of fibroblasts to surround individual collagen bundles.

The thick collagen fibers results in firmness uponpalpation

Image A: Hemorrhage and hemosiderin pigmentresults in brown/ tan color of the lesion

Dermatofibromas resemble small round firm brownscars, but there is usually no injury recalled.


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Neurofibroma

Image A: hemangioma on the tongueImage B: histology of juvenile capillary hemangiomaImage C: image of cavernous hemangioma

Image D: pyogenic granuloma of the lip Hemangiomas commony present as:

large rapidly growing tumors in infancy (strawberry angioma=infantile capillary hemangioma)small rapidly growing ulcerating tumors at any age (pyogenic granuloma) image Dsmall slowly growing tumors in adulthood (senile angioma= cherry angioma= Campbell demorgan spot

It is a circumscribed nodule of dermal blood vessels which gives rise it a discrete bright red papule ornodule


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D. Epidermal Infections

Tinea Corporis

Pityriasis Versicolor

Image of neurofibromatosis (Cecil Textbook of Medicine) showingcaf au lait spots. Multiple neurofibromas indicate the hereditary systemic disease

neurofibromatosis Intact epidermis: results in a smooth surface

Dermal proliferation of cells with wavy nuclei having pointedends : results in papules, nodules or polyps.

Delicate collagen fibers produces a soft texture on palpation Presence of numerous mast cells Lack of cells with increased pigment: hence the lesions are

usually skin colored

Image A: characteristic plaque of tineacorporisImage B: shows the picture of mildeczematous (spongiotic) dermatitis,Image C: periodic acid-Schiff stain revealsdeep red hyphae and yeast forms within thestratum corneum.

Hyper keratosis and parakeratosis (image

B) produces and obvious scale seen inimage A

Numerous inflammatory cells in thedermis and epidermis results in a pruriticred plaque also seen in image A

Sparse fine branching hyphae seen inimage C

Caused by Trichophyton, Epidermophyton andMicrosporum. Which commonly cause skin, hair and naildiseases but are not present on health skin.

Application of KOH to scrapings from diseased skindissolves keratinocytes allowing identification of the smallnumbers of fungi

On biopsies, the pathologyic features often resemble psoriasis or eczema unless special stains are performedto identify the sparse fungi


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Herpes Simplex and Varicella-Zoster

E) Other Epidermal Inflammatory Disorders

Also called tinea versicolor, is caused by Malassezia( Pityrosporum), which normally lives as a yeast in hairfollicles, but in some people, travels out onto the surfaceof the epidermis as a yeast and hyphae

The organism secretes a compound that is toxic to

melanocytes (note hypopigmentation in image) A KOH prep shows numerous organisms Hyperkeratosis without parakeratosis results in subtle

fine scale Minimal inflammation results in macules or patches with

little redness or itching Numberous yeast and plump hyphae, resembling

sausages and meatballs

Necrosis of all epidermal cell types: results in vesicles and erosions Multinucleated keratinocytes Dermal inflammation: results in redness These viruses cause cold sores, genital herpes, chicken pox (varicella) and shingles (herpes

zoster). The pathologic changes are the same in all types of infection. The distinctive multinucleated keratinocytes can be rapidly identified by a Tzanck

preparation, performed by smearing scrapings from a vesicle onto a slide, staining andexamining, under a microscope

Top Left: Herpes in adermatomal distributionTop Right: Herpes Vesicles onPalmBottom Left: vesicles anderosions on palateBottom Right: Herpes causingerythema multiforme withtypical targetoid papules of palm


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Psoriasis

Eczema

Top Left: Early and eruptive lesions may be dominated by signs of inflammation and erythemaTop Right: Established, chronic lesions demonstrate erythemasurmounted by characteristic silver-white scale (Robbins)Bottom Left and Right: Pustular psoriasis (from emedicine) Predisposition to this very common type of cutaneoous

inflammation is hereditary, with lesions precipitated by minortrauma, cutaneous or systemic infections or drugs

Punctate bleeding when the scales are removed, sometimeshelpful in diagnosis, is called Auspitz sign

Elegated rete ridges (epidermal hyperplasia), resultsin planar papules or plaques

Uniform hyperkeratosis and parakeratosis, results innumerous prominent scales

Neutrophils in the epidermis, hence sometimesvisible pustules

Thinning of the portions of the epidermis directlyoverlying the dermal papillae, with dilated vesselsclose to the epidermis : hence bright redness andpresence of Auspitz sign
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Stages of eczema development.

A , Initial dermal edema and perivascular infiltration by inflammatory cells isB followed within 24 to 48 hours by epidermal spongiosis and microvesicle formation .C Abnormal scale, including parakeratosis,D follows, along with progressive epidermal hyperplasia andE hyperkeratosis as the lesion enters into a more chronic stage. Eczema can be triggered by heredity (atopic dermatitis), irritants (irritant contact dermatititis),

contact with allergens (allergic contact dermatitis, excessive drying of the skin (asteatoticeczema), or insufficiency of veins in the legs (stasis dermatitis)

A, In an acute allergic contact dermatitis, numerous vesicles appear at the site of antigen exposureB Histologically, intercellular edema produces widened intercellular spaces within the epidermis,eventually resulting in small, fluid-filled intraepidermal vesicles. Elongated rete ridges (epidermal hyperplasia) results in papules or plaques Variable hyperkeratosis and parakeratosis: hence variable scale Lymphocytes and increased lLangerhans cells, triggering by external agents Increased fluid(serous fluid) space between keratinocytes in the epidermis (spongiosis) : resulting in

vesicles, weeping and crusting Lymphocytes surrounding dermal vessels results in redness


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Acne

A Inflammatory acne is characterized clinically by erythematous papules and pustules, with the possibility of eventual scarring.B A portion of a hair shaft piercing the follicular epithelium and eliciting an inflammatory response and fibrosis.

Initial pathogenetic event is plugging of the superficial portions of haif follicles by excessive keratin. This can result in rupture of the follicle aided by the bacterium Proprionibacterium acnes followed by

inflammation and scarring Plugging of hair follicle by keratin resulting in open comodones (black heads) and closed comedones (white

heads) Inflammation in and around the follicles results in red follicular papules, pustules and nodules Replacement of normal dermal structures by fibroblasts and excess collagen results in scarring

Pathology of Common Skin Diseases With Clinical Correlates

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