The Skin

Skin Tumor Benign epithelial tumors Premalignantepidermal tumor Malignant epidermal tumor Disorders of pigmentation and melanocytes
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Histopatologi-& clinical patologic correlations of skinlesions

Benign epithelial tumors

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Seborrheic keratoses Fibroepithelial tumor (skin tag acrochordon, soft fibroma, fibroma molle) Keratoacanthoma Appendage tumor

1. Seborrheic keratoses
Ins: common Age:middle/older Predileksi;trunk-extrimiti,head,neck Ins: male > female Mac: round,flat,coin plaqmm to cm dark brown, always impacted with keratingive impression stuck on Mic exophytic, demarcated sharplyfr epidermis Hyperkeratosishorncyst (inside)

2. Fibroepithelial tumor

Ins: most common of thew cutaneus tumor Age:midle/older Predileksi: neck, trunk, face, Intertrigo areas Mac:soft flesh color, small stalk Mic: fibrovascular cores covered by squamous epithel Biologically : associated: DM, intestinal polyposis pregnancy

3. Keratoacanthoma
Age: >50y of age -caucasians Predilecti: sun exposed skin cheeks nose,ears,hands Mac: flesh colored,dome shapedwith central keratinplugcrater,1cm to sev cm Mic central keratin filledcrater surounded with proliferating epithelial cells

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4. Appendage tumor

Cylindromas: lesi:nodules on forehead and scalp.appear early in life Mic:appocrine differentiation Syringoma: lesion of eccrine differentiation Lesi occur as multiple on the lower eye lids Trichoepithelioam: hair follikel differentiation Lesi occur on the face,scalp,neck and upper trunk
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Premalignant epidermal tumor

Actinic keratosis (solar keratosis) prior developt malignancy!epidermis Ac keratosis progresive dysplasia sun exposure Keratin , other causes: radiation, hydrocarbon, arsens12
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Actinic keratosis
Mac: diameter lesi <1cm Red,brownskin color,efl: papule/plaqprod keratin(keratin horn) Mic: epidermis(lowermost layer)atypic cells Basal layer evidence of dyskeratosis with pink or red cytoplasma Basal membrane intake Dermis: thickened, bluegray, elasticfiberselastosis (abn fiber synt, sun damage fibroblast)

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Malignant tumor
1. Squamous cell carcinoma Most common type Sun exposed sites, older people Male. female Predisposisi fact: sun light, chronic ulcers, old burns scar, industrial carcinogens (tars & oils), arsen, radiation Mucosa (oral cav); tobacco
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1. Squamous cell carcinoma

Mac:

well demarcated, red scalling plaqs, or nodular, hyperkeratotic ulceration Mucosal leukoplakia Mic: epidermal atypia, Well diufferentiated (with prominent keratinisasition ) to highly anaplastic with necrosis and abortive keratinisation

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2. Basal cell carcinoma

Common, slow growing, very rare metastase Chronic sun exposure lightly pigmented people Age: middle >40y Predileksi; face,head not occur in mucosal surface Pattern growth: multifoka l(extended) Nodular (down ward) Mic: like normal basal layer of the epidermis(palisading)basal cell proliferating

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Disorder of pigmentation
Lentigo

dont involve proliferation of melanocyt cel Ins: all ages (also infancy & childhood) All sex No racial predilection Cause; unknown Mac: can involve skin &mucosa membrane

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Lentigo
Mac:

5-10 mm,oval,brown macules Mic : hyperplasia melanocytichyperpigmented basal cell layer in the epidewrmis

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Pigmented naevus

Mac: congg/acquired 1cm, uniform pigmented Papules & well defined, rounded borders Dark brown Mic: junctional naevus:naevus cell along the dermoepidermal junction

Compound naevus: when the melanocyt nest within both dermis &epidermis Dermal naevus: the naevus cell in the dermis

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Dysplastic naevus
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characteristic features Mic : compound naevus with architecture and cytologic evidence of abnormal growth (atypia) This type is precursor of malignant melanoma.

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Malignant melanoma

Common (relative)deadly Sun light important role Lightly pigmented individuhigher risk, than darkly pigmented (tanning fad?) Predisp: sunlight pre existing naevus: eg dysplastic naevus Mic: melanoma cells(individual) (>naevus cell) Large nuclei, irregular chromatin, prominent nu

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Endocrine pancreas
The

islet of Langerhans form 1-2% of the pancreatic tissue. Three types of cell make up the islets The majority are cells Insulin &glucagon have virtually opposite actions
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Clinical effects & biochemical changes

Insulin Non

dependent diabetes

insulin dependent diabetes(maturity or late onset diabetes)

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Tumors of the islets

Are apudomas (amine precursor uptake and decarboxylation) The clinical effects vary with the hormone produced; Insulin-secreting tumours Gastrin-secreting tumours Glucagonoma inducing a diabetic condition Inapropriate hormone secretion e.g carcinoid & cushing syndrome

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