? usually present at or soon after birth.
? Term should always be qualified according to the cell or tissue of
origin, for example "connective tissue nevus" or "vascular nevus".
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? Nevi generally represent clones of genetically altered cells arising
from mosaicism.
Benign tumor
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? A localized proliferation of cells of one type,
? which has some degree of autonomous control of growth,
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? but a normal differentiation.In situ tumor
? A localized collection of morphologically malignant epidermal cells,
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? which have still not invaded the basement membrane
? so it essentially applies to epidermal tumors.
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Malignant tumor
? A collection of morphologically malignant cells
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? with full capacity to metastasize to lymph nodes and other organs.? Others:
? Underlying skin diseases
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? oculocutaneous albinism? Xeroderma pigmentosum
? Epidermodysplasia verruciformis
? Chronic venous ulcers
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EPIDERMAL TUMORS AND NEVI
? SEBORRHEIC KERATOSIS
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? Benign epidermal tumor,? seen after age of 50.
? Morphology: Multiple, well-defined, hyperpigmented papules with a
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"stuck on" appearance, a greasy surface, and keratinous plugs.
? Sites: Face, trunk, and upper extremities.
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? Treatment: Can be left alone, remove if cosmetically disfiguring.Biopsy if diagnosis is in doubt (to rule out malignant melanoma).
? Biopsy- horn pseudocysts
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? small black papules, limited to
the upper part of face.
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?
Skin Tags
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? Familial
? Associated with obesity.
? Acanthosis nigricans.
? Diabetes.
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? Soft, skin-colored or pigmented, pedunculated papules? Neck, axillae, and groins.
? radiofrequency
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Melanocytic NevusCongenital melanocytic nevi
? Derived from epidermal melanocytes and nevus cel s have a predilection
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for deeper penetration.
? Present at birth.
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? single,multiple.? Color varies from brown to black
? lesions darken and enlarge as the child grows.
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? With age, the lesions also become raised and develop rugosities
(cerebriform appearance).
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? Coarse hair develops in 90% of lesions?
? Giant lesions are usually seen on the trunk and because they may
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cover large areas of the trunk, are called "bathing trunk nevi".? Complications: potential for malignant transformation is definitely
more in giant congenital melanocytic nevi (bathing trunk nevi).
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? Meningeal involvement and spina bifida, seen in lesions located over
vertebral column.
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ACQUIRED MELANOCYTIC NEVI
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JUNCTIONAL MELANOCYTIC NEVUS
COMPOUND MELANOCYTIC NEVUS
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INTRADERMAL MELANOCYTIC NEVUS
OTHERS
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? MONGOLION SPOTS
? Bluish ill-defined macules
? Lumbosacral region.
? Regress by age of 4 years
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?
? NEVUS OF OTA
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? Present at birth.? Or appears in infancy.
? Macular pigmentation, which has two components: More prominent
slate grey hyperpigmentation due to dermal melanocytes. Brownish
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epidermal pigmentation.
? Distribution along the maxillary division of the trigeminal nerve.
? Pigmentation of sclera (slate gray) and conjunctiva (brown) often
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present
?
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? Halo nevus or Sutton's nevus:
? Melanocytic nevus which develops a halo of depigmentation
? over period of many years, the nevus involutes and
? the depigmented halo repigments.
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COMPLICATIONS
? INFLAMMATION
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? MALIGNANT CHANGE-? The following changes in a melanocytic nevus are suspect and
warrant a biopsy:
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? Change in size and pigmentation.? Change in shape and contour.
? Itching, inflammation, ulceration, and bleeding.
?
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Verrucous Epidermal Nevus ? localised/
generalised
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Variants
? ILVEN
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? NEVUS COMEDONICUS
? NEVUS SEBACEOUS
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?
Becker's Nevus
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? Common condition.? More frequent in men.
? Begins shortly before, at or after puberty.
? Appears as a hyperpigmented (light-dark brown) patch, which has a
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characteristic splashed appearance.? Over period of time, coarse dark hairs appear on the lesion
? Chest and shoulders.
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Epidermoid and Trichelemmal Cysts
? freely mobile over underlying
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structures? tethered to the skin.
? Characteristically, have a central
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punctum through which cheesymaterial can be expressed
? Sites
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? Complications
? Epidermoid cyst: Face, upper
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? Secondary infection.back, and retroauricular region
? Rupture in the dermis and
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induce a foreign body reaction.
? Trichilemmal cyst : Most
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? Dystrophic calcificationfrequent on the scalp.
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? MILIA:? small subepidermal keratin cysts.
? small, firm, white papules,
which are less than 2 mm in
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diameter.
? De novo on the face
? At sites of healed subepidermal
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blisters e.g., bullous pemphigoid
Premalignant Lesions
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? cutaneous horn? keratoacanthoma
? Bowen's disease
? actinic keratoses
? arsenical keratoses
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cutaneous horn
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?Cutaneous horn (cornu cutaneum)
? A conical hypertrophic protuberance emanating from a skin-
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colored to erythematous papular base? Height at least one-half of the largest diameter
? Thirty-eight percent to 40 percent of all cutaneous horns
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represent AKs
? Is a morphological diagnosis.
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? Occurs secondary to:? Epidermal nevus.
? Warts.
? Seborrheic keratoses.
? Rarely, underlying squamous cell carcinoma.
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keratoacanthoma
? Rapidly growing, skin-colored
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nodule, which develops a centralhorny plug ; the plug falls off to
leave a crater.
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? Most lesions resolve
spontaneously, leaving a
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depressed (cosmeticallyunacceptable) scar.
? Few (very few!!) transform into
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squamous cell carcinoma.
Keratoacanthoma
? Solitary or multiple
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? rapid growth? 1 to 2.5 cm
? ulcer with keratinous material
? spontaneous resolution
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Bowen's Disease? Carcinoma in situ
? erythematous plaque
? irregular borders
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? enlarging psoriasiform plaque? indentations (reniform margin)
BOWEN'S DISEASE
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? A: psoriasiform plaque, showing
irregular indentations.
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? B: infiltration of the lesionindicates development of
squamous cell carcinoma
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? Treatment
? Excision,
? cryotherapy, or
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? topical 5-fluorouracil (5-FU).? Actinic keratoses: pink irregular
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macules and papules with dryadherent scales.
? middle aged and elderly.
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? Face, scalp, and dorsae of hand.? Suspect transformation into
squamous cell carcinoma (a rare
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occurrence), if the lesionenlarges rapidly, ulcerates or
bleeds.
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? arsenic keratoses: multiple corn-
like papules.
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? rain drop pigmentationMALIGNANT EPIDERMAL TUMORS
? BASAL CELL CARCINOMA
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? SQUAMOUS CELL CARCINOMA? MALIGNANT MELANOMA
1. BASAL CELL CARCINOMA
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? The most common cancer
affecting humans
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? Slow growing? At least 75% first tumours are on
the face
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? Relatively `benign' in most cases
? but if left untreated can be
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disfiguring and life threateningBasal Cell Carcinoma
? Raised, with pearly border
? prominent vasculature
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? ulceration? nodular most common
TYPES OF BCC
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NODULAR? Usually begin as a small
pink `pearly' papule
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? Develop a depression inthe centre
? Rolled edge
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? Overlying telangiectasia
Superficial Basal Cell
? Scaly patches
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? irregular borders? extremities, less common in head
and neck
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MORPHOEIC? White or waxy
? Always on face
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? Presents as a spontaneous `scar'
? Margins are usually much wider than
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what is clinically visiblePigmented BCC
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? Basal Cell Carcinoma----histopathology is diagnostic
? Cells resemble those of stratum
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basale
? peripheral palisading
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? stromal retraction? Course
? Slowly progressive,
? locally invasive (especially noduloulcerative variant) neoplasm,
? eating into underlying structures like cartilage or bone, if left
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untreated.
? Lymphadenopathy and distant metastasis do not occur.
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? Surgical excision is treatment of choice in most cases.? All variants of BCC except the morphoeic variant are excised with a
0.5 cm of skin margin.
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? Morphoeic variant is excised with wider margin (up to 2 cm) because
the lateral extent is often indistinct.
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Squamous cell carcinoma
? Etiology:
? Damaged skin (photodamaged/scarred/ulcerated skin/leucoplakia/
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erythroplasia),
? topical and systemic carcinogens- Pitch tar, mineral oils, and inorganic
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arsenic? human papilloma virus
? immunosuppression - HIV
? Certain rare genetic disorders, with defective DNA repair
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mechanisms, such as xeroderma pigmentosum
? A: raised ulcer with indurated
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base and everted margin(cauliflower-like) on the lower lip.
? B: raised ulcer with indurated
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base and everted margin at site
of radiation dermatitis.
? Metastases
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? Lymphadenopathy: Regional lymphadenopathy. Nodes hard andsometimes fixed to underlying structures and tethered to skin.
? Visceral metastases: Infrequent.
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? scc
? characteristic histology.
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Malignant Melanoma? Etiology:
Clinical variants :
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? Multifactorial.
lentigo maligna melanoma,
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? Actinic damage important.superficial spreading melanoma
? Evidence of nevi in 25% of
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(SSM),
patients with MM.
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acral lentiginous melanoma, andnodular malignant melanoma
(NMM).
SSM most frequent while NMM is
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the most aggressive.
? Asymmetrical pigmented nodule,
? Border irregularity,
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? Color variability,? Diameter >0.5 cm,
? Elevation irregularity.
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SubungualMetastatic melanoma
melanoma
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? histological grading using
Breslow's method.
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? measures the vertical distance
(in mm) from granular cell layer
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to the deepest part of tumor,using a microscopic micrometer.
? prognostic predictor.
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Benign Tumors of Skin Appendages
Malignant Tumors of Skin Appendages
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Paget's Disease
? Paget's disease of breast:
? sharply marginated plaque with
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a slightly raised edge and an
irregular outline.
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? If the crusts are removed, a red,glazed, moist surface is revealed.
? Note destruction of nipple.
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Benign Tumors and Nevi of Dermis
? Port-wine stain: deeply
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erythematous, telangiectatic
slightly bosselated lesion on the
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face.? Usually present at birth.
? Salmon patch
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? Is a capil ary malformation
? Commonest vascular malformation
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present at birth.? salmon patch involutes by the age
of one.
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? Presents as telangiectatic macules.
? Nape of neck, forehead, and
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eyelids.? Treatment None required.
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? Venous malformation: a softcompressible bluish swelling,
which increases in size when
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dependent
? Lymphatic malformations
? Usually present at birth.
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? Characterized by a cluster of
thin walled vesicles (resembling
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frog spawn).Infantile hamangioma
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? Lesion appears within a fewweeks of birth and grows for a
few months.
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? Spontaneous regression occurs
with minimal atrophy in most
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patients.? Soft, brightly red (strawberry
colored) nodule with pale
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stippling indicating resolution
? Complications:
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? Treatment? Large swellings near orifices
? Small lesions: Resolve
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(oral, nasal, anogenital)
spontaneously.
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interfere with function.? Large symptomatic lesions:
? Bleeding may follow trauma.
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? Systemic steroids
? Ulceration especially in large
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? Propranolollesions and in intertriginous area. ? Lasers: pulsed dye laser in
residual lesions.
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Beningn acquired
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hemangioma/ pyogenic
granuloma
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Malignant Tumors of Dermis
Cutaneous T Cell Lymphoma (Mycosis Fungoides)
? Lymphoma of helper T cel s.
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? Initial patch stage of wel -defined, bizarre
shaped, atrophic patches; poikiloderma
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? later infiltrated plaque stage and then? tumor stage with aggressive course.
? Characteristic histology with presence of
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atypical cel s (Pautrier's microabscesses);
epidermotropism
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? Treatment: Early stage: Topical steroids,topical nitrogen mustard, PUVA, acitretin
and electron beam treatment.
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? Tumor stage: Chemotherapy.
? Others:
? LCH
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? Kaposi sarcomaQUESTIONS (please answer in one word)
? 1. Horn pseudocysts are a feature of ?
? 2. Virus which is implicated in the pathogenesis of skin malignancies-
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? 3. Bathing trunk nevus is a type of-? 4. melanocytic nevus surrounded by a depigmented halo is
? 5.Name a premalignant lesion of skin
? 6.Pautrier microabscesses are seen in
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? 7. What is the diagnosis in case of pigmented macules present overleft cheek distributed over maxillary division of trigeminal nerve-
? 8. Which of the malformation is most likely to involute
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spontaneously?
? 9. Grouped open and closed comedones arranged linearly are seen in
? 10. . Breslow's method is used for histological staging of
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