Pre- Cancerous Lesions of
the Skin & Mucosa
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ACTINIC KERATOSESAka solar keratosis, or senile keratosis
Precursor lesions of cutaneous squamous cel carcinoma
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(SCC).Consists of proliferations of atypical epidermal
keratinocytes ,that may progress to invasive SCC
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The overal risk of progression to invasive SCC is (5 -10)%.
ACTINIC KERATOSES
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Risk factors
cumulative UV radiation exposure (most important)- outdoor
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work/hobbyfair skin, red or blond hair, blue eyes (Fitzpatrick type 1).
age,
immunosuppression,
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prior history of non-melanoma skin cancer.certain genetic syndromes, namely albinism, xeroderma
pigmentosum,
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ACTINIC KERATOSESSite: sun-exposed areas,
balding scalp, head, neck, forearms,
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dorsal hands, dorsal legs in women
asymptomatic, pruritus, burning or
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stinging pain, bleeding.2- to 6-mm, erythematous, flat, rough,
gritty or scaly papule
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more easily felt than seen.
against a background of
photodamaged skin
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ACTINIC KERATOSESA punch biopsy with depth upto mid-reticular dermis
Common indications for a biopsy
1. Rapidly enlarging lesions,
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2. bleeding or ulceration,3. Evidence of inflammation,
4. strong induration,
5. lesions extending beyond 1 cm of size,
6. resistance to treatment.
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ACTINIC KERATOSES
DD
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seborrheic keratosis, arsenical keratosismelanocytic nevi, Senile lentigo,
cutaneous lupus erythematosus
Established AKs chronic course
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lesions persist, spontaneously regress, or progress to invasive SCCs.Spontaneous resolution range from 20% to 30%
limiting sun exposure, use of sunscreen promote regression.
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PROGRESSION TO INVASIVE SCCeach AK : potential to progress into SCC (5-10% in reality)
Direct cancerous invasive transformation of basaloid atypical keratinocytes
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is the most common mechanism of disease progressionIn situ SCC
AK I
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basal,
AK II
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AK IIIsuprabasal
lower two-thirds
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> two-thirds
SCC
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ACTINIC KERATOSESTreatment
treat entire actinically
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damaged areas
PREVENTION of AK
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SUNSCREENS : Broad-spectrum against UVB and UVA, minimum SPF 30
RETINOIDS:
Systemic retinoids in preventing nonmelanoma skin cancer, Ak
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only effective while taking them; limited by systemic toxicitiesOral nicotinamide: doubtful
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BOWEN DISEASEsquamous cel carcinoma (SCC) in situ.
Progress to Bowen carcinoma (invasive SCC) - 5% of
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cases.Etiologic factors include
1. UV radiation,
2. arsenic,
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3. previous therapy with psoralen and UVA radiation (PUVA),4. immunosuppression,
5. exposure to ionizing radiation,
6. infection with HPV(16, 18, 31, 34, 35, 54, 58, 61, 62, and 73)
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BOWEN DISEASESlow growing, usually
asymptomatic.
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erythematous plaques with
irregular, clearly demarcated
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borders.Surface scaly, crusted,
hyperkeratotic. measure up to
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several centimeters.
Bowen Disease
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Clinical variants
pigmented, intertriginous,
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periungual, and subungual BD.HPE
full-thickness epidermal atypia with
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large, round cells and possible
adnexal involvement.
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Differential Diagnosis of Bowen DiseaseTreatment of Bowen Disease
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Surgical &Destructive therapiesTopical Therapies
1. Excision
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1. 5-Fluorouracil
2. Mohs micrographic surgery
3. Curettage with or without
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4. ElectrosurgeryNonsurgical Ablative
5. Cryosurgery
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Therapies
1. Photodynamic(PDT)
2. Laser ablation
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3. Chemoablation :TCA4. Radiation therapy
ARSENICAL KERATOSES
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result from chronic exposure to arsenicpotential to become squamous cell carcinoma (SCC)
punctuate, keratotic, yellow papules overlying pressure points
Palms and soles.
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HPV ASSOCIATED EPITHELIAL
PRECANCEROUS LESIONS
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BOWENOID PAPULOSISBP is a precancerous
condition of the genitalia
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infection with high-risk
HPV, (16, 18, and 33)
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young to middle-agedsexual y active, M>F
multiple red to brownish
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flat papules on the penis
or vulva.
BOWENOID PAPULOSIS
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location
on the glans penis, prepuce, and penis in males,
around the labia minora and majora in females.
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BP : transitional state between genital warts and in situ SCC.
Benign, clinical course: spontaneous regression, persistence, rarely
transformation into BD and invasive SCC (1% to 2.6%).
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DD
lichen planus, condylomata acuminata, erythroplasia, mol uscum
contagiosum, and seborrheic keratoses.
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Treatment of Bowenoid Papulosis
Local destructive
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Topical1. curettage with or without
1. Tretinoin,
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electrosurgery
2. 5-FU,
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2. CO2-laser3. Cidofovir
3. neodymium:YAG laser,
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4. Imiquimod
4. cryosurgery
5. excision.
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HPV-specific vaccination for types 6, 11, 16, and 18 in prevention: ?
EPIDERMODYSPLASIA VERRUCIFORMIS
inherited skin condition
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Loss-of-function mutations of the genes EVER1 and EVER2High local susceptibility to infection with HPV, commonly types
5 and 8.
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Factors contributing to pathogenesis1. host genetic background
2. HPV infection,
3. UV exposure
4. immunosuppression
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EPIDERMODYSPLASIA VERRUCIFORMIS
develop skin lesions early in life
clinical presentation
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1. numerous thin, pink, flat-topped papules and plaques thatresemble verrucae planae ; knees, elbows, and trunk.
2. widespread scaly, erythematous, or hypopigmented macules
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and flat papules resemble tinea versicolor
High risk to develop AK, BD, invasive SCC in future
Sun avoidance, sun-protective measures, regular fol ow up,
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screening of family members
topical 5% imiquimod cream and retinoids ? mixed results
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EPIDERMODYSPLASIA VERRUCIFORMIS
POTENTIALLY MALIGNANT DISORDERS
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OF THE ORAL CAVITYLEUKOPLAKIA
white lesion of the oral mucosa that cannot be rubbed off or characterized
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by any other definable lesion or known disease.most common potentially malignant lesion of the oral mucosa
potential to become oral SCC is 0.2% to 3.4%.
LEUKOPLAKIA
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Etiologic factors for leukoplakia
1. Chronic chemotoxic exposure,
Tobacco is the strongest risk factor: either as smoke or by
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chewing2. mechanical trauma with poor oral hygiene
il -fitting prosthesis, chronic cheek biting,
3. HPV (16 and 18)
4. alcohol consumption
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Differential Diagnosis of Oral Leukoplakia
1. Tobacco-associated
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7. Frictional lesionlesion
8. Oral white sponge nevus
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2. Candida-associated
9. Oral hairy leukoplakia
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lesion10.Verrucous carcinoma
3. Leukoedema
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11.Squamous cel
4. Lichen planus
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carcinoma5. Lupus erythematosus
6. Habitual cheek biting
LEUKOPLAKIA treatment
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OMMISSION
1. consumption of tobacco products, alcohol, bethel nuts,
2. chronic mechanical trauma
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Surgical excision is the first treatment of choice.recurrence after surgical excision : cryotherapy or CO2-laser
the patient should be followed closely
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ERYTHROPLAKIAa red macule or patch on a mucosal surface that cannot
be categorized as any other known disease entity caused
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by inflammatory, vascular, or traumatic factors.
commonly seen with leukoplakia
least common of al oral potential y malignant lesions
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greatest potential to become oral squamous celcarcinoma
Males
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Risk factors tobacco products, alcohol consumption.ERYTHROPLAKIA
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asymptomatic,solitary, erythematous
macule or patch.
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sharply demarcated fromthe surrounding pink
mucosa,
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surface is smooth and
homogeneous in color
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ERYTHROPLAKIA - DDErythematous candidiasis
Chronic al ergic contact
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Atrophic lichen planus
dermatitis
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Lupus erythematosusChronic mechanical trauma
Pemphigus
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Thermal or mechanical injury
Cicatricial pemphigoid
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Squamous cel carcinomaKaposi sarcoma
? High potential for malignant transformation : early treatment.
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? Surgery or excision with CO2- laser: treatment of choice
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