Download MBBS Venereology and Leprosy Presentations 2 Pre Cancerous Lesions of The Skin Lecture Notes

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ACTINIC KERATOSES

Aka 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/hobby

fair 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 KERATOSES

Site: 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 KERATOSES

A 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 keratosis
melanocytic 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 SCC

each 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 progression

In situ SCC

AK I

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basal,

AK II

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AK III

suprabasal

lower two-thirds

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> two-thirds

SCC

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ACTINIC KERATOSES

Treatment

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 toxicities

Oral nicotinamide: doubtful

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BOWEN DISEASE

squamous 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 DISEASE

Slow 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 Disease


Treatment of Bowen Disease

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Surgical &Destructive therapies

Topical Therapies

1. Excision

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1. 5-Fluorouracil

2. Mohs micrographic surgery
3. Curettage with or without

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4. Electrosurgery

Nonsurgical Ablative

5. Cryosurgery

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Therapies

1. Photodynamic(PDT)
2. Laser ablation

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3. Chemoablation :TCA
4. Radiation therapy

ARSENICAL KERATOSES

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result from chronic exposure to arsenic
potential 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 PAPULOSIS

BP 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-aged

sexual 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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Topical

1. curettage with or without

1. Tretinoin,

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electrosurgery

2. 5-FU,

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2. CO2-laser

3. 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 EVER2
High local susceptibility to infection with HPV, commonly types

5 and 8.

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Factors contributing to pathogenesis
1. 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 that

resemble 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 CAVITY

LEUKOPLAKIA
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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chewing
2. 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 lesion

lesion

8. Oral white sponge nevus

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2. Candida-associated

9. Oral hairy leukoplakia

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lesion

10.Verrucous carcinoma

3. Leukoedema

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11.Squamous cel

4. Lichen planus

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carcinoma

5. 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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ERYTHROPLAKIA

a 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 cel

carcinoma

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 from

the surrounding pink

mucosa,

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surface is smooth and

homogeneous in color

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ERYTHROPLAKIA - DD

Erythematous candidiasis

Chronic al ergic contact

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Atrophic lichen planus

dermatitis

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Lupus erythematosus

Chronic mechanical trauma

Pemphigus

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Thermal or mechanical injury

Cicatricial pemphigoid

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Squamous cel carcinoma

Kaposi 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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