Download MBBS (Bachelor of Medicine, Bachelor of Surgery) 1st Year, 2nd Year, 3rd Year and Final year Venereology and Leprosy 2 Pre Cancerous Lesions of The Skin PPT-Powerpoint Presentations and lecture notes
Pre- Cancerous Lesions of
the Skin & Mucosa
ACTINIC KERATOSES
Aka solar keratosis, or senile keratosis
Precursor lesions of cutaneous squamous cel carcinoma
(SCC).
Consists of proliferations of atypical epidermal
keratinocytes ,that may progress to invasive SCC
The overal risk of progression to invasive SCC is (5 -10)%.
ACTINIC KERATOSES
Risk factors
cumulative UV radiation exposure (most important)- outdoor
work/hobby
fair skin, red or blond hair, blue eyes (Fitzpatrick type 1).
age,
immunosuppression,
prior history of non-melanoma skin cancer.
certain genetic syndromes, namely albinism, xeroderma
pigmentosum,
ACTINIC KERATOSES
Site: sun-exposed areas,
balding scalp, head, neck, forearms,
dorsal hands, dorsal legs in women
asymptomatic, pruritus, burning or
stinging pain, bleeding.
2- to 6-mm, erythematous, flat, rough,
gritty or scaly papule
more easily felt than seen.
against a background of
photodamaged skin
ACTINIC KERATOSES
A punch biopsy with depth upto mid-reticular dermis
Common indications for a biopsy
1. Rapidly enlarging lesions,
2. bleeding or ulceration,
3. Evidence of inflammation,
4. strong induration,
5. lesions extending beyond 1 cm of size,
6. resistance to treatment.
ACTINIC KERATOSES
DD
seborrheic keratosis, arsenical keratosis
melanocytic nevi, Senile lentigo,
cutaneous lupus erythematosus
Established AKs chronic course
lesions persist, spontaneously regress, or progress to invasive SCCs.
Spontaneous resolution range from 20% to 30%
limiting sun exposure, use of sunscreen promote regression.
PROGRESSION TO INVASIVE SCC
each AK : potential to progress into SCC (5-10% in reality)
Direct cancerous invasive transformation of basaloid atypical keratinocytes
is the most common mechanism of disease progression
In situ SCC
AK I
basal,
AK II
AK III
suprabasal
lower two-thirds
> two-thirds
SCC
ACTINIC KERATOSES
Treatment
treat entire actinically
damaged areas
PREVENTION of AK
SUNSCREENS : Broad-spectrum against UVB and UVA, minimum SPF 30
RETINOIDS:
Systemic retinoids in preventing nonmelanoma skin cancer, Ak
only effective while taking them; limited by systemic toxicities
Oral nicotinamide: doubtful
BOWEN DISEASE
squamous cel carcinoma (SCC) in situ.
Progress to Bowen carcinoma (invasive SCC) - 5% of
cases.
Etiologic factors include
1. UV radiation,
2. arsenic,
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)
BOWEN DISEASE
Slow growing, usually
asymptomatic.
erythematous plaques with
irregular, clearly demarcated
borders.
Surface scaly, crusted,
hyperkeratotic. measure up to
several centimeters.
Bowen Disease
Clinical variants
pigmented, intertriginous,
periungual, and subungual BD.
HPE
full-thickness epidermal atypia with
large, round cells and possible
adnexal involvement.
Differential Diagnosis of Bowen Disease
Treatment of Bowen Disease
Surgical &Destructive therapies
Topical Therapies
1. Excision
1. 5-Fluorouracil
2. Mohs micrographic surgery
3. Curettage with or without
4. Electrosurgery
Nonsurgical Ablative
5. Cryosurgery
Therapies
1. Photodynamic(PDT)
2. Laser ablation
3. Chemoablation :TCA
4. Radiation therapy
ARSENICAL KERATOSES
result from chronic exposure to arsenic
potential to become squamous cell carcinoma (SCC)
punctuate, keratotic, yellow papules overlying pressure points
Palms and soles.
HPV ASSOCIATED EPITHELIAL
PRECANCEROUS LESIONS
BOWENOID PAPULOSIS
BP is a precancerous
condition of the genitalia
infection with high-risk
HPV, (16, 18, and 33)
young to middle-aged
sexual y active, M>F
multiple red to brownish
flat papules on the penis
or vulva.
BOWENOID PAPULOSIS
location
on the glans penis, prepuce, and penis in males,
around the labia minora and majora in females.
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%).
DD
lichen planus, condylomata acuminata, erythroplasia, mol uscum
contagiosum, and seborrheic keratoses.
Treatment of Bowenoid Papulosis
Local destructive
Topical
1. curettage with or without
1. Tretinoin,
electrosurgery
2. 5-FU,
2. CO2-laser
3. Cidofovir
3. neodymium:YAG laser,
4. Imiquimod
4. cryosurgery
5. excision.
HPV-specific vaccination for types 6, 11, 16, and 18 in prevention: ????
EPIDERMODYSPLASIA VERRUCIFORMIS
inherited skin condition
Loss-of-function mutations of the genes EVER1 and EVER2
High local susceptibility to infection with HPV, commonly types
5 and 8.
Factors contributing to pathogenesis
1. host genetic background
2. HPV infection,
3. UV exposure
4. immunosuppression
EPIDERMODYSPLASIA VERRUCIFORMIS
develop skin lesions early in life
clinical presentation
1. numerous thin, pink, flat-topped papules and plaques that
resemble verrucae planae ; knees, elbows, and trunk.
2. widespread scaly, erythematous, or hypopigmented macules
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,
screening of family members
topical 5% imiquimod cream and retinoids ? mixed results
EPIDERMODYSPLASIA VERRUCIFORMIS
POTENTIALLY MALIGNANT DISORDERS
OF THE ORAL CAVITY
LEUKOPLAKIA
white lesion of the oral mucosa that cannot be rubbed off or characterized
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
Etiologic factors for leukoplakia
1. Chronic chemotoxic exposure,
Tobacco is the strongest risk factor: either as smoke or by
chewing
2. mechanical trauma with poor oral hygiene
il -fitting prosthesis, chronic cheek biting,
3. HPV (16 and 18)
4. alcohol consumption
Differential Diagnosis of Oral Leukoplakia
1. Tobacco-associated
7. Frictional lesion
lesion
8. Oral white sponge nevus
2. Candida-associated
9. Oral hairy leukoplakia
lesion
10.Verrucous carcinoma
3. Leukoedema
11.Squamous cel
4. Lichen planus
carcinoma
5. Lupus erythematosus
6. Habitual cheek biting
LEUKOPLAKIA treatment
OMMISSION
1. consumption of tobacco products, alcohol, bethel nuts,
2. chronic mechanical trauma
Surgical excision is the first treatment of choice.
recurrence after surgical excision : cryotherapy or CO2-laser
the patient should be followed closely
ERYTHROPLAKIA
a red macule or patch on a mucosal surface that cannot
be categorized as any other known disease entity caused
by inflammatory, vascular, or traumatic factors.
commonly seen with leukoplakia
least common of al oral potential y malignant lesions
greatest potential to become oral squamous cel
carcinoma
Males
Risk factors tobacco products, alcohol consumption.
ERYTHROPLAKIA
asymptomatic,
solitary, erythematous
macule or patch.
sharply demarcated from
the surrounding pink
mucosa,
surface is smooth and
homogeneous in color
ERYTHROPLAKIA - DD
Erythematous candidiasis
Chronic al ergic contact
Atrophic lichen planus
dermatitis
Lupus erythematosus
Chronic mechanical trauma
Pemphigus
Thermal or mechanical injury
Cicatricial pemphigoid
Squamous cel carcinoma
Kaposi sarcoma
? High potential for malignant transformation : early treatment.
? Surgery or excision with CO2- laser: treatment of choice
THANK YOU
This post was last modified on 08 April 2022