Keratosis and Skin Cancer Flashcards
Curettage
Scraping the skin away with a curette, a ring-shaped instrument
Electrodessication
High-frequency current is applied to the lesion, destroying the tissue by drying it out
Cryotherapy
Tissue is destroyed by freezing to -40 C or below using liquid nitrogen
Biopsy
Incisional (portion)
Excisional (whole)
Solar Lentigo
“Age spot” “Senile freckle”
- Local proliferation of melanocytes (UV damage in sun exposed areas)
Very Common
Clinical Presentation of Solar Lentigo
Well circumbscribed
Small brown macule often found in groups
Seborrheic Keratosis (SK)
Common benign epidermal lesion
- Proliferation of immature keratinocyte
Develop typically after age 50
- “barnacles of aging”
Genetic link to excess multiple SKs
Clinical Presentation of Seborreic Keratosis
Tan to black with warty, waxy, “stuck-on” appearance
Well demarcated, oval/round/irregular shape
May have single SK or hundreds
- Chest, back, head, and neck
- “Christmas tree” appearance on back due to Blaschko Lines
ISK: Irritated SK
- caused by rubbing/friction
- may have pruritus, pain, bleeding
Leser-Trelat Sign
Associated with SK
Sudden onset of multiple SKs with inflammatory base
- skin tags
- acanthosis nigricans (A skin condition characterized by dark, velvety patches in body folds and creases.)
Possible association with GI and lung cancers
Clinical Presentation of Keratocanthoma
Hallmark: rapid growth over 6-8 weeks
Round, flesh colored nodule, with central keratin plug
- More commonly found in sun exposed areas +/- hair distribution
Risk Factors of Keratocanthoma
Middle-age to elderly with fair skin
Increased UV radiation or chemical carcinogens
Management of Keratocanthoma
Majority resolve spontaneously in 6-9 months
Due to difficult dx, requires biopsy and treatment
- Excisional biopsy preferred (Mohs)
Actinic Keratosis (AK)
Also known as solar keratosis
Originate from keratinocyte
Considered pre-cancerous
- May progress to SCC (disease continuum, 8% risk per year)
Risk Factors Actinic Keratosis (AK)
Increasing age
M>F
Light skin complexion (Fitz I,II)
Chronic UV light exposure
History of sunburns
Immunosuppression
Genetic syndromes
Clinical Presentation of Actinic Keratosis
Erythematous, scaly/gritty macule or papule
May be tender
Subtypes:
- Hypertrophic: thickened
- Atrophic: scale absent
- AK w/ cutaneous horn
- Pigmented
- Actinic cheilitis (lip)
Diagnosis of Actinic Keratosis
Typically clinical diagnosis based on visualization and touch
Dermoscopy may be helpful
Shave or punch biopsy
- lesion > 1cm
- rapid growth
- ulceration or pain associated
*If lesion is >6mm: consider SCC in situ
Management of Actinic Keratosis
May spontaneously resolve (20-30%) but could reoccur
Isolated lesions: cryotherapy or surgical intervention
Multiple lesions: field treatment
- Topical fluorouracil cream: preferred
- Photodynamic therapy (PDT): topical photosensitizer selectively destroy target cells
- Imiquimod (Aldara)
Basal Cell Carcinoma (BCC)
Arises from basal layer of the epidermis
Nodular BCC is most common type
Flesh-colored or pinkish
Pearly papule/nodule
Telangiectasias
May have central ulceration w/ rolled border
Most common on head and neck
Sebaceous Hyperplasia
BCC DDx
Enlarged oil gland with central clearing
Look for telangiectasias
Fibrous Papule
BCC DDx
Benign angiofibroma
Skin colored/ pinkish papule on the nose
No telangiectasias and lacks pearly texture
BCC Treatment
Surgical: preferred
- Curettage & dessication
- Excision with 4 mm margins
- Mohs for high risk or cosmetic reasons
Nonsurgical
- Radiation for poor surgical candidates
Superficial BCC
- Imiquimod cream
- 5% fluorouracil cream
- Photodynamic therapy
Squamous Cell Carcinoma (SCC)
Originates from keratinocytes
Males 50-70 years
Risk Factors: UV exposure including tanning beds, genetic alterations, chemical carcinogen exposure
May arise from previous skin injuries: burns, scars, etc.
Clinical Presentation of SCC
Papule, plaque, or nodule
Pink, red, or skin colored
Often asymptomatic, may be pruritic or tender
Lesion appears scaly, exophytic, indurated, and/or friable
Commonly appears warty
Treatment of SCC
Surgical: preferred
- Wide excision: margins based on risk
- Mohs: recommended for high risk and cosmetic
Non-surgical
- Radiation (poor surgical candidate, residual tumor)
- Curettage & Dessication or cryotherapy (select low-risk or SCC in situ)
Less effective options for SCC in situ
- Imiquimod cream
- 5% fluorouracil cream
- Photodynamic therapy
Risk Factors of Malignant Melanoma
Fair skin, blue eyes, red/blonde hair, freckling
> 5 atypical nevi, >25 nevi
Immunosuppression
Personal or family history of melanoma: genetic
predisposition in small percentage
Prolong UV exposure
Melanoma
Usually asymptomatic
Most de novo with some arising from pre-existing nevus
Pigmented papule, plaque, or nodule
ABCDEs
ABCDEs of Detecting Melanoma
A - Asymmetry: shape or color
B - Border: irregular
C - Color: dark or variations
D - >6mm (pencil eraser)
E - Evolving: changes in the above
Superficial Spreading Melanoma
Most common subtype (70%)
Confined to epidermis
Often younger population
Radial spread > Vertical growth
Men: back
Woman: legs and back
Nodular Melanoma
Rapid vertical growth
Minimal radial growth
Aggressive
Nodule is inflamed and friable
Lentigo Melanoma
Elderly w/ chronic sun exposure
Slow progression radially with rapid vertical growth
- typically remains more superficial
Acral Lentiginous
Darker skin (african/asian ancestry)
Spreads superficial, then vertical
M > F
Larger lesions due to delay in dx
- palmar, plantar, or subungual
Melanoma Considerations
Subungual
- Great toe or thumb
- history of trauma
- dark streak & involves proximal nail fold
Amelanotic
- minimal or absent pigment
- extensive ddx
Treating Melanoma
Wide surgical excision is the gold standard w/ 2cm clear margins
Regional lymph node dissection/sentinel node biopsy
Advanced metastatic disease:
- radiation
- chemotherapy
- immunotherapy/targeted therapy: adjunct therapy
Follow up every three months
