AK & SCC Flashcards
squamous cell carcinoma (SCC) most commonly occurs:
in who?
Where?
WHITE/FAIR SKIN people
SUN-EXPOSED AREAS (head, neck, forearms, dorsal hands)
SCC vs BCC mortality
SCC has INCREASED mortality, mostly due to high rate of metastasis
SCC etiology
cell of origin: KERATINOCYTE
cumulative UV exposure->genetic alterations accumulate, provide selective growth advantage
SCC in NON sun-exposed areas may be due to chemical carcinogens (eg. arsenic)
SCC morphology
varies:
- papule, plaque or nodule
- pink, red or skin colored
- scale
- Exophytic (grows outward)
- Indurated (lesion feels thick, firm)
- cutaneous horm
FRIABLE: bleed w/minimal traum then crust
(U) asymptomatic, may be pruritic
SCC in situ
aka Bowen’s dz
circumscribed pink-to-red patch
or
thin plaque w/scaly or rough surface
keratinocyte atypia is confined to epidermis, DOES NOT invade past dermal-epidural junction
Shave biopsy use
diagnosis
Surgical excision use
treatment of choice for SCC in situ
specimen must be sent to pathology to document clear margins (complete excision)
Liquid nitrogen cryotherapy use
to tx pre-cancerous actinic keratosis
“Invasive squamous cell carcinoma” means
there are SCC cells IN THE DERMIS
unrelated to metastatic potential
SCC in situ means
there is NO DERMAL INVOLVEMENT
“Atypical squamous proliferation” means
often used when biopsy is too superficial
if dermis cannot be seen in the biopsy, invasive SCC cannot be excluded
SCC treatment options:
surgical (invasive, in-situ)
- surgical excision (invasive SCC):
- wide local excision, Mohs -micrographic surgery - curette & desiccation (in situ SCC)
SCC non-surgical tx options
radiation therapy for poor surgical candidates
5-fluorouracil cream, imiquimod cream, photodynamic therapy-(U) used for in situ SCC when excision is suboptimal choice
SCC: rates of mets
SCC in sun exposed area=5% rate of mets to regional lymph nodes
higher rates of metastasis if:
- large (diameter>2cm), deep (>4mm) and recurrent tumors
- tumor involvement of bone, muscle & nerve
- location on scalp ears nose & lips
- tumor arising in scars chronic ulcers, burns, sinus tracts or on genitalia
- Immunosuppressed patients
- tumors caused by arsenic ingesion
SCC patient follow up
surveillance for the early recognition & management of:
- tx-related complications
- local or regional recurrences
- development of new skin cancers
patients with a hx of SCC should have close follow-up
patients are often seen every 6 to 12 months
Actinic Keratosis:
cell of origin
what is it
prognosis/risk
keratinocyte is cell of origin
AK is premalignant lesion;
almost all AKs that become CA will become SCC
1/1000 risk of malignant transformation from AK to SCC in one year
risk factors: persistence of AK, hx of skin CA, immunosuppression
Etiology of AK
cumulative & prolonged UV exposure, resulting in UV-induced p53 tumor suppressor gene mutations
Individual risk factors that can increase susceptibility to AK (4)
- increasing age
- fair skin, light eyes/hair (skin types I,II)
- immunosuprresion
- genetic syndromes, such as xeroderma pigmentosum and albanism
AK clinical manifestations (5)
- may be symptomatic (tender)
- on sun-exposed areas (head neck extensor forearms, dorsal hands)
- (U) on background of sun damages skin
- erythematous paule or thin plaque w/rough, gritty scale
- often dx by feel (like sandpaper)
AK is often dx how?
by feel (like sandpaper)
*be cautious in lesions>6mm since they may represent SCC in situ or superficial BCC
Skin features of chronic sun damage: (5)
- combination of atropy & hypertrophy
- telangiectasias
- spotty depigmentation & hyperpigementation
- wrinkles
- skin appears “leathery” and “prematurely aged”
Solar Lentigo (lentigines):
cause
distribution
appearance
result from UV damage
sun-exposed areas
once/many small brown macules
Cutis rhomboidalis nuchae
red neck with rhomboidal furrows
an effect of sun damage
solar elastosis
fine nodularity pebbly surface
an effect of sun damage
