SCC and its precursors Flashcards
(25 cards)
List treatment options for Actinic Keratoses
**Liquid nitrogen **
Curettage
**Shave excision **
TOPICALs
5 - Fluorouracil 5% cream
5 FU - 0.5% cream with 10% salycylic acid
**Imiquimod 5% cream or 3.75% cream **
Diclofenac gel 3%
Tribanibulin 1% ointment
Procedural:
- PDT - daylight / red light / blue light
- chemical peels: Trichloroacetic acid
- ablative laser techniques (CO2, erbium YAG)
AK risk of progression to SCC
Rates vary - commonly quoated at 1/1000 risk
A patient with 7.7AK has a 10% risk of one transforming to SCC over a ten year period.
Cryotherapy risks
Blistering
Oedema
Crusting
soreness
Hypopigmentation
Scarring
Recurrence
How is diclofenac used to treat AKs?
3% diclofenac in 2.5% hyaluronic acid
Needs daily for 90 days
Complete clearance rates of only 47%
How to use imiquimod for the treatmnt of AKs?
5% or 3.75%
Three times a week for four to six weeks, repeated if necessary after a break of four weeks
What is PDT?
Administration of a photosensitising compound (which selectively accumulates in the hyperproliferating target cells)
Followed by local irradiation with visible light
Causing target tissue damage (necrosis and apoptosis)
What photosensising agents might be used for PDT?
5-aminolaevulinic acid (ALA)
Methyl ester of 5-aminolaevulinic acid (Metvix)
What is an arsenic keratoses?
A corn like punctate keratoses caused by arsenic, characteristically affecting the palms and soles
Clinical features of Arsenic poisioning?
Punctate keratoses
Hyperpigmentation in a rain drop like pattern
Hypopigmented areas
Mees lines - transverse white bands on the fingernails
sensory changes - numbess and tingling in a glove and stocking distribution
headache
weakness
What is disseminated superifical actinic porokeratoses?
An Autosomal dominant condition
Due to mutations in MVK or MVD
- requires a second hit to the wildtype allell of the gene
Characterised by:
- 1 -3 mm conical papules, brownish red
- keratotic ring
- skin within the ring is somewhat atrophic, red or hyperpigmented
What is the risk of malignant transformatin of Bowens Disease?
3 - 5 %
Dx?
Bowens disease with an inflammatory infiltrate
Bowens disase on perianal skin carriers a higher risk of invasion, recurrence and an ass with vulval / cervical dysplasia
T
rook
Treatment of choice for bowens disease?
Cryotherapy - 30s freeze
Currettage
Topical 5 FU
Topical Imiquimod - once daily for 16 weeks
PDT
Excision
2nd LIne
- radiotherapy
Common gene mutations in SCC
NOTCH 1
NOTCH 2
CDKN2A
FAT1
Immunosuppressent meds in order of risk of developing SCC?
AZA
Calcinurin inhibitors (tacro)
MMF
Pred
MTOR inhibitors
Role of HPV in SCC pathogenesis
Beta HPV in particular (E6 and E7) is implicated
Exact mechanism is unclear
Rate of SCC metastatsis
5%
High risk features for SCC
Diameter 20 - 40mm
Thickness 4 -6 mm
Invasion in to sub cut fat
PNI (nerve diameter < 0.1mm)
Poorly differentiated
Lymphovascular invasion
Tumour site ear or lip
Tumour arising within a scar or site of chronic inflammation
immunosuppressed patients
Fraily and comorbidities
Very high risk factors for SCC
Diameter > 40mm
Thickness > 6mm
Invasion beyond subcut fat
Any bone invasion
PNI (nerve >0.1 mm or named nerve or nerve beyond the dermis)
High grade histological subtype
In transit mets
Immunosuppressed patients
Fraily and comorbidities
How is SCC staged?
TNM
SCC overall stage
Histological variants of SCC
o Grading: well – poorly differentiated
o Adenoid/pseudoglandular: tubular pattern, keratinocyte acantholysis
o Clear cell: Keratinocytes appear clear from accumulation of lipid vacuoles & swelling
o Spindle Cell: spindle shaped atypical cells – poor prognosis
o Signet ring: rare, concentric rings composed of keratin & large vacuoles
o Verrucous: acanthosis & papillomatosis (warty), deeper component extends downward displacing collagen bundles
o Acantholytic and
o Basaloid
what is a verrucous carcinoma?
a low grade, locally destructive SCC associated with HPV 6 & 7
