Skin Cancer Flashcards

1
Q

What are the 2 mechanisms of skin cancer?

A
  • direct action of UV on target cells (keratinocytes) for neoplastic transformation by DNA damage
  • effects of UV on the host’s immune system (immune suppression)
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2
Q

Describe basal cell carcinoma

A
  • lesion with a shiny shouldered edge, with a degree of ulceration
  • mutation of DNA in basal cells results in multiplication and growth of basal cells when they would normally die
  • PTCH gene mutation may predispose
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3
Q

Describe the treatment of basal cell carcinoma

A
  • surgical excision with 3-4mm margin (gold standard)
  • curettage and cautery (scrape away damaged tissue)
  • cryotherapy
  • photodynamic therapy (immune response induced with UV light to attack cancer cells)
  • topical imiquimod/5FU cream
  • mohs micrographic surgery (surgery with pathology technician assistance)
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4
Q

Describe the different subtypes of basal cell carcinoma

A
  • nodular (most common)
  • superficial (red patch, crusting and involvement of blood vessels, flatter)
  • pigmented (rolled shiny margin, depressed ulcerated area with dark brown pigmentation)
  • morphoeic/sclerotic (subtle area of skin colour change, shiny, what you see is not representative of true margins)
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5
Q

Describe the features of squamous cell carcinoma

A
  • may occur in normal skin, injured skin, or chronically inflamed skin
  • originates in keratinocytes
  • pre-malignant variants (actinic keratoses, Bowen’s disease)
  • most occur on skin regularly exposed to sunlight/UV radiation
  • appears as keratin crust and scaling, inflammation + areas of pigmentation
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6
Q

What is the treatment for squamous cell carcinoma?

A
  • surgical excision with 4mm margin (high rate of relapse so increased margin) = gold standard
  • curettage and cautery (in certain scenarios)
  • premalignant syndrome = topical imiquimod/5FU cream, cryotherapy, photodynamic therapy, sun protection
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7
Q

Describe the features of melanoma

A
  • tumour of melanocytes
  • most common in skin (but can occur in bowel/eye)
  • DNA damage (mainly UV, rarely genetic)
  • has radial growth phase, then deeper vertical growth
  • can spread by lymphatic system
  • has a premalignant form
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8
Q

What are the risk factors of melanoma?

A
  • genetic markers
  • family history
  • UV radiation
  • sunburns during childhood
  • melanocytic/congenital/atypical nevi
  • personal history of melanoma
  • very fair skin
  • DNA repair defects eg. Xeroderma pigmentosum
  • immunosuppression
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9
Q

Describe the subtypes of melanoma

A
  • superficial seeding
  • nodular
  • acral (affecting digits and toes)
  • subungual (under nail)
  • amelanotic (red rather than pigmented)
  • lentigo meligna (pre-malignant precursor in sundamaged skin of face and neck)
  • lentigo meligna melanoma
  • melanoma in situ (precursor for melanoma in other areas)
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10
Q

What is the treatment of melanoma?

A
  • surgical excision (breslow <1mm = 1cm margin, >1mm = 2cm margin)
  • immunotherapy (ipilimumab, nivolumab)
  • immune checpoint/MEK inhibitor (trametinib)
  • biologic antibodies for genetic defects (eg. BRAF defects)
  • imaging/scanning CT/MRI/PET
  • long term follow up, assessment of lymph nodes/organ spread, genetic testing in family with multiple primary melanomas
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11
Q

Describe different cutaneous tumour syndromes

A
  • Gorlin’s syndrome (multiple BCCs, jaw cysts, risk of breast cancer)
  • Brooke Spiegler syndrome (multiple BCCs, trichepitheliomas)
  • Gardner syndrome (soft tissue tumours, polyps, bowel cancer)
  • Cowden’s syndrome (multiple hamartomas, thyroid, breast cancer)
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