Clinical: Melanoma, Non Melanoma and Benign Skin Lesions Flashcards
What is the most common non-melanoma skin cancer?
Basal Cell Carcinoma
What are the 3 types of basal cell carcinomas?
Superficial, Nodular and Infiltrative
How does BCC arise?
Derived from immature pluripotent epidermal cells and is composed of cells with similarities to basal cell layer of epidermis and appendages
Who does BCC commonly affect?
Middle aged, sun exposed patients
Is BCC slow/fast growing and locally/widely destructive?
Slow growing and locally destructive. May ulcerate.
How can BCC kill?
By invading the eye and damaging the brain
What is the typical transformation of BCC from an early lesion to a developed one?
Early: pale, translucent papules or nodules with overlying superficial telangiectasis.
Late: ulcerated with raised, rolled edge
What does a superficial BCC look like?
- Brown plaques with raised thread like edge
- Tissue needs to be resected
What does an infiltrative BCC look like?
- Morphoeic causes destruction if neglected
- Ill defined edge and slow growing
- May infiltrate tissue widely
What does a nodular BCC look like?
- Well defined nodule, looks stuck on
- Shiny and pearly
What is the best management for BCC?
- Early nodular BCC is best excised
- At difficult lesions around the eyes- Mohs’ micrographic surgery
- Clearance of more than 90% of tumours should be achieved
- Cryotherapy for small, localised, low risk lesions
What does squamous cell carcinoma arise from?
Epidermal keratinocytes
Where does a patient typically present with SCC?
On sun exposed areas such as bald scalp, tops of ears, face and back of hands
When does SCC behave most aggressively?
- In immunocompromised patients
- On the lips and ears
What is the first choice management for SCC?
Complete surgical excision
What is the cure rate for most SCC if the excision is cut with a 3-4mm margin?
90-95% for most SCC
What can be given to patients with high risk for further SCCs?
Systemic retinoids
What is Actinic Keratosis?
Hyperkeratotic Erthythematous lesions arising on chronically sun exposed areas
What is the risk of progression Actinic Keratosis to SCC?
0.1%
Does SCC always have to arise from Actinic Keratosis?
No, it can arise de-novo
What may indicate a transformation of Actinic Keratosis to SCC?
Increase in size, ulceration, bleeding, pain or tenderness
What is the histology of Actinic Keratosis?
Moderate squamous cell dysplasia. Not as dysplastic as Bowen’s disease.
What is Bowen’s disease?
In situ, SCC on lower leg of elderly woman
What can Bowen’s disease mimic?
Inflammatory diseases
What is the presentation of Bowen’s disease?
Slow growing, well demarcated, scaly, erythematous plaque
What may be difficult to distinguish Bowen’s from?
Superficial BCC
What does Bowen’s disease often co-exists with?
Venous stasis
What is the % chance of Bowen’s disease developing into SCC?
3%
What is the histology of Bowen’s disease?
Crowding, hyperkeratosis, parakeratin
How is Bowen’s disease managed?
Non surgical procedures are often preferred. Incisional biopsy to confirm diagnosis.
What is keratoacanthoma?
A benign squamous tumour, difficult to distinguish from SCC as it clinically and histologically similar.
How does keratoacanthoma develop?
Rapid growth over weeks-moths then spontaneous resolution
What does keratoacanthoma look like?
Isolated dome shaped nodule with central keratin plug
What is the most common type of cutanous T cell lymphoma?
Mycosis Fungiodes
“scaly rash (like psoriasis) tumour that can on for 20-30 years”
Mycosis Fungiodes (cutaneous lymphoma)
What is the defective gene copy in freckles?
MCIR gene
Often referred to “age spots” or “liver spots”, what are they?
Actinic Lentigines
What is Actinic Lentingines?
“Age spots” related to UV exposure
-Increased number of melanocytes along the basement membrane but without the formation of nests that occur in melanocytic naevi
How does Seborrheoic Keratosis arise?
Benign proliferation of epidermal keratinocytes
What do Seborrheoic Keratosis commonly look like and where do they appear?
- Very common in ageing skin, found on face and trunk
- Warty, ‘stuck on’ appearance with a greasy hyperkeratotic surface with a visible pinpoint keratin plug
Are Melanocytic naevi most commonly congential or acquired?
Acquired before the age of 25
What is melanocytic naevi?
Localised, benign clonal proliferations of melanocytes
What is the % of babies typically born with melanocytic naevi?
1%
What are the 3 types of acquired naevi and in what stage of life do they develop?
1) Junctional naevus in childhood
2) Compound naeves in adolescence/ early adulthood
3) Intradermal naevus in adulthood
Describe where Junctional, compound and Intradermal Naevi are found
Junctional: clusters of melanocytes found at the DEJ
Compound: clusters of melanocytes found at the DEJ and in dermis
Intradermal: clusters of melanocytes found entirely in the dermis
How does the difference in appearance vary between the junctional, compound and intradermal naevi and how do these differences arise?
Junctional: macular, circular or oval mid-dark brown appearance
Compound and Intradermal: both seen as nodules due to dermal content. Intradermal is less pigmented than compound.
What are the 2 clinical settings of dysplastic naevi?
- Sporadic: not inherited
- Familial: strong FHx of melanoma, autosomal inheritance, high lifetime risk of developing melanoma
Give some examples of rarer naevi
Blue naevi, Halo naevi, Spitz naevi
How does a congenital naevus differ from an acquired naevus in how it looks?
Congenital: larger, slightly raised, becomes more rugose and elevated as the child grows older
