Skin Flashcards
Where can skin cancers arise?
MECA O
- Epidermis
- Connective Tissue
- Melanocytes
- Adnexae
- Other Components
Skin tumours of the epidermis
Seborrhoeic keratosis*
Keratocanthoma
Basal cell carcinoma*
Squamous carcinoma*
Skin tumours of the connective tissue
Dermatofibroma DFSP (Dermatofibrosarcoma) Haemangioma Leiomyoma/Sarcoma Angiosarcoma Kaposi’s sarcoma
Skin tumours of melanocytes
Melanocytic naevi*
Melanoma*
Skin tumours of adnexae
Hair follicle
Sweat gland
Sebaceous gland
Benign epidermal tumours
◦ Seborrhoeic keratosis/wart
◦ Viral wart (HVP)
◦ Keratoacanthoma
Malignant epidermal tumours
◦ Basal cell carcinoma
◦ Squamous carcinoma
What’s a seborrhoeic keratosis/wart
Syn. Basal cell papilloma
◦ Very common - middle-old age
◦ Greasy, warty plaques
◦ Uniform small-medium sized basaloid cells
Basal cell carcinoma
Terminology: BASAL CELL: Cells resemble epidermal basal cells CARCINOMA: Malignant tumour Commonest malignant tumour BCC:SCC = 4:1 Not a truly epidermal tumour ◦ related to hair follicle epithelium
What’s the commonest malignant skin tumour?
BCC
What causes ageing and skin wrinkling?
UVA
Basal Cell Carcinoma: Risk factors
UVB- intermittent exposure
Skin type -pale skin, red/blond hair, freckles etc
(The lower the skin type the higher the risk)
Genetic conditions:
Gorlin’s syndrome –PTCH-1 gene mutation
Xeroderma pigmentosum (of nucleotide excision repair)
Immunosuppression
Others – e.g. radiation
Basal Cell Carcinoma: Clinical
“Rodent ulcer” as it eats through structures
Sun-exposed sites (UVB)
Middle-old age (cumulative sun exposure)
“pearly nodule with telangiectasia” But also plaques, ulcers (depends on growth pattern)
Slow growing
Small (Usually <2cm but occ. much larger)
Behaviour:
10% recur (Depends on growth pattern and resection margins)
1:10,000 - 1:50,000 metastasise (HARDLY EVER)
Prognostic factors of BCC
Diameter of lesion
Site (head and neck worse)
Tumour type (pattern- infiltrative and micronodular are more likely to recur)
What does squamous carcinoma look like?
Squamous cell: Tumour cells resemble the keratinocytes of then epidermis
Often show keratinisation like the stratum corneum of the epidermis
Is squamous carcinoma malignant?
Yes but... Terminology confusing as it may be ◦ Invasive (truly malignant) ◦ In-situ (premalignant): Solar/actinic keratosis Bowen’s disease
Squamous Carcinoma: Risk factors
UVB (cumulative exposure, p53 mutations) Skin type Immunosuppression (more so than BCC) HPV (as in uterine cervix) Genetic conditions e.g. XP Others e.g. scars, chronic ulcers,etc
What’s actinic keratosis?
Scaly papules/small patches on sundamaged skin (UVB)
Common in elderly pale-skinned individuals
Histology of actinic keratosis and what can it become?
Histo:
- Variable dysplasia (akin to CIN of cervix)
- Only severe dysplasia = in situ scc
Evolution of lesions
- development of invasive scc
What’s Bowen’s disease?
Type of squamous carcinoma in situ
Middle - old age
Large red-brown scaly (“flaky”- keratin ) patches
More common in sun-exposed skin
Severe dysplasia
Pathology of squamous cell carcinoma
◦ Malignant squamous cells
Keratinised frequently
Pink
◦ Infiltrate the dermis/subcutis
◦ Variable degrees of differentiation (grade)
Well, moderate, poor
Depending on how much the cells resemble normal epidermal cells
Behaviour of squamous cell carcinoma
◦ Locally destructive
◦ More likely to metastasise than bcc
Local lymph nodes
Lungs, etc
◦ Less than 5% metastasise BUT depends on site, grade and thickness of tumour
◦ Stage of tumour depends on how early it is discovered (and how thick it is)
Poor prognostic features for squamous carcinoma
Sites with poor prognosis: ◦ Lips- at least 15% metastasise ◦ Ears - about 10% metastasise ◦ Vulva ◦ Anus
Histological features:
◦ Tumour thickness
◦ Tumour grade
◦ Completeness of excision
Immunosuppression
How is Keratoacanthoma similar and different to SCC?
Common features with SCC:
Sun-exposed skin
Nodule with keratin BUT within a central crater
Histo: Well differentiated SCC BUT central crater
Differentiating features fromSCC:
Grows quickly (weeks) and spontaneously regresses (months)
Does not recur or metastasise
Stages of progression of melanocytic tumours
1.Benign ◦ Melanocytic naevi: - Common acquired (usual “run of the mill”) - Congenital - Special naevi: Blue, Spitz, etc
- Dysplastic (premalignant)
◦ Dysplastic naevi
3.Malignant
◦ Melanoma
Moles aka
melanocytic naevi
sometimes look blue if the melanin is deep in the skin
Features of melanocytic naevus
Initial presentation:10 and 25 years old
Variable numbers (some families and skin types more prone)
Natural evolution:
- Usually arise at epidermal-dermal junction
(junctional)
- Evolve over many years with nests of melanocytes
entering the dermis (compound)
- Eventually become totally intradermal (intradermal)
Very few may become malignant
Melanoma: Risk factors
UVB
◦ Intermittent exposure (“ordinary” melanoma)- burning episodes in childhood
◦ Chronic exposure in some – lentigo maligna on face
◦ NOT in acral or nail melanoma
Skin type
Family history - familial melanoma/dysplastic naevus syndrome
Multiple benign naevi
Congenital naevi - “giant
Clinical signs of melanoma
(ABCD)
Brown/blue/black pigmentation
◦ melanin, depends on its location within the skin
Macules, patches (generally if in situ), papules and nodules (generally if invasive)
Bigger, more irregularly shaped and pigmented
than benign naevi
Changes in previously stable naevus
Itching and bleeding
Directions of melanoma growth
Large, pleomorphic melanocytes arranged singly, in nests and large nodules
Majority grow for a prolonged period in the epidermis
+/-superficial dermis - RADIAL GROWTH PHASE
Later develop capacity for deeper invasion/metastatic spread = VERTICAL GROWTH PHASE
Melanoma prognosis
Age - worse with increasing age Sex - women better than men Site - arms and legs better than other sites STAGE - localised > LN > systemic BRAF mutations do better due to better therapy TUMOUR THICKNESS ◦ <1mm = 99% (pT1) ◦ >4.00mm = <40% Mitotic count (pT1a vs pT1b) Presence of ulceration Level of invasion (Clark) Host lymphocyte response and regression
Treatment of melanoma
Primary excision
Re-excision
Sentinel lymph node bx (pT1b and above)
Lymphadenectomy
Medical treatment
◦ BRAF mutant- “nibs”- Signalling inhibitors that stop cell cycle
◦ BRAF wild type- “mabs”- Immunotherapy that activates immune system
Basal cell carcinoma main points
Slow growing
Locally destructive
Local recurrence
Virtually never metastases
Squamous cell carcinoma main points
Variable growth rate
Locally destructive
Local recurrence
Metastases much commoner
Sometimes melanomas contain large areas that are non-pigmented. What are these called and how do they arise?
amelanotic. In these areas the malignant melanocytes have lost the capacity to produce melanin pigment.
What are the clinical features which might help distinguish a melanoma from a benign naevus?
‘ABCD’
‘A’ stands for asymmetry. Melanoma is often asymmetrical whereas benign naevi should show a uniform symmetrical appearance.
‘B’ stands for borders. In melanoma the border of the lesion is often ill defined or irregular.
‘C’ stands for colour. In melanomas it is not unusual to see different shades of colouring ranging from red to brown, black and even grey. The more colourful a pigmented skin lesion the more suspicious it is of malignancy.
‘D’ stands for diameter, i.e. size (>6 mm).
Other pointers are: new pigmented lesion, change of pigmentation or growth in a pre-existing naevus, itching or bleeding. If in doubt, a pigmented lesion should be excised and the majority of melanomas are cured by early surgical excision.
Risk factors for melanoma
ultraviolet radiation (UVB
- intermittent (i.e. burning episodes, particularly in childhood)
- chronic (cumulative)
There is some evidence now that the genetic abnormalities vary between melanomas occurring on chronically sun-exposed sites (C-kit) and those occurring on intermittently sun-exposed sites (NRAS and BRAF). This is increasingly important because of targeted chemotherapy for metastatic melanomas.
Skin type (pale freckled skin, red / blond hair) is also an important risk factor. Others are family history (dysplastic naevus syndrome), multiple benign naevi and large congenital naevi.
How would you explain the findings? In the dermis and subcutaneous tissue there is a well circumscribed darkly pigmented nodule. The overlying skin surface shows no obvious pigment.
The absence of surface involvement suggests that this is most likely a metastatic melanoma deposit. In fact, the skin / subcutis between a primary melanoma and local lymph nodes is a common site of metastasis (so-called in-transit metastasis). Melanoma may recur locally, spread via the lymph nodes and systemically via the blood stream most commonly to liver, lung, brain and skin. It may recur many years after removal of the primary melanoma.
What is the most important prognostic factor for melanomas?
The most important prognostic factor is the thickness of the lesion at the time of primary excision. It is called the Breslow thickness and is measured in mm. The presence or absence of surface ulceration is also important. The cure rate for completely excised non-ulcerated melanomas <1mm approaches 100%, whereas the 5-year survival for lesions >4mm is < 40%. Clearly, increasing age, site (arms and legs are better than other sites) and overall stage (localised > lymph node metastasis > systemic metastasis ) also play a role.
How do nodular melanoma grow?
Nodular melanoma invade rapidly without a discernible radial growth phase.
What are the most common sites for nodular melanoma?
trunk, head and neck
It is more common for nodular melanoma to begin in normal skin rather than in a pre-existing lesion.
What’s the tumour?
On the head, ulcerated lesion with rolled everted edges, tumour does not appear to reach the deep margin formed by the aponeurosis
BCC
What’s the tumour?
On the skin, pearly papules or nodules +/- ulceration.
BCC
Nests of darkly staining atypical cells invade the dermis but do not invade the subcutaneous fat. The nests show peripheral palisading (cells lined up like a fence around the edge of the nests) which is characteristic of….
basal cell carcinoma
Surface crusting suggestive of…
keratinisation and the most likely diagnosis is that of a squamous cell carcinoma (SCC)
Which malignant epidermal tumour are you more at risk of if you’re immunosuppressed?
SCC
What are the precursor lesions of squamous cell carcinoma in the skin?
Invasive carcinoma of the skin often develops from premalignant dysplastic epithelium following sun-damage. These lesions are termed actinic or solar keratoses. Severely dysplastic lesions are termed squamous carcinoma in-situ or Bowen’s disease.
What is a keratoacanthoma and how does it differ from squamous cell carcinoma?
Keratoacanthoma is a rather curious lesion which may mimic squamous cell carcinoma. However, clinically it is a benign lesion and it regresses. It is characterised by a symmetrical crater-like appearance, often occurs on sun-damaged skin, grows very rapidly for several months and then regresses. Histologically, it is virtually indistinguishable from a well differentiated squamous cell carcinoma. However, it never invades deeply and does not metastasise. The architectural symmetry may not be appreciated unless the lesion is excised intact rather than curetted. This tumour may represent a special form of squamous cell carcinoma, which is clinically benign because of its ability to totally regress.
Histology of SCC
- squamous eddies
- keratin pearls
- some cells stain deeply pink because of the keratinisation
- intercellular bridges (or prickles)
What are cutaneous horns and what are they made of?
A conical projection above the surface of the skin which resembles a miniature horn. It is composed of compacted keratin similar to that of the very superficial layers of the epidermis.
