Skin Flashcards
Layers of the skin
Epidermis: (CLGSB)
- Stratum Corneum
- Stratum Lucidum
- Stratum Granulosum
- Stratum Spinodum
- Stratum Basale
Dermis:
- Papillary Dermis
- Reticular Dermis
What is squamous cell carcinoma (SCC)?
Malignant tumor from squamous epithelial cells.
Commonly affects skin; can involve lungs, mouth, genitals.
2nd most common skin cancer.
Main risk factors for SCC?
UV radiation (sun/tanning beds).
Immunosuppression (HIV, transplants).
Carcinogens (arsenic, tobacco).
Chronic inflammation (scars, ulcers).
HPV infection, fair skin.
How does SCC develop?
DNA damage (e.g., UV, carcinogens) mutates squamous cells.
p53 gene mutations disrupt cell cycle, causing growth.
Progresses from actinic keratosis to invasive SCC.
How does skin SCC present?
Scaly, red patch or firm nodule.
Non-healing ulcer, bleeding/crusting.
Found on sun-exposed areas (face, hands).
SCC presentation in non-skin?
Mouth/Esophagus: Painful ulcer, difficulty swallowing.
Lungs: Persistent cough, hemoptysis, chest pain.
Key histopathological features of SCC?
Atypical squamous cells invade dermis.
Keratin pearls (well-differentiated SCC).
High mitotic activity in poorly differentiated SCC.
What is Bowen’s Disease
Intra-epidermal SCC/ in-situ SCC
How does SCC differ from BCC and melanoma?
BCC: Less metastatic, pearly nodules.
Melanoma: Aggressive, arises from melanocytes, changing mole
Questions in the history for skin cancer?
PC:
Onset, development
Ulcerating, itching, bleeding, pain
Systemic/constitutional symptoms: cough, WL, tiredness, night sweats, headache
RFs: , PMHx/FHx of skin cancer, Sun exposure, history of blistering sunburn, outdoor occupation, tanning beds
PMHx: FIT, Genetic cancer syndromes: Gorlin’s Syndrome for BCC
DHx: immunosuppressants, anticoagulants, allergies
SHx: Smoking, alcohol, Home situation, social support
What examination would you perform in skin cancer clinic?
General: Pale skin, freckles
Lesion
A: Asymmetry
B: Border (irregular or poorly defined border)
C: Colour (>3 colours)
D: Diameter (>6mm)
E Evolving (change in colour or shape)
F: Fixed to underlying structures
Locoregional examination: Satellite lesions, local metastasis, Lymph nodes
Full skin examination with chaperone
Clinical photography with consent
What are the specific body areas for site assessment in classification cSCC?
- Head, neck, trunk, and limbs
- Genital/perianal
- Eyelid
If the cSCC lesion is located on the genital or perianal area, what is the next step?
Refer to a site specialist team.
What are the clinical staging size thresholds for cSCC lesions on the head, neck, trunk, or limbs?
T1: ≤ 20 mm
T2: > 20 to ≤ 40 mm
T3: > 40 mm
What are the clinical staging size thresholds for cSCC lesions on the eyelid?
T1: ≤ 10 mm
T2: > 10 to ≤ 20 mm
T3: > 20 mm
What additional clinical features are included in staging for cSCC eyelid lesions (apart from diameter)?
Involving the tarsal plate or lid margin:
T1b, T2b, or T3b if involved
T1a, T2a, or T3a if not involved
Full thickness of eyelid:
T1c, T2c, or T3c
What is the next step when assessing cSCC, if there is clinically positive nodes?
USS/FNAC and/or FNAB
If no nodes: incision/excision biopsy
How can be cSCC lesions be classified in terms of risk?
Low risk
High risk
Very high risk
Features of low risk cSCC
Clinical:
Tumour diameter <20mm (T1)
Histological:
Tumour thickness <4mm
No invasion into Dermis
No perineural/lymphovascular invasion
Patient:
Immuno-competent
Features of high risk cSCC
Clinical:
Tumour diameter 20 - 40 mm (T2)
Ear/Lip
From scar/chronic inflammation
Histological:
Tumour thickness 4 - 6mm
Invasion into Subcut fat
Perineural (dermal only)
Lymphovascular invasion
Patient:
Iatrogenic/biological immunocompromised
Features of very high risk cSCC
Clinical:
Tumour diameter >40mm (T3)
In transit metastasis
Histological:
Tumour thickness >6mm
Invasion beyond Subcut fat/into bone
Perineural (nerve beyond dermis/named nerve)
Lymphovascular invasion
Patient:
Iatrogenic/biological immunocompromised. Solid organ transplant recipient. Haematological malignancy (CLL/myelofibrosis)
Excision margins for Low risk cSCC?
Peripheral: ≥ 4 mm
Deep: “For mobile lesions the deep margin should be within the next clear surgical plane, and on the scalp the excision should include the galea.”
Excision margins for high risk cSCC?
Peripheral: ≥ 6 mm
Deep: “For mobile lesions the deep margin should be within the next clear surgical plane, and on the scalp the excision should include the galea.”.
Excision margins for very high risk cSCC?
Peripheral: ≥ 10 mm
Deep: “For mobile lesions the deep margin should be within the next clear surgical plane, and on the scalp the excision should include the galea.”
Follow up for low risk cSCC?
Single post-treatment appointment
Risk of recurrence for low risk cSCC?
40%: further keratinocyte cancer within 5 years
Follow up for high risk cSCC
4monthly for 12 months
6 monthly for second year
Risk of recurrence for high/very high risk cSCC?
Patients with more than one proior keratinocyte cancer have 80% chance of further keratinocyte cancer within 5 years
Follow up for very high risk cSCC?
4monthly for 2 years
6 monthly for third year
What is the first step in the management pathway for cSCC?
Freely mobile: offer surgical excision/Mohs/C&C
What margins following cSCC would indicate clearance?
> 1mm (peripheral and deep)
How would you manage a patient with cSCC with positive margins
Positive margin or <1mm peripheral/deep.
SSMDT discussion
Offer: re-excision/Mohs/Radiotherapy
How do you classify nodal staging (TNM) in cSCC?
Non-head and neck
N1: single node ≤ 3 cm
N2: single ipsilateral node 3-6 cm, multiple nodes <6cm
N3: node > 6 cm
Head and neck region
N1 single ipsilateral node ≤ 3 cm without ENEa (extra nodal extension)
N2a: single ipsilateral node 3-6 cm without ENE
N2b: multiple ipsilateral nodes <6 cm without ENE
N2c: Bilateral or contralateral nodes <6cm without ENE
N3a: single or multiple nodes > 6 cm without ENE
N3b: nodes with ENE
How do you classify metastasis staging (TNM) in cSCC?
M0: No distant metastasis
M1: Distant metastasis (including contralateral nodes in non-head and neck cSCC)
How do you classify tumour staging (TNM) in cSCC?
T1: ≤ 2 cm
T2: > 2 to 4 cm
T3: > 4 cm or minor bone erosion or specified perineural invasion (≥ 0.1 mm diameter and/or deeper than the dermis and/or a named nerve) or deep invasion (thickness > 6 mm and/or beyond the subcutaneous fat)
T4a: Tumour with gross cortical bone/marrow invasion
T4b: Tumour with skull base or axial skeleton invasion including foraminal involvement and/or vertebral foramen involvement to the epidural space
What is Basal Cell Carcinoma (BCC)?
Most common type of skin cancer.
A slow-growing, locally invasive skin cancer arising from basal cells in the epidermis.
Types of BCC
27 Types
Nodular (most common): Pearly, dome-shaped papule with telangiectasia.
Superficial: Erythematous, scaly plaque with a thread-like border.
Morpheaform/Sclerosing: Waxy, scar-like lesion; more aggressive.
Basisquamous
Pigmented: Brown/black pigmentation, mimicking melanoma.
How can you classify BCC by risk?
Low risk
High risk
Features of low risk BCC?
Area Lb < 20 mm
Trunk and extremities but excluding hands, nail units, genitals, pretibia, ankles and feet.
Area Mc < 10 mm
Cheeks, forehead, scalp, neck and pretibia
Well defined borders
Immuno-competent
Type: Nodular/superficial
Contained within subcut fat
<6mm depth
No perineurial/lymphovascular invasion
Features of high risk BCC?
Area Lb > 20 mm
Trunk and extremities but excluding hands, nail units, genitals, pretibia, ankles and feet.
Area Mc > 10 mm
Cheeks, forehead, scalp, neck and pretibia
Area Hd
Periorbital, temple, ear, lips, mandibular margin
Poorly defined borders
Immunocompromised
Type: Infiltrative
Invading beyond subcut fat
>6mm depth
Perineurial/lymphovascular invasion
Excision margins for BCC?
Low risk: >4mm
High risk: >5mm
“Excise BCC by ensuring adequate excision at the deep margin to a clear plane, including a fat layer where pre- sent, and other deeper structures if needed.”
Treatment options for low risk BCC?
Standard surgical excision
Topical imiquimod/5-fluorouracil
Cryosurgery
Curette & cautery
Photodynamic therapy
Radiotherapy
Treatment options for high risk BCC?
Standard excision
Mohs
Treatment options for high risk BCC, if patient unsuitable or declines surgery?
Primary: Radiotherapy
Recurrent or advanced: Radiotherapy or Vismodegib
Mechanism of action of Vismodegib
Vismodegib selectively binds to and inhibits the transmembrane protein smoothened homologue (SMO) to inhibit the Hedgehog signalling pathway.
Mechanism of action of Imiquimod
Activate toll like receptor 7 (TLR7), which activates innate immune system
Mechanism of action of 5-fluorouracil
Thymidylate synthesis inhibitor.
Blocks production of dTMP damaging and preventing DNA replication
What is melanoma?
Malignant tumor of melanocytes, commonly occurring on the skin, but also in other melanocyte-containing sites like eyes (uveal melanoma) or mucosal surfaces.
Types of melanoma?
Superficial Spreading (70% of cases): Common on sun-exposed skin. Irregular borders, color variation.
Nodular (15-20%):
Aggressive, vertical growth phase dominates. Dark, raised lesion.
Lentigo Maligna Melanoma (5-10%):
Found in older individuals with chronic sun damage. Slowly progressive; starts as lentigo maligna (in situ).
Acral Lentiginous Melanoma (<5%): palms, soles, or under nails. More common in darker-skinned individuals.
Desmoplastic Melanoma: Rare
What will you look for in the histology report for melanoma?
Breslow thickness
Differentiation
Subtype
Ulceration
Lymphovascular invasion
Mitotic Rate
What factors affect tumour staging (TNM) for melanoma?
Breslow thickness
Ulceration
Lymphovascular invasion
Mitotic index of 2 or more
Melanoma: T1a
Breslow Thickness: <0.8mm
No Ulceration/Lymphovascular Invasion/
Mitotic rate <2
Melanoma: T1b
Breslow Thickness: <0.8mm
Ulceration/Lymphovascular Invasion/ Mitotic rate>2
or
Breslow Thickness: 0.8-1mm
Melanoma: T2a
Breslow Thickness: 1-2mm
No Ulceration/Lymphovascular Invasion/
Mitotic rate <2
Melanoma: T2b
Breslow Thickness: 1-2mm
Ulceration/Lymphovascular Invasion/ Mitotic rate >2
Melanoma: T3a
Breslow Thickness: 2-4mm
No Ulceration/Lymphovascular Invasion
Mitotic rate <2
Melanoma: T3b
Breslow Thickness: 2-4mm
Ulceration/Lymphovascular Invasion/ Mitotic rate>2
Melanoma: T4a
Breslow Thickness: >4mm
No Ulceration/Lymphovascular Invasion
Mitotic rate <2
Melanoma: T4b
Breslow Thickness: >4mm
Ulceration/Lymphovascular Invasion/ Mitotic rate>2
Excision margins for T1 MM
1cm
Excision margins for T2 MM
2cm
Excision margins for T3/T4 MM
> 2cm
What is the next step in management for stages IB - IIB MM
WLE +/- SNLB
What is the next step in management of IIB - IV MM
CT Scan
What is the next step in management if SLNB is positive in MM
Lymph node dissection +/- Adjuvant SACT
Differential Diagnosis for MM
Cherry angioma.
Angiokeratoma.
Dermatofibroma.
Freckles (ephelides).
Kaposi’s Sarcoma.
Lentigo.
Junctional naevus.
Compound Naevus.
Halo naevus.
Blue naevus.
Spitz naevus. E
Pigmented BCC.
Pyogenic granuloma.
Seborrhoeic keratosis.
Cherry Angioma
Benign vascular lesions caused by proliferating endothelial cells. Small firm, papular angioma. Red, purple or blue inn colour. 1-10mm in diameter.
Kaposi’s Sarcoma.
Malignant growth of blood vessels. Most commonly associated with HIV. Reddish/purplish macules which develop into modules or plaques. Usually, multiple lesions which may ulcerate or bleed.
Angiokeratoma
Asymptomatic hyperkeratotic vascular skin lesion. Small (rarely >5mm) dark red to purple papules, nodules or plaques. Lesions are prone to thrombosis results in sudden colour change.
Lentigo
Flat pigmented, well defined benign lesion. Doesn’t fade in winter. Types: Lentigo simplex, Solar lentigo, ink spot, lentigo, PUVA lentigo, mucosal. Can be associated with syndromes: Noonan with multiple lentigines (formerly LEOPARD), Peutz-Jeghers.
Dermatofibroma
Benign fibrous nodule usually found in lower legs. Tethered to the surface, mobilse over subcutaneous tissue. Usually 5-15mm in diameter. Pink to light brown on white skin.
Junctional naevus.
Groups or nests of naevus calls at the junction of epidermis and dermis. Flat, well defined, pigmented lesion.
Compound Naevus
Nests of naevus cells at the epidermal-dermal junction as well as within the dermis. Raised central area surrounded by a flat patch.
Freckles (ephelides)
Light to dark macules. More prominent in summer and fade in winter
Halo naevus.
Naevus surrounded by a white patch and fade away after several years. Consider to be autoimmune process against melanoctyes.
Blue naevus
Blue because of Tyndall effect in which shorter wavelengths of light are scattered by dermal melanocytes. Blue because deeper into tissues.
Pyogenic granuloma
Acquired benign proliferation of capillary blood vessels of skin, which can develop in response to trauma, hormone changes, medication, infection. Painless, red, fleshy nodule, Typically 5-10mm that grows rapidly over a few weeks. Fingers and face most common sites. Smooth surface that is fragile and crust, ulcerate or bleed.
Spitz naevus.
Epithelioid cell naevus. Pink (classic Spitz) or pigmented dome shaped mole that arises in children and young adults.
Seborrhoeic keratosis
Caused by proliferation of epidermal keratinocytes. Raised plaques with “stuck on” appearance
