6- Dermatology (skin cancer) Flashcards
(37 cards)
BCC RF
Risk factors
- Caucasian (type I and II)- fair
- Sun exposure (UV)/ sun burn
- Older age
- Previous skin cancer
- Immunosuppression
- Albinism
- Inherited syndrome e.g. Gorlin syndrome
BCC presentation
- Slow growing plaques or nodules
- Early lesions are small, translucent or pearly and have raised areas with telangiectasia
- Varies in size
- Spontaneous bleeding
- Occurs in sun exposed sites apart from the ear
- Indurated edge and ulcerated centre
- Slow growing but can spread deeply to cause considerable destruction
investigations for BCC
- Visual inspection
- Punch biopsy if treatment other than standard surgical excision is planned
BCC management
Depends on size, type and location.
- Can be managed in primary care as long as GP trained to perform skin surgery
Surgical excision is the mainstay of treatment
1) Normal surgical excision of cancer
2) Mohs micrographic surgery (4mm margins) Best treatment: gold standard but not used that often
–> Involves examining carefully marked excised tissue under microscope later by layer to ensure complete excision
->Very high cure rates
Non-surgical
e.g. superficial BBC or if they decline or unfit for surgery
- Curettage and cautery
- Cryotherapy (liquid nitrogen)
- Imiquimod cream
- 5-Fluorouracil
- Radiotherapy if margins incomplete
management of advanced or metastatic BCC
- Surgery
- Radiotherapy
- Target therapy
Prevention of BCC
- Avoid sunburn esp in fair skinned
- Oral nicotinamide (vitamin B3)
Prognosis for BCCs
- Most BCCs cured by treatment
- 50% develop second one within 3 years of first
o At increased risk of melanoma - Advanced BCC very rare- often neglected tumours
- Metastaic BCC very rare
squamous cell carcinoma
Squamous cell carcinoma
Background
- Malignant tumour arising from keratinising cells of the epidermis
- Locally invasive (passes basement membrane) and has the potential to metastasise
- Types e.g.
o Cutaneous horn
o Keratoacanthoma
SCC causes
- Older patients
- Previous skin cancer
- Smoking
- Inherited syndromes e.g. xeroderma pigmentosum
- Related to sun exposure (UVR)
- Fair skin
- Chemical carcinogens- arsenic
- HPV
- Chronic inflammation
- May arise in pre-existing solar keratoses
- Immunosuppression after transplant
SCC presentation
- Grow quickly over weeks to months (much faster than BBC)
- Indurated nodular keratinising or crusted tumour that may ulcerate without evidence of keratinisation
- Non healing ulcer or growth in one of the highest risk sun exposed area
- Centre becomes necrotic and becomes an ulcer
- Ulcer with hard, raised edges
- Bleeding
- Size varies from a few mm to several CM
Investigations for SCC
- Visual inspection
- Biopsy for histology
- If high risk: imaging using US, Xray, CT, MRI, lymph node biopsy
Classification of SCC
Based on low-risk or high-risk, depending on the chance of the tumour recurrening or metastasing
High-risk SCC
- Diameter greater than or equal to 2 cm
- Location on the ear, vermilion of the lip, central face, hands, feet, genitalia
- Arising in elderly or immune suppressed patient
- Histological thickness greater than 2 mm, poorly differentiated histology, or with the invasion of the subcutaneous tissue, nerves and blood vessels.
SCC staging
Staging: TNM
management of SCC
1) Nearly always treated surgically
- Wide local excision – repeat surgery to gain adequate margins may eb required
- Mohs’ micrographic surgery- precise technique in which excision of skin lesion is carried out in stages and checked histologically
Other non-surgical procedures
- Curettage and cautery
- Crytotherapy
- Imiquimod cream
- Photodynamic therapy (PDT)
- Electrochemotherapy
- Radiotherapy
Prevention of SCC
- Avoid sunburn esp in fair skinned
- Oral nicotinamide (vitamin B3)
- Patients with multiple SCC may be prescribed oral retinoid (acitretin or isotretinoin)
- Self examination important
Prognosis
of SCC
- Most SCCs cured by treatment
- 50% develop a second within 5 years
- Increased risk of melanomas
melanoma
- In situ- tumour confined to epidermis
- Invasive- tumour spread into dermis
- Metastatic- tumour spread to other tissues
pathophysiology of melanoma
Pathophysiology
- Melanocytes are found in equal numbers in black and in white skin; however, the melanocytes in black skin produce much more melanin. People with dark brown or black skin are very much less likely to be damaged by ultraviolet (UV) radiation than those with white skin.
- Non-cancerous growth of melanocytes results in moles (benign melanocytic naevi) and freckles (ephelides and lentigines).
- Most skin melanomas spread out within the epidermis. If all the melanoma cells are confined to the epidermis then the lesion is a melanoma in situ, which can be cured by excision because it has no potential to spread around the body.
- When the cancer has grown through the dermis it is known as invasive melanoma malignant melanoma
metastasis sites for melanoma
Metastasis everywhere
- Lymph nodes
- Lungs
- Liver
- Bone
- brain
Risk factors of melanoma
- Previous primary invasive melanoma
- Fair – highest incidence in Australia and new Zealand
- Increasing age
- Many melanocytic naevi – moles
- Sun exposure
- Family history
- Immunosuppressed
Presentation of melanoma
- Can occur anywhere on the body e.g. the back or legs
- Usually start as skin lesions- can also grow on mucus membranes e.g. lips or genitals
- Bleeding
- > 6mm
- Key features- ABCDE
ABCDE of melanoma
- Asymmetry.
- Border irregular.
- Colour irregular.
o Tan, dark borwn, black, blue, red - Diameter greater than 7 mm.
- Evolving.
investigations for melanoma
- Visual inspection
- Dermatoscopy
- Removal for histology
- Imaging to look for metastasis e.g. PET CT
