Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
102 Cards in this Set
- Front
- Back
|
Where do basal cell carcinomas arise? |
The keratinocytes within the basal layer |
|
|
What changes should be considered when melanoma is suspected? |
Asymmetry Border Colour Diameter Evolution |
|
|
What is the ugly ducking sign? |
This is the observation that naevi in the same individual tend to resemble each other and with MM, this is abnormal compared to the others. |
|
|
What are the non-melanoma skin cancers? |
This is basal and squamous cell carcinoma and these are the most common representing about 95% of cases |
|
|
What are the clinical manifestations of BCC? |
Slow growing lump or ulcer which does not heal that is often painless. It is translucent with visible ulceration "rodent ulcer" |
|
|
What does superficial BCC present as? |
Scaly plaque |
|
|
Does BCC metastases? |
Very rarely however it is locally invasive |
|
|
When does BCC commonly present? |
Around 40 years of age usually |
|
|
Is it possible for BCC to be pigmented? |
Yes |
|
|
What are the clinical manifestations of SCC? |
Hyperkeratotic lump or ulcer which arises on sun-damaged skin and grows relatively fast and can be painful and bleed. |
|
|
If SCC is well differentiated, how does this affect the prognosis? |
Tends to be low risk SCC |
|
|
What is a concerning feature of SCC? |
High risk of metastases |
|
|
What pre-cursors are associated with SCC? |
Actinic keratoses and Bowen's disease |
|
|
What are actinic keratosis? |
These are pre-cancerous lesions which form due to chronic sun-exposure and are associated with high risk of the development of BCC or SCC. |
|
|
What is the appearance of Bowen's disease |
Erythematous plaque |
|
|
What feature is seen with keratoacathoma? |
Central crater |
|
|
What are the high risk sites for SCC? |
Scalp, ears and lips |
|
|
What are some of the risk factors of skin cancer? |
Genetic predisposition Immunosuppression Environmental carcinogens- smoking, radiation |
|
|
What damage does UVB cause? |
Sunburn and solar lentigo |
|
|
What damage does UVA cause? |
Solar elastosis |
|
|
What is the role of sunburn? |
Protective role whereby badly damage UV keratinocytes undergo apoptosis |
|
|
What is solar lentigo? |
Freckles which form in individuals that cannot tan to protect their skin from the sun |
|
|
What dictates your skin type? |
1- always burns, never tans 2- usually burns, can tan 3- can burn but usually tans 4- always tans, never burns 5- brown skin 5- black skin |
|
|
What is the sun-exposure pattern of SCC? |
Intermittent intense sunburn episodes |
|
|
What is the sun-exposure pattern of BCC? |
Chronic cumulative UV exposure |
|
|
What is the sun-exposure pattern of melanoma? |
Intermittent intense sunburn episodes |
|
|
What is xeroderma pigmentosum? |
This is a genetic skin disorder where there is a defect in one of the 7 nucleotides excision repair (NER) genes. |
|
|
What are the risks associated with xeroderma pigmentosum? |
This causes photosensitivity- skin cancer on UV exposed areas- median average onset of skin cancer is 8 Neurological degeneration Increased risk of other cancers |
|
|
What is the most common type of melanoma associated with xeroderma pigmentosum? |
Lentigo maligna melanoma |
|
|
What is Gorlin's syndrome? |
This is an autosomal dominant familial cancer syndrome. |
|
|
What are the major features associated with Gorlin's syndrome? |
-Early onset - Palmar pits - Ecoptic calcification falx - Jaw cysts |
|
|
What are the minor factors associated with Gorlin's syndrome? |
-Skeletal abnormalities - Ovarian/cardiac fibroma - Medulloblastoma |
|
|
Name 5 photo toxic drugs? |
Thiazide diureitcs, anti-TNF, NSAIDs, BRAF inhibitors and voriconazole (anti-fungal) |
|
|
Name 3 types of epidermal tumours? |
- Seborrhoeic keratosis (benign) - Bowen's disease, actinic keratosis and viral lesions - BCC and SCC |
|
|
What is seborrhoeic keratosis? |
Very common in ageing skin which forms due to the benign proliferation of epidermal keratinocytes which is common on the face and trunk |
|
|
What histological features would be seen with seborrhoeic keratosis? |
Epidermal acanthosis, hyperkeratosis and horn cysts. |
|
|
What is the appearance of seborrhoeic keratosis? |
Greasy hyperkeratotic surface |
|
|
What is Leser-Trelat sign? |
This is the sudden eruption of many lesions which indicates internal malignancy |
|
|
What are the 3 types of basal cell carcinoma? |
Superfical Nodular Infiltrative |
|
|
What are the histological features seen with BCC? |
Numerous apoptosis and mitosis Peripheral palisading |
|
|
What is peripheral palisading? |
This is the appearance of the nuclei lining up with a similar appearance to a fence around the tumour. |
|
|
Which type of BCC is the most significant? |
Infiltrative as this may spread along nerves |
|
|
What histological features would be seen with infiltrative BCC? |
Poorly defined margin with a prominent desmoplastic fibrous stroma (looks like pods) |
|
|
Where is Bowen's disease most commonly found? |
The legs |
|
|
Where is actinic keratosis most commonly found? |
The head/scalp |
|
|
Where are viral lesions most commonly found? |
Anogenital skin |
|
|
What is the appearance of Bowen's disease? |
Irregular border which gives the appearance of a scaly patch |
|
|
What is seen on histological slides with actinic keratosis ? |
Squamous dysplasia |
|
|
What is erythroplasia of Queryat? |
This is Bowen's disease affecting the glans of the penis |
|
|
What causes erythroplasia of Queryta? |
HPV 16 and nearly always results in penile dysplasia |
|
|
What histological feature is seen with Bowenoid dysplasia of the glans? |
Atypical elevated mitoses |
|
|
What is a dermofibroma? |
Common benign skin tumours which are attributed to a reactive reaction to trauma e.g. an insect bite |
|
|
What is the appearance of a dermofibroma? |
Single nodules that develop on the extremities, most commonly the lower legs which are free moving and firm |
|
|
Where are melanocytes derived from? |
The neural crest |
|
|
Where do melanoblasts migrate to from the neural crest? |
Skin Uveal tract- pigmented middle of the 3 concentric layers of the eye Leptomeninges- layers covering the brain and the spinal cord |
|
|
When do melanoblasts become melanocytes? |
When they settle in the skin |
|
|
What does the MC1R mean? |
This is the melanocortin 1 receptor gene which encodes for the MC1R protein which sits on the cell surface. |
|
|
What is the function of the MC1R gene? |
This determines the balance of pigment in the skin and the hair |
|
|
What causes red hair? |
Phaeomelanin |
|
|
What is the function of MC1R gene? |
This converts phaeomelanin into eumelanin (which gives a hair colour other than red) |
|
|
What does one defective copy of MC1R mean? |
This will result in the individual having freckles |
|
|
What does two defective copies of the MC1R gene mean? |
This will result in the individual having red hair and freckles |
|
|
What is the other name given to freckles? |
Ephilides |
|
|
When do freckles occur and what this their role? |
Occurs after UV exposure which reflects the clumpy distribution of melanocytes |
|
|
What is actinic lentigines? |
These are known as age or liver spots and are related to UV exposure and are formed due to the increased of melanin and basal melanocytes |
|
|
What are melanocytic naevi? |
Moles |
|
|
What are congenital melanocytic naevi? |
Theses are congenital moles Small <2cm in diameter Medium >2cm but less than 20cm Large> 20cm which are associated with a 20% risk of melanoma |
|
|
Are melanocytic naevi congenital or acquired? |
Both |
|
|
What happens to the number of melanocytes during infancy |
The keratinocyte: melanocyte ratio breaks at a normal of cutaneous sites |
|
|
What is clinical significant about the naevi and immunosuppressed children? |
They appear to have more than the normal child leading many to believe that naevus induction is immune regulated |
|
|
What are the 3 stages of naevus development? |
Junctional Compound Intradermal |
|
|
What are junctional naevus and when do these appear? |
Melanocytes proliferate forming a cluster of cells at the dermo-epidermal junction. This stage occurs in childhood. |
|
|
What are compound naevus? |
These are junctional clusters and groups of cells in the dermis and this occurs in adolescence and early adulthood. |
|
|
What are intradermal naevus? |
All junctional activity has ceased and the melanocytic clusters are all dermal and this occurs in adulthood. |
|
|
What are dysplastic naevi? |
Generally greater than 6mm with an asymmetrical border and variable pigment |
|
|
What are the 2 types of dysplastic naevi? |
Sporadic and familial |
|
|
What is sporadic dysplastic naevi? |
Not inherited with one or several dysplastic naevi present with a slight increase in the risk of melanoma |
|
|
What is familial dysplastic naevi? |
There is a strong familial history of melanoma Autosomal dominant Will develop melanoma |
|
|
What is the appearance of dysplastic naevi? |
They are architecturally and cellularly abnormal |
|
|
How do dysplastic naevi look different from melanoma? |
In dysplastic naevi, the epidermis is not affected |
|
|
What are halo naevi? |
Peripheral halo of depigmentation which show inflammatory regression and overrun by lymphocytes |
|
|
What are blue naevi? |
Entirely dermal and consist of pigment rich dendritic spindle cells |
|
|
What is Spitz naevus? |
Uncommon type of mole which usually appears face, limbs and chest which may mimic melanoma and are benign |
|
|
What is the appearance of Spitz-naevi? |
Dome-shaped red, reddish-brown which may be 1cm or 2cm in diameter which grow rapidly over a few weeks to months |
|
|
What causes the pink colourisation of Spitz-naevi? |
Prominent vascular |
|
|
What histological feature is seen with Spitz-naevi? |
Epidermal hyperplasia |
|
|
When should you suspect melanoma? |
Change in shape Irregular pigmentation Bleeding Development of satellite nodules Ulceration New pigmented lesions which develop in adulthood |
|
|
What are the 4 types of malignant melanomas? |
1. Superficial spreading- commonest in the trunk and limbs 2. Acral lentiginous- acral and mucosa 3. Lentigo maligna- sun damaged areas e.g. neck, face and scalp 4. Nodular- varied but often found on the trunk |
|
|
What is the radial growth phase |
Grow as macules either in situ or with dermal microinvasion |
|
|
What is the vertical growth phase? |
When the melanoma cells invades the dermis |
|
|
What is nodular melanoma? |
This melanoma displays no clinical or microscopic evidence of the rapid growth phase and only VGP. |
|
|
What lesions have RGP and VGP |
Superficial spreading melanoma Acral or mucral lentigenous melanoma- acral or mucosal Lentigo maligna melanoma |
|
|
What lesions only display VGP? |
Nodular melanoma |
|
|
What is the Breslow measurement? |
The depth of the tumour measured from the granular layer in mm as well as the extent of ulceration. |
|
|
What is the classification? |
pT1 tumour <1mm- 90% survival pT2 tumour 1-2mm- 80% survival pT3 tumour 2-4mm- 55% survival pT4 tumour >4mm- 20% survival |
|
|
What if ulceration is present? |
Then the suffix b is added to the report e.g T3b |
|
|
How does malignant melanoma spread? |
Local dermal lympathics- satellite deposits of MM Regional lymph node metastases Blood spread to other organs |
|
|
What is the management of melanoma? |
Primary excision to confirmation of diagnosis and assessment of Breslow Sentinel node biopsy may be required- if positive- regional lymphadenectomy |
|
|
What if the melanoma is in situ only? |
Then clear by 5mm |
|
|
What if the melanoma is invasive but <1mm thick |
1cm clearance |
|
|
What is the BRAF gene? |
BRAF is a weak cytoplasmic protoncogene
|
|
|
What happens if there is a mutation in BRAF gene? |
It drives cell proliferation by upreguating MEK and ERK leading to uncontrolled cell growth |
