Management of Skin Cancer Flashcards
Can also occur in internal organs due to abnormal migration of melanocytes from the neural crest during embryogenesis.
Wild type=normal variant ie it isn’t mutated so wouldn’t cause activation of this pathway.
MM=malignant melanoma (there is no such thing as benign melanoma though!)
Apart from E for evolving the ABCDE rule is not helpful for nodular melanoma as it doesn’t tend to have the ABCD changes.
In melanoma have amelanotic type ie non-pigmented type and also BCC can be pigmented, so they can look similar
The black swan rule is not a thing in diagnosing melanoma, but there is the ugly duckling sign, which is where you are looking for the mole that doesn’t look for the others, to help with diagnosis.
C=BRAF if you have a BRAF mutated melanoma, that is associated with worst prognosis. This can inform treatment decision as if it is positive for BRAF you can use BRAF inhibitor as a treatment.
If just take punch through lesion wont be able to analyse whole architecture of lesion so may miss out important features and have a misrepresentation of severity, so generally you have to exicse it, unless large malignant melanoma where can just biopsy darkest part.
Only offer sentinel lymph node biopsy for PT1b+ melanomas ie 0.8mm+ or ulcerated melanoma.
LDH is helpful in metastatic melanoma when used as a prognostic indicator.
AK-can evolve into SCC but the majority don’t.
BCC, not as likely as SCC to metastasise, hardly ever metastasises.
BCC is 4x as common as SCC (think B before S in alphabet)
BCC almost never metastasises, but is highly destructive to local structures eg salivary glands, ocular glands, can even go into bone etc. So they should be treated. Exception: if person has a short life expectancy, but generally treatment is required.
A=true, shown on top right
B=bottom right-shown as scar
Vismodegib is a sonic hedgehog patched pathway inhibitor
BCC-if see and confident with clinical and dermoscopic signs, you can proceed to excision. If any doubt eg there will be a large defect or you want to consider subtype to see if indication for Mohs micrographic surgery then you may choose to biopsy
Topical only suitable for superficial BCC but not for others
Mohs micrographic surgery-few people trained to perform this and very time consuming and expensive and whole point is to ensure complete excision margins, so generally we would take safety margin. Mohs is only used for areas around eyes or nose or for aggressive subtypes which spreads around quickly or for recurrent BCC.
SCC and keratocanthoma can be difficult even histiologically to tell apart. Typically k ressolve over weeks or months after reaching their full size. Genetic studies say they are different.
SCC-can represent AK, warts or ulcers so A is incorrect
C is incorrect, Cemplimab is a PD1 checkpoint inhibitor
C=can be itchy, sometimes it isn’t, when is, it usually isn’t very itchy
Rapid progression is not typical at all. Called indolent as it is slow and lazy, takes years to develop
B is incorrect, clinical features and histological features can be very non specific, takes about 5-6 years from onset to get diagnosis because there aren’t the features to confirm the diagnosis yet.
D-we know p53 and CDKN2a are involved but they seemed to be secondary events, we only have theories for the primary event of pathogenesis.
A=vascular sarcoma so appearnace depends on level of skin it is, ie dark violet if superficial, nodule if pushing through skin, pink if deep in skin.
Can have other forms of immunosuppression that cause it eg transplant drugs, not just HIV, or normal immune people can have it-this is the endemic form.
HHV8 is involved in this!
It name is msileading as we don’t think it believes from merkel cells, it was named as it has structural and immunohistochemical (ie proteins on surface) are similar
Polyomavirus and UV light play a role in development
40% develop metastases so is more severe
D-radiation is not an option, can be alternative to surgery in the elderly in BCC, or post excision as adjuvant in SCC
Radiotherapy can actually cause SCC, can arise in radiotherapy sites, so no point using in something which has a low chance of becoming malignant anyway, when have so many other options with lower risk.
Perineural invasion if present is bad.
All the others are high risk features
SCC are not all equal, some are low risk and less likely to metastasise but some are much more risky.
Mycosis fungoides-early when patches or sightly raised patches, we tend to treat gently ie with topical steroids or phototherapy or radiation (these are for symptomatic reasons), but then we use aggressive treatment in later stage eg brentuximab vedotin (anti CD30). There is no shown increased survival advantage in treating aggressively early.
Sezary syndrome should always get systemic chemo, despite being primary skin involvement. Extracorporesis phototherapy also used (blood out and light shine etc)
