Skin cancer basics Flashcards

1
Q

What is melanoma

A

Malignant tumour arising from melanocytes

most common sc death

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2
Q

Where can melanoma arise besides regular skin

A

Can arise on mucosal surfaces (e.g. oral, conjunctival, vaginal) and within uveal tract of eye

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3
Q

genetic risk factors for skin cancer

A

Family history (CNKN2A mutations), MC1R variants
Lightly pigmented skin
Red hair
DNA repair defects (e.g. xeroderma pigmentosum)

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4
Q

environmental risk factors for melanoma

A
Intense intermittent sun exposure
Chronic sun exposure
Residence in equatorial latitudes
Sunbeds
Immunosuppression
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5
Q

phenotypic risk factors for melanoma

A

> 100 Melanocytic nevi

Atypical melanocytic nevi

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6
Q

What does BRAF substitution result in

A

BRAF mutations substitution leads to activation of mitogen-activated protein kinase (MAPK) pathway
melanoma

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7
Q

host response to melanoma

A

CD8+ T-cell recognise melanoma-specific antigens and if activated appropriately, are able to kill tumour cells.

CD4+ helper T-cells and antibodies also play a critical role

Cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) is natural inhibitor of T-cell activation by removing the costimulatory signal (B7 on APC to CD28 on T-Cel

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8
Q

immunotherapy for melanoma based on

A

CTLA-4 blockade – ipilimumab

- Also checkpoint inhibitors (PD-1, PDL1)

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9
Q

subtypes of melanoma

A
Superficial spreading
Nodular
Lentigo maligna
Acral lentiginous
Unclassifiable
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10
Q

features of superficial spreading melanoma

A

Most frequently seen on trunk of men and legs of women
regression (visible as grey, hypo-or depigmentation), due to reaction of host immune system with tumour
After a slow horizontal (radial) growth phase, limited to epidermis, a more rapid vertically oriented growth phase, which presents clinically with development of nodule

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11
Q

nodular melanoma epidemiology

A

2nd most common type of melanoma in fair skinned individuals
Most commonly trunk, head and neck
M>F

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12
Q

presentation of nodular melanoma

A

Usually present as blue to black, but sometimes pink to red, nodule – may be ulcerated, bleeding
Develops rapidly
Nodular melanoma is believed to arise as a de novo vertical growth phase without the pre-existing horizontal growth phase
Tend to present more advanced stage, with poorer prognosis.

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13
Q

lentigo maligna epidem

A

Occurs in chronically sun-damaged skin, most commonly on the face
>60 years old
rarer

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14
Q

presentation of lentigo maligna

A

Slow growing, asymmetric brown to black macule with colour variation and an irregular indented border
sun exposed areas e.g neck

Invasive Lentigo Maligna Melanoma arises in a precursor lesion termed lentigo maligna (in situ melanoma) in sun damaged skin).

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15
Q

epi acral lentiginous

A

Typically occurs on palms and soles or in and around the nail apparatus
Incidence similar across all racial and ethnic groups

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16
Q

why BAME groups get acral lentiginous melanomas?

A

As more darkly pigmented Africans and Asians do not typically develop sun-related melanomas, ALM represents disproportionate percentage of melanomas diagnosed in Afro- Caribbean (up to 70%) or Asians (up to 45%)

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17
Q

public awareness of early detection of skin cancer

A
ABCDE
Asymmetry
Border irregularity
Colour variegation
Diameter greater than 5mm
Evolving
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18
Q

poor prognosis indicators (melanoma)

A
Increased Breslow thickness >1mm
Ulceration
Age
Male gender
Anatomical site – trunk, nhead, neck
Lymph node involvement
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19
Q

how to measure breslow thickness

A

From granular layer to bottom of tumor

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20
Q

what is dermoscopy

A

Investigation that can improve correct diagnosis of melanoma by nearly 50%

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21
Q

main features of general melanoma

A

Asymmetry
Presence of multiple colours
Reticular, globular, reticular-globular, homogenous
Starburst

22
Q

removal of melanomas

A

primary excision - 2mm peripheral margin

wide excision - margin determined by breslow depth - 5mm in situ, 10mm for 1mm invasion

23
Q

staging of melanomas

A

thickness
ulceration
TNM

24
Q

unresecrtable melanoma management or metastatic

A

Immunotherapy

Mutated oncogene targeted therapy

25
mutated oncogene melanoma therapy
BRAF inhibitor and MEK inhibitor
26
keratinocyte dysplasia epi
Predominantly pale skin types | Solar induced UV damage
27
types of skin carcinoma
Actinic keratoses - Dysplastic keratinocytes Bowen’s disease (Squamous cell carcinoma in situ) Squamous cell carcinoma - Potential for metastasis/death Basal cell carcinoma (more common) - rarely metastasises - Locally invasive
28
BCC pathogenesis
stroma produced by dermal fibroblasts crosstalk between tumour cells and mesenchymal stroma cells proteolytic activity (invasion) via metalloproteinases and collagenases
29
UV radiation role in SCC
Develops through addition of genetic alterations – alterations in p53 are most common
30
risk factors of all keratinotye carcinomas (SCC,BCC etc)
``` Genetic syndromes Xeroderma pigmentosum Oculocutaneous albinism Muir Torre syndrome Organ transplantation (immunosuppressive drugs) Chronic non-healing wounds Ionising radiation + Occupational chemical exposures Airline pilots ```
31
what is actinic keratoses
Atypical keratinocytes confined to epidermis Erythematous macule or scale or both-> thick papules or hyperkeratosis or both Develop on sun-damaged skin - usually head, neck, upper trunk and extremities
32
what is bowens disease
Squamous cell carcinoma in situ Erythematous scaly patch or slightly elevated plaque may arise from existing actinic keratinosis can resemble AK, psoriasis, chronic eczema
33
treatment of AK and bowens
5-fluorouracil cream Cryotherapy Imiquimod cream Photodynamic therapy Curettage and cautery Excision
34
SCC presentation
Arises within background of sun-damaged skin - Erythematous to skin coloured - Papule - Plaque-like - Exophytic - Hyperkeratotic - ulcerated
35
red flags of SCC
``` rapid growth immunosuppressed patient inflammation poorly differentiated invasion beyond subcut fat ```
36
what is keratocanthoma
sharply circumscribed, crateriform nodule with keratotic core Most occur on head or neck / sun exposed areas hard to distinguish from SCC
37
diagnosis of SCC
clinical sufficient | biposy maybe, ultrasound of lymph nodes if concerned
38
treatment SCC
Examination of rest of skin and regional lymph nodes Excision Radiotherapy - Unresectable - High risk features e.g. perineural invasion Cemiplimab for metastatic SCC
39
types of basal cell carcinoma
``` Nodular Superficial Morpheic Infiltrative Basisquamous Micronodular ```
40
most common type of BCC
Nodular | Accounts for approximately 50% of all Basal cell carcinomas
41
how does BCC often present
Typically presents as shiny, pearly papule or nodule | or superficial BCC - Well-circumscribed, erythematous, macule / patch or thin papule /plaque
42
diagnosis of BCC
clinical sufficient | biopsy maybe
43
BCC treatment
Standard surgical excision Mohs micrographic surgery Other options
44
when to use Mohs micrographic surgery
recurrent BCC aggressive subtype - morpheic, micronodular criticla sites
45
cutaneous t cell lymphoma subtypes
Sézary syndrome and mycosis fungoides
46
mycosis fungoides diagnosis
Diagnosis requires skin biopsy Diagnosis may take years as skin lesions may be present that are neither clinically nor histologically diagnostic for many years Atypical T-cell infiltrates may also be found in lymphomatoid drug eruptions Patches or plaques
47
mycosis fungoides treatment
topical corticosteroids, radiotherapy phototherapy
48
what is sezary syndrome
Triad of: Erythroderma Generalised lymphadenopathy Presence of neoplastic T-cells (Sézary cells) in the skin, lymph nodes and peripheral blood
49
sezary syndrome treatment
Systemic treatment is required Extracorporeal photophoresis Skin-directed therapies like PUVA or potent topical corticosteroids may be used as adjuvant therapy
50
main features of merkel cell carcinoma
Solitary, rapidly growing nodule- pink-red to violaceous, firm, dome shaped, - Ulceration can occur
51
merkel cell carcinoma treatment
Treated with surgery, radiation therapy | anti-PD1 (Pembrolizumab) / anti-PDL1 (Avelumab)