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BRS Year 2 > Skin cancer basics > Flashcards

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
Q

mutated oncogene melanoma therapy

A

BRAF inhibitor and MEK inhibitor

26
Q

keratinocyte dysplasia epi

A

Predominantly pale skin types

Solar induced UV damage

27
Q

types of skin carcinoma

A

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
Q

BCC pathogenesis

A

stroma produced by dermal fibroblasts
crosstalk between tumour cells and mesenchymal stroma cells
proteolytic activity (invasion) via metalloproteinases and collagenases

29
Q

UV radiation role in SCC

A

Develops through addition of genetic alterations – alterations in p53 are most common

30
Q

risk factors of all keratinotye carcinomas (SCC,BCC etc)

A 
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
Q

what is actinic keratoses

A

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
Q

what is bowens disease

A

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
Q

treatment of AK and bowens

A

5-fluorouracil cream
Cryotherapy

Imiquimod cream
Photodynamic therapy
Curettage and cautery
Excision

34
Q

SCC presentation

A

Arises within background of sun-damaged skin

  • Erythematous to skin coloured
  • Papule
  • Plaque-like
  • Exophytic
  • Hyperkeratotic
  • ulcerated
35
Q

red flags of SCC

A 
rapid growth
immunosuppressed patient
inflammation
poorly differentiated
invasion beyond subcut fat
36
Q

what is keratocanthoma

A

sharply circumscribed, crateriform nodule with keratotic core
Most occur on head or neck / sun exposed areas
hard to distinguish from SCC

37
Q

diagnosis of SCC

A

clinical sufficient

biposy maybe, ultrasound of lymph nodes if concerned

38
Q

treatment SCC

A

Examination of rest of skin and regional lymph nodes
Excision
Radiotherapy
- Unresectable
- High risk features e.g. perineural invasion
Cemiplimab for metastatic SCC

39
Q

types of basal cell carcinoma

A 
Nodular
Superficial
Morpheic
Infiltrative
Basisquamous
Micronodular
40
Q

most common type of BCC

A

Nodular

Accounts for approximately 50% of all Basal cell carcinomas

41
Q

how does BCC often present

A

Typically presents as shiny, pearly papule or nodule

or superficial BCC - Well-circumscribed, erythematous, macule / patch or thin papule /plaque

42
Q

diagnosis of BCC

A

clinical sufficient

biopsy maybe

43
Q

BCC treatment

A

Standard surgical excision

Mohs micrographic surgery

Other options

44
Q

when to use Mohs micrographic surgery

A

recurrent BCC
aggressive subtype - morpheic, micronodular
criticla sites

45
Q

cutaneous t cell lymphoma subtypes

A

Sézary syndrome and mycosis fungoides

46
Q

mycosis fungoides diagnosis

A

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
Q

mycosis fungoides treatment

A

topical corticosteroids,
radiotherapy
phototherapy

48
Q

what is sezary syndrome

A

Triad of:
Erythroderma
Generalised lymphadenopathy
Presence of neoplastic T-cells (Sézary cells) in the skin, lymph nodes and peripheral blood

49
Q

sezary syndrome treatment

A

Systemic treatment is required
Extracorporeal photophoresis
Skin-directed therapies like PUVA or potent topical corticosteroids may be used as adjuvant therapy

50
Q

main features of merkel cell carcinoma

A

Solitary, rapidly growing nodule- pink-red to violaceous, firm, dome shaped,
- Ulceration can occur

51
Q

merkel cell carcinoma treatment

A

Treated with surgery, radiation therapy

anti-PD1 (Pembrolizumab) / anti-PDL1 (Avelumab)

BRS Year 2 (67 decks)

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