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Year 2 Derm > Skin Cancers > Flashcards

Skin Cancers Flashcards

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Dermatology Board Prep flashcards
1
Q

What is melanoma?

A

Malignant tumour arising from melanocytes
Leads to >75% of skin cancer deaths
Rising incidence rates observed worldwide

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2
Q

Where can melanoma arise?

A

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

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3
Q

What are the 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

What are the 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

What are the phenotypic risk factors for melanoma?

A

> 100 Melanocytic nevi

Atypical melanocytic nevi

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6
Q

What is the molecular pathogenesis for melanoma?

A

MAPK (RAS-RAF-MEK-ERK) pathway regulates cellular proliferation, growth and migration

KIT mutations - 30-40% of acral and mucosal melanomas

melanomas from chronically sun-exposed skin harbour activating mutations or copy number amplifications of KIT gene

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7
Q

What are some genes that link to melanoma?

A
  • NRAS gene (15-20% of melanomas)

- BRAF gene (50-60%) – high in melanomas of skin with intermittent UV exposure

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8
Q

What does BRAF substitution result in?

A

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

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9
Q

What other gene can cause MAPK pathway dysfunction?

A

Inherited CDKN2A mutations also cause MAPK pathway activation
P16 - tumour suppressor encoded by CDKN2A

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10
Q

How does CDKN2A cause melanoma?

A
  • Binds to CDK4/6, p16 prevents formation of cyclin D1-CDK4/6 complex
  • Cyclin D1-CDK4/6 complex phosphorylates Rb, inactivating it,
    leading to E2F release (once released, E2F promotes cell cycle progression)
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11
Q

What is the 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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12
Q

What is immunotherapy for melanoma based on?

A

Immunotherapy based on CTLA-4 blockade – ipilimumab

- Also checkpoint inhibitors (PD-1, PDL1)

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13
Q

What are the subtypes of melanoma?

A 
Superficial spreading 
Nodular
Lentigo maligna 
Acral lentiginous
Unclassifiabl
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14
Q

What are the features of superficial spreading melanoma?

A

60-70% of all melanomas

Most frequently seen on trunk of men and legs of women

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15
Q

What are the features of superficial spreading melanoma tumours?

A

In up to 2/3 of tumours, regression (visible as grey, hypo-or depigmentation), reflecting the interaction 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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16
Q

What are the main features of nodular melanoma?

A

2nd most common type of melanoma in fair skinned individuals
15-30% of all melanomas
Most commonly trunk, head and neck
M>F

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17
Q

What are the main features of nodular melanoma tumours?

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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18
Q

What are the features of lentigo maligna?

A

Minority of cutaneous melanomas (around 10%) and is
>60 years old
- Occurs in chronically sun-damaged skin, most commonly on the face

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19
Q

What are the features of lentigo maligna tumours?

A

Slow growing, asymmetric brown to black macule with colour variation and an irregular indented border.

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

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20
Q

What is the disease course for maligna tumors?

A

It has been estimated that 5% of lentigo maligna lesions progress to invasive melanoma

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21
Q

What are the features of acral lentiginous?

A

Relatively uncommon: ~5% of all melanomas
Diagnosed most frequently in 7th decade of life
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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22
Q

Why are a large percentage of acral lentiginous melanomes diagnosed in BAME groups?

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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23
Q

What is important re early detection?

A

History of change in colour, shape or size of a pigmented skin lesion

Garbe’s rule: If a patient is worried about a single skin lesion, do not ignore their suspicion and have a low threshold for performing a biopsy

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24
Q

What were the steps in the public awareness campaign for early detection?

A 
Asymmetry
Border irregularity
Colour variegation
Diameter greater than 5mm 
Evolving
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25
Q

What are some poor prognosis features?

A 
Increased Breslow thickness >1mm
Ulceration
Age
Male gender
Anatomical site – trunk, nhead, neck
Lymph node involvement
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26
Q

What are the prognosis for thin vs. thick melanomas?

A

Stage 1A melanoma have 10 year survival of >95% whereas thick melanomas >4mm and ulceration pT4b have a 10 year survival rate of 50%

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27
Q

How is breslow thickness measured?

A

From granular layer to bottom of tumor

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28
Q

What is dermoscopy?

A

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

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29
Q

What are global features of melanomas?

A

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

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30
Q

What is key regarding dermoscopic findings?

A

Dermoscopic findings should not be considered n isolation

History and risk factor status are important

Excise lesion for histological assessment if in any doubt

“If in doubt, take it out”

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31
Q

How are melanomas removed?

A

Primary excision down to subcutaneous fat
- 2mm peripheral margin

Wide excision

  • Margin determined by Breslow depth
    • 5mm for in situ
    • 10mm for =1mm

Prevents local recurrence or persistent disease

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32
Q

How are melanomas staged?

A

Thickness
Ulceration
TNM

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33
Q

How is TNM staging done in melanomas?

A

Imaging
Stage III, IV
And Stage IIc without SLNB

PET-CT
MRI Brain

LDH is MAJOR prognostic factor in metastatic melanoma

34
Q

How are unresectable or metastatic melanomas managed?

A

Immunotherapy

Mutated oncogene targeted therapy

35
Q

What immunotherapy is used in melanoma?

A

CTLA-4 inhibition – unresectable or metastatic BRAF negative melanoma (Ipilimumab)

PD-L1 (Programmed cell death ligand) inhibitors (Nivolumab)Combination immunotherapy not much better than ingle agent in

  • Combination immunotherapy leads to 60% response vs 20% monotherapy alone
36
Q

What mutated oncogene targeted therapy is used in melanoma?

A

Combination of aBRAFinhibitor (e.g. encorafenib, vemurafenib, dabrafenib) andMEK inhibitor (e.g. trametinib

37
Q

What are the features of keratinocyte dysplasia (carcinoma)?

A

Predominantly pale skin types

Solar induced UV damage

38
Q

What are the different types of carcinoma?

A

Actinic keratoses
- Dysplastic keratinocytes

Bowen’s disease (Squamous cell carcinoma in situ)

Squamous cell carcinoma
- Potential for metastasis/
death

Basal cell carcinoma

  • (Virtually) never metastasises
  • Locally invasive
39
Q

Describe the pathogenesis of basal cell carcinoma?

A

Dependent on stroma produced by dermal fibroblasts
Cross talk between tumour cells and mesenchymal cells of stroma
- Receptors for PDGF are upregulated in Stroma but PDGF is upregulated in tumour cells
BCC has proteolytic activity e.g. metalloproteinases and collagenases – degrade pre-existing dermal tissue and facilitate spread of tumour cells

40
Q

Why does UV radiation play such an important role in squamous cell carcinoma?

A

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

  • CDKN2A also
    NOTCH1 or NOTCH2 (Wnt / β-catenin signalling) also plays role
41
Q

What are the main features of keratinocyte carcinoma?

A

Basal cell carcinoma is most common skin cancer

BCC:SCC 4:1

Both commoner in pale skin types

Both more common in men vs women (2-3:1)

Median age at diagnosis of BCC is 68

42
Q

What are risk factors for keratinocyte carcinomas?

A 
UV exposure
Fair skin 
Genetic syndromes
- Xeroderma pigmentosum
- Oculocutaneous albinism
- Muir Torre syndrome
- Nevoid basal cell carcinoma syndrome*
Nevus sebaceous
Porokeratosis 
Organ transplantation (immunosuppressive drugs)
Chronic non-healing wounds 
Ionising radiation
- Airline pilots
Occupational chemical exposures
- Tar, polycyclic aromatic hydrocarbons
43
Q

What is actinic keratoses?

A

Atypical keratinocytes confined to epidermis

Develop on sun-damaged skin - usually head, neck, upper trunk and extremities

Erythematous macule or scale or both-> thick papules or hyperkeratosis or both

44
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ
Erythematous scaly patch or slightly elevated plaque
May arise de novo or from pre-existing AK
May resemble actinic keratoses, psoriasis, chronic eczema

45
Q

What is the treatment for Actinic Keratoses and Bowen’s treatment?

A 
5-fluorouracil cream
Cryotherapy
Imiquimod cream
Photodynamic therapy
Curettage and cautery
Excision
46
Q

What are the main features of squamous cell carcinoma tumours?

A 
Arises within background of sun-damaged skin
May be:
- Erythematous to skin coloured
- Papule
- Plaque-like 
- Exophytic
- Hyperkeratotic
- Ulceration
47
Q

What are some high risk features of squamous cell carcinoma?

A

Localisation: Trunk and limbs > 2cm; Head / neck > 1cm; Periorificial zones
Margins: Ill-defined
Rapidly growing
Immunosuppressed patients
Previous radiotherapy or site of chronic inflammation
Histology

48
Q

What features in the histology of SCC is worrying?

A
  • Grade of differentiation: poorly differentiated
  • Acantholytic, adenosquamous, demosplastic subtypes
  • Tumour thickness - Clark level: >6mm, Clark IV, V
  • Invasion beyond subcutaneous fat
  • Perineural, lymphatic or vascular invasion
49
Q

What is keratoacanthoma?

A

Controversial entity
- Pseudo-malignancy vs variant of SCC

sharply circumscribed, crateriform nodule with keratotic core

Resolves slowly over months to leave atrophic scar

Most occur on head or neck / sun exposed areas

Difficult to distinguish clinically and histologically from squamous cell carcinoma

50
Q

How is SCC diagnosed?

A

Often clinical diagnosis sufficient

Diagnostic biopsy may be taken if diagnostic uncertainty

Ultrasound of regional lymph nodes ± FNA if concerns regarding regional lymph node metastasis

51
Q

How is SCC treated?

A

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

52
Q

What secondary prevention is advised in those with SCC?

A
  • Skin monitoring advice

- Sun protection advice

53
Q

What are the main types of basal cell carcinoma?

A 
Nodular
Superficial
Morpheic
Infiltrative
Basisquamous 
Micronodular
54
Q

What is the most common subtype of BCC?

A

Nodular

Accounts for approximately 50% of all Basal cell carcinomas

55
Q

How does nodular BCC typically present?

A

Typically presents as shiny, pearly papule or nodule

56
Q

How does superficial BCC typically present?

A

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

57
Q

How does morphoeic BCC typically present?

A 
Less common 
Slightly elevated or depressed area of induration
Usually light-pink to white in colour 
More aggressive behaviour
- Extensive local destruction
58
Q

How does basisquamous BCC typically present?

A

Histological features of both basal cell carcinoma and squamous cell carcinoma

59
Q

What are the features of micronodular basal cell carcinoma?

A

Resembles nodular basal cell carcinoma clinically

More destructive behaviour – high rates of recurrence and subclinical spread

60
Q

How is BCC diagnosed?

A

Often clinical diagnosis sufficient

Diagnostic biopsy may be taken

61
Q

What is the treatment for BCC?

A

Standard surgical excision

Mohs micrographic surgery

Other options

62
Q

When is Mohs micrographic surgery used?

A
  • Recurrent basal cell carcinoma
  • Aggressive subtype (morpheic / infiltrative / micronodular)
  • Critical site
63
Q

What are the other features of BCC?

A

Topical therapy e.g. 5-Fluorouracil, Imiquimod
Photodynamic therapy
Curettage
Radiotherapy
Vismodegib - selectively inhibits abnormal signalling in Hedgehog (Hh) pathway

64
Q

What is Mohs micrographic surgery?

A

Remove visible path of lesion

Take secessional onion layer and examine it before taking more tissue

65
Q

What are the features of cutaneous T-cell lymphomas?

A

75% of cutaneous lymphomas are T-cell
Heterogenous group of neoplasms of skin-homing T-cells that show considerable variation in clinical presentation, histological appearance, immunophenotype and prognosis

66
Q

What are the most common subtypes of cutaneous T-cell Lymphoma?

A

Sézary syndrome and mycosis fungoides are most common subtypes

67
Q

What is the pathogenesis of CTCL?

A

Underlying molecular pathogenesis of CTCL is unknown

- Inactivation of genes controlling cell cycle and apoptosis has been identified

68
Q

What is mycosis fungoides?

A

Common variant of primary CTCL and accounts for 50% of all primary cutaneous lymphoma
Indolent clinical course
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

69
Q

What is the progression of myocsis fungoides?

A

Patients progress from patch stage → plaque stage → (finally) tumour stage disease
Protracted clinical course over years → decades
Generally many years of nonspecific eczematous or psoriasiform skin lesions

70
Q

What is the avergae time from onset to diagnosis in MF?

A

Median duration of onset of skin lesions to diagnosis of MF is 4-6 years, but may vary from several months to more than 5 decades

71
Q

What is the early patch stage of MF characterised by?

A

Early patch stage is characterised by variably sized erythematous, finely scaling lesions which may be mildly pruritic

72
Q

What is the pathogenesis of MF?

A

Considered to be a stepwise accumulation of genetic abnormalities → clonal proliferation → malignant transformation → progressive and widely disseminated disease
Molecular events remain unidentified
Genetic abnormalities described, but no constitute pattern
P53, CDKN2A, PTEN, STAT3 identified in advanced MF, but not early
e.g. likely secondary genetic events
Persistent antigenic stimulation plays a crucial role in various lymphomas but no antigens known in MF

73
Q

How is MF evaluated?

A

Evaluation requires examination with attention to:

Type and extent of skin lesions
Presence of palpable lymph nodes
Skin biopsies
Complete blood counts and serum chemistries

74
Q

What is the treatment for MF?

A

Plaque / patch stage treatments include topical corticosteroids, phototherapy and radiotherapy

Systemic chemotherapy is only indicated in advanced stage when there is nodal or visceral involvement or in patients with rapidly progressive tumours unresponsive to less aggressive therapies

Brentuximab vedotin (anti-30) - for advanced disease

75
Q

What is the prognosis for MF?

A

Depends on stage
10 year survival rates are:

> 95% in limited patch / plaque disease
85% in generalised patch / plaque disease
42% in tumour stage disease
20% in those with histological lymph node involvement

76
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

77
Q

What is the treatment for Sezary syndrome?

A

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

78
Q

What are the main features of Kaposi Sarcoma?

A

Multifocal systemic disease
May be endemic or related to immunosuppression
Cutaneous lesions can vary from pink patches to dark violet plaques, nodules or polyps
Treatment with chemotherapy (vincristine, doxorubicin, etoposide, bleomycin) and / or radiation is favoured over surgery

79
Q

What are the main features of Merkel cell carcinoma?

A

Malignant proliferation of highly anaplastic cells which share structural and immunohistochemical features with various neuroectodermally derived cells, including Merkel cells

80
Q

What are risk factors for Merkel Cell Carcinoma?

A

80% are associated with polyomavirus
UV exposure is also an aetiological factor
Predilection for the head and neck region of older adults

81
Q

What are the features of MCC tumours?

A

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

82
Q

What is the behaviour and treatment of Merkel Cell Carcinoma?

A

Aggressive, malignant behaviour
>40% develop advanced disease
Treated with surgery, radiation therapy
anti-PD1 (Pembrolizumab) / anti-PDL1 (Avelumab)

Year 2 Derm (3 decks)

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