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skin cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

What are melanomas?

A

Malignant tumors arising from melanocytes (pigment cells)

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2
Q

What percentage of skin cancer deaths are caused by melanomas?

A

75% (but it is not the most common type)

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3
Q

Give a possible reason for the rising worldwide incidence of melanomas.

A

Might be due to detecting more

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4
Q

What surfaces can melanomas be found on?

A

Skin, mucosal surfaces (oral, vaginal, conjunctival) and within uveal tract of eye

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5
Q

What are the broad types of risk factors for melanoma?

A

Genetic factors
Environmental factors
Phenotypic factors

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6
Q

What are some genetic risk factors for melanoma?

A

Family history (CDKN2A mutation, MC1R variants)
Lightly pigmented skin
Red hair
DNA repair defects (e.g. xeroderma pigmentosum)

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7
Q

What are some environmental risk factors for melanoma?

A

Intense intermittent sun exposure
Chronic sun exposure
Living in equatorial regions
Sunbeds
Immunosuppression

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8
Q

What are some phenotypic risk risk factors for melanoma?

A

> 100 melanocytic nevi

atypical melanocytic nevi

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9
Q

What constitutes the MAPK pathway and what does this pathway regulate?

A

RAS-RAF-MEK-ERK

Regulates cell proliferation, growth and migration

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10
Q

What is the contribution of KIT mutations towards melanoma causation?

A

30-40% of acral and mucosal melanomas

Also melanomas from chronically sun-exposed skin bear activation mutations and copy number amplifications of KIT gene

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11
Q

In what genes are activation mutations present in?

A

NRAS genes (15-20% of melanomas)

BRAF genes (50-60% of melanomas)- high in melanomas of skin with intermittent UV exposure but low in melanomas of skin with high cumulative UV exposure

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12
Q

What gene mutations lead to MAPK pathway activation?

A

BRAF mutation substitution

CDKN2A mutation

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13
Q

What is P16 and what is its functions?

A

Binds to CDK4/6 and prevents the formation of the cyclin D1-CDK4/6 complex

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14
Q

What is the function of the cyclin D1-CDK4/6 complex?

A

Phosphorylates Rb, inactivating it and leading to the release of E2F (once released, E2F promotes cell cycle progression

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15
Q

What is the host immunological response to melanoma?

A

Host CD8+ T cells can recognise melanoma specific antigens and, if activated appropriately, can kill tumour cells

CD4 helper T cells and antibodies also play a critical role

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16
Q

What is CTLA4 and what does it do?

A

Cytotoxic T-lymphocyte-associated antigen 4 is a natural inhibitor of T cell activation by blocking costimulatory signal (B7b on APC to CD28 on T-cell

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17
Q

What drug classes are associated with melanoma immunotherapy?

A 
CTLA-4 inhibitors (ipilimumab)
Checkpoint blockade (PD-1, PDL-1)
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18
Q

What is the distribution of melanoma?

A

Develops predominantly in caucasian populations
Incidence low among darkly pigmented populations

less per year in Europe than in Australia/NZ (x3 in Au/NZ)

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19
Q

What are the subtypes of melanoma?

A

Superficial spreading
Nodular
Lentigo maligna
Acral lentiginous
Unclassifiable

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20
Q

What is the most common type of melanoma in fair-skinned individuals?

A

Superficial spreading (60-70%)

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21
Q

Where are superficial spreading melanomas localised?

A

Trunk of men

Legs of women

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22
Q

How do superficial spreading melanomas arise?

A

De novo or from a pre-existing nevus

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23
Q

How is interaction of host immune system with superficial spreading melanoma reflected in the tumor?

A

Areas of regression (visible as grey, hypo- or depigmentation) in 2/3 of tumours

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24
Q

In a superficial spreading melanoma, what are the growth phases of the tumour?

A

Slow horizontal (radial) growth phase limited to the epidermis

Rapid vertically oriented growth phase associated with nodule development

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25
Q

What is the second most common type of melanoma in fair skinned individuals?

A

Nodular

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26
Q

Where are nodular melanomas localised?

A

Usually head, neck, trunk

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27
Q

What is the gender distribution of nodular melanomas?

A

M>F

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28
Q

What do nodular melanomas present as and in what stage?

A

Generally present as blue to black but may be pink to red- may be ulcerated, bleeding

Tend to present more advanced stage with poorer prognosis

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29
Q

Describe nodular melanoma development

A

Develop rapids

Believed to arise as a de novo vertical growth phase without the pre-existing horizontal growth phase

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30
Q

What type of melanoma accounts for the minority of cutaneous melanomas?

A

Lentigo maligna

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31
Q

What age group does lentigo maligna arise in?

A

> 60 years old

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32
Q

Where is lentigo maligna localised?

A

In sun-damaged skin, most commonly on the face

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33
Q

What does a lentigo maligna lesion look like?

A

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

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34
Q

What precursor lesion does invasive lentigo maligna melanoma arise from?

A

Lentigo maligna (in situ melanoma) in sun damaged skin- it has been estimated that 5% of lentigo malignant lesions progress to invasive melanoma

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35
Q

How common is acral lentiginous melanoma and at what age is it usually diagnosed?

A

Relatively uncommon- 5% of all melanomas

most frequently diagnosed in the 7th decade of life

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36
Q

Where are lesions localised in acral lentiginous melanoma?

A

Typically occurs in palms, soles and around the nail apparatus

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37
Q

What is the racial/ethnic distribution of acral lentiginous melanoma?

A

Incidence similar across all racial/ethnic groups

As darkly pigmented Africans and Asians do not typically develop sun-related melanomas, ALM represents a disproportionate percentage of melanomas diagnosed in Afro-Caribbean or Asians

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38
Q

What are amelanotic melanomas?

A

Melanomas which do not produce melanin, therefore do not look like other melanomas (may appear pink or reddish, with grey or brownish edges)

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39
Q

What is the ABCDE melanoma self detection campaign?

A 
Asymmetry
Border irregularity
Colour variaton
Diameter > 5mm
Evolving
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40
Q

What are differential diagnoses for melanoma?

A

Basal cell carcinoma
Dermatofibroma
Sebborrhoeic keratosis

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41
Q

What are poor prognostic features for melanoma?

A 
Age 
Anatomical site - head, neck, trunk
Ulceration
Increased Breslow thickness (>1mm)
Lymph node involvement
Male gender

stage 1A melanoma has a 10 year survival of 95% but a melanoma with thickness >4mm and ulceration (pT4b) has a 10 year survival of 50%

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42
Q

What is breslow thickness?

A

Measurement from granular layer to the bottom of tumour

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43
Q

Name a technique used in melanoma investigation

A

Dermatoscopy- can improve correct diagnosis of melanoma by nearly 50%

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44
Q

What are some global features of melanomas?

A

Asymmetry
Colour variation
Reticular, globular, reticular-globular, homogeneous
Starbust

Atypical networks, streaks, atypical dots or globules, irregular blood vessels, blue-white veil, regression structures

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45
Q

Can dermatoscopic findings be considered in isolation in melanoma?

A

No- history and risk factor status are important

Excise lesion for histological assessment if in any doubt

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46
Q

What are the 2 stages of excision in melanoma management?

A

Primary excision- down to the subcutaneous fat, 2mm peripheral margin

Wide excision- margin determined by Breslow depth (5mm for in situ, 10mm for thickness >=1mm)

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47
Q

Why are melanomas excised with a peripheral margin?

A

TO prevent local recurrence/ persistent disease

48
Q

What are the 2 types of staging used in melanoma?

A

Pathological

TNM

49
Q

What are sentinel lymph nodes and how are they significant in melanoma?

A

Lymphatic drainage from a finite region of skin occurs specifically into an initial lymph node in a given nodal basin known as the ‘sentinel node.’

This represents the most likely nodes to contain metastatic disease

50
Q

For what stage of melanoma is SLNB offered?

A

pT1b+

51
Q

What is needed if extra capsular lymph node spread is observed on lymph node biopsy?

A

Lymph node dissection

52
Q

In what stage of melanoma is imaging offered?

What types of imaging is carried out?

A

Stage III, IV
Stage Iic without SLNB

PET-CT
MRI brain

53
Q

Serum levels of ___ are a major prognostic factor in metastatic melanoma

A

LDH

54
Q

What kinds of treatment are offered in cases of unresectable/ metastatic melanoma?

A

Immunotherapy

Mutated oncogene targeted therapy

55
Q

Give examples for immunotherapy used in treating unresectable/ metastatic melanoma

A

CTLA-4 inhibtion (ipilimumab)- unresectable/ metastatic BRAF negative melanoma

PDL-1 (nivolumab)

56
Q

Give an example of mutated oncogene targeted therapy used in treating unresectable/ metastatic melanomas

A

Comination of BRAF (encorafenib, vemurafenib, dabrafenib) and MEK inhibitors (trametinib)

57
Q

What are risk factor for keratinocyte dysplasia?

A

Pale skin

UV-induced skin damage

58
Q

Name 4 types of keratinocyte dysplasia/ 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

59
Q

Describe the pathogenesis of basal cell carcinoma

A

Depends on stroma production by desmolytic fibroblasts

Cross talk between tumour cells and mesenchymal cells in stroma- there is up regulation of PDGF receptors in stroma, but PDGF is unregulated in tumour cells

BCC has proteolytic activity- metalloptroteases and collegenases- which leads to destruction of existing dermal tissue and facilities spread of tumour cells

Loss of function in chromosome 8q (PTCH gene)- sonic hedgehog patched signalling pathway/ sonic hedgehog signalling is required fir growth of established BCCs

P53 mutations- mostly missense mutations with a UV signature

60
Q

What are common genetic alterations which can lead to the development of SCC?

A

p53 mutations are the most common

CDKN2A
NOTCH1 or NOTCH2 (Wnt/ B-catenin signalling)

61
Q

What is the most common type of skin cancer?

A

Basal cell carcinoma

62
Q

What is the ratio BCC:SCC?

A

4:1

63
Q

Are BCCs and SCCs more common in men/ women?

A

Men

64
Q

BCC median age of diagnosis?

A

68

65
Q

Give examples for risk factors for keratinous carcinomas.

A

Fair skin
UV exposure
Ionising radiation (airline pilots)
Occupational chemical exposure (tar, polycyclic aromatic hydrocarbons)
Genetic syndromes (xeroderma pigmentosum, oculocutaneous albinism, Muir Torre syndrome, Nevoid basal cell carcinoma syndrome
Nevus sebaceous
Porokeratosis
Organ transplantation (immunosuppression)
Chronic non-healing wounds

66
Q

What are actinic keratoses?

Where are they localised?

What do they look like?

A

Atypical keratinocytes confined to epidermis

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

Erythematous macule/scale/both–> thick papule/ hyperkeratosis/ both
sometimes cutaneous horn

67
Q

How are acting keratoses distinguished from SCCs?

A

sometimes difficult, requiring biopsy

68
Q

What do skin lesions look like in Bowen’s disease?

A

Erythematous scaly patch or slightly elevated papule

69
Q

How does Bowen’s disease arise?

A

De novo/ from pre-existing actinic keratoses

70
Q

What can Bowen’s disease resemble?

A

Actinic keratoses, psoriasis, chronic eczema

71
Q

Actinic keratoses/ Bowen’s disease treatment

A 
5-fluorouracil cream
imiquimod cream
cryotherapy
photodynamic therapy
curettage and cautery
excision
72
Q

What do skin lesions look like in SCC?

A

Erythematous to skin-coloured

May be papules, plaque-like, hyperkeratotic, exophytic, ulceration

73
Q

What are high risk features for squamous cell carcinoma?

A 
Localisation: Trunk and limbs>2cm, head and neck >1cm, periorificial regions
Margins ill-defined
Rapidly growing
Immunosuppression
Previous radiotherapy
chronic inflammation site

Histology
Invasion beyond subcutaneous fat
Perineural, lymphatic, vascular invasion
Tumor thickness (>6mm/ Clark level IV,V)
Grade of differentiation- poorly differentiated
Acantholytic, Adenosquamous, desmoplastic subtypes

74
Q

What is keratoacanthoma?

A

Pseudomalignancy/ variant of SCC

75
Q

What does a keratoacanthoma skin lesion look like?

A

Rapidly enlarging papule which evolves into a sharply circumscribed, cratereiform nodule with a keratitis core which resolves slowly over months to give an atrophic scar

76
Q

Where a skin lesions localised in keratoacanthoma?

A

Mostly head/ neck/ sun-exposed areas

77
Q

What type of carcinoma can keratoacanthoma resemble?

A

Squamous cell carcinoma

78
Q

What investigations are carried out to diagnose SCC?

A

Often clinical diagnosis is sufficient

Diagnostic biopsy if diagnosis is uncertain

Ultrasound of regional lymph nodes +/- FNA if regional lymph node involvement is a concern

79
Q

Differential diagnoses for SCC?

A

Basal cell carcinoma
Merkel cell carcinoma
Viral wart

80
Q

How is squamous cell carcinoma treated?

A

Examination of regional lymph nodes
Excision
Radiotherapy (unresectable tumours, tumours with high risk features like perineurial invasion)
Cemiplimab for metastatic SCC
Secondary prevention (Skin monitoring advice, sun protection advice)

81
Q

What are the main subtypes of BCC?

A 
Nodular
Micronodular
Morphoeic
Superficial
Infiltrative
Basisquamous
82
Q

What is the most common subtype of basal cell carcinoma?

A

Nodular (accounts for about 1/2 of all BCCs)

83
Q

How does nodular BCC typically present

A

Shiny, pearly papule or nodule

84
Q

How does superficial BCC present?

A

Well defined, erythematous macule/patch or thin papule/ plaque

85
Q

What do skin lesions in morphoeic BCC look like and is it comparatively more/less aggressive than other BCCs?

A

Slightly elevated/depressed area of induration
Usually light-pink to white in colour

More aggressive in behaviour- aggressive local tissue destruction

86
Q

what types of carcinomas do the histological features of basisquamous carcinomas resemble?

A

BCCs

SCCs

87
Q

Does micro nodular BCC resembles nodular BCC?

A

It resembles nodular BCC clinically but shows more destructive behaviour (high rates of recurrence and subclinical spread

88
Q

What investigations are carried out for BCC?

A

Often clinical diagnosis is sufficient

Diagnostic biopsy may be taken

89
Q

Basal cell carcinoma differential diagnoses?

A

SCC
Merkel cell carcinoma
Adnexal (sebaceous) carcinoma

90
Q

How is basal cell carcinoma treated?

A

Standard surgical excision
Mohs micrographic surgery (recurrent BCC, aggressive subtypes- micro nodular, infiltrative, morphoeic, critical sites
Curettage
Topical therapy (Imiquimod, 5-fluorouracil)
Photodynamic therapy
Radiotherapy
Vismodegib- selectively inhibits abnormal signalling in Hedgehog (Hh) pathway

91
Q

What is cutaneous T cell lymphoma?

A

Heterogeneous group of neoplasms of skin-homing T-cells that show considerable variation in clinical presentation, histological appearance, immunopheotype and prognosis

92
Q

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

A

Sézary syndrome

Mycosis fungoides

93
Q

What is the underlying molecular pathogenesis of cutaneous T cell lymphoma?

A

Unknown- inactivation of genes controlling cell cycle and apoptosis has been identified

94
Q

which is more common- Sezary syndrome or mycosis fungoides?

A

Mycosis fungicides (Sézary syndrome is rare- on 5% of CTCL)

95
Q

What is the median age of diagnosis of CTCL?

A

55-60 years

96
Q

Describe the clinical course, diagnosis and skin lesions in CTCL

A

Indolent clinical course

Diagnosis requires biopsy
Diagnosis may take years as skin lesions may be present that are neither clinically nor histologically relevant for years

patches or plaques

97
Q

Other than CTCL where else may atypical T cell infiltrates be found?

A

Lymphomatous drug eruptions

98
Q

What are the stages of progression of mycosis fungoides?

A

Patch stage–> plaque stage–> (finally) tumour disease stage

99
Q

What is the median duration of onset of skin lesions to diagnosis of mycosis fungoides?

A

4-6 years, but may vary from several months to more than 5 decades

100
Q

Describe skin lesions in the early patch stage of mycosis fungoides.

A

variably sized, erythematous, finely scaling lesions

may be mildly pruritic

101
Q

What considerations are important in examination for mycosis fungoides?

A

type and extent of skin lesions
presence of palpable lymph nodes
skin biopsy
FBC and serum chemistries

102
Q

Describe the pathogenesis of mycosis fungoides

A

considered to be a stepwise accumulation of genetic abnormalities–>clonal proliferation–>malignant transformation–> progressive and wildly disseminated disease
Molecular events remain unidentified
Genetic abnormalities described but no constitute pattern
P53, CDKN2A, PTEN, STAT3 identified in advanced MF but not early (likely secondary genetic events)
Persistent antigenic stimuli play a crucial role in some lymphomas but no antigens known in MF

103
Q

How is mycosis fungoides treated?

A

Plaque/patch stage treated with topical corticosteroids, phototherapy, radiotherapy
systemic chemotherapy is only indicated in advanced stage where there is visceral/ nodal disease or in rapidly progressive tumours unresponsive to less aggressive therapies
brentuximab vedotin (anti-30)

104
Q

What are the 10 year survival rates for mycosis fungoides?

A

95% in limited patch/ plaque stage disease
85% in generalised patch/ plaque stage disease
42% in tutor stage disease
20% if there is histological lymph node involvement

105
Q

What are differentials for mycosis fungoides?

A

Psoriasis
Parapsoriasis
Eczema (Discoid)

106
Q

What triad of symptoms can be seen in Sézary syndrome?

A

Erythroderma
Generalised lymphadenopathy
Presence of neoplastic T-cells (Sézary cells) in skin, lymph nodes, blood

107
Q

What are the criteria for diagnosis for Sézary syndrome?

A

Demonstrate the presence of a T-cell clone in the blood by molecular/ cytogenetic methods

An absolute Sézary cell count of at least 1000 cells per micro litre

Demonstration of an immunophenotypical abnormality (expanded CD4+ T cell population such that the CD4/CD8 ratio is greater than 10 and/ or aberrant expression of pan T-cell antigens

108
Q

How is Sézary syndrome treated?

A

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

109
Q

Whta is Kaposi Sarcoma?
What do skin lesions look like in Capos sarcoma?
What viral infection can lead to Kaposi sarcoma?

A

A multifocal, systemic disease that may be endemic or may be related to immunosuppression

Can vary from pink patches to dark purple plaques, polyps, nodules

110
Q

How is Kaposi Sarcoma treated?

A

Chemotherapy (vincristine, doxorubicin, etoposide, bleomycin) and radiotherapy preferred over surgery

111
Q

What is Merkel cell carcinoma?

A

Malignant proliferation of highly anaplastic cells which share structural and immunohistochemical properties with neuroectoderm derived cells including Merkel Cells

Agressive, malignant behaviour (40% develop advanced disease)

112
Q

Name two etiological factors that can lead to MCC

A

80% are associated with polyomavirus

UV exposure

113
Q

Where are skin lesions localised in MCC?

What age group of the population does MCC present in

A

Generally head and neck region in older adults

114
Q

Describe skin lesion in Merkel cell carcinoma

A 
Solitary, rapid-growing nodule
pink-red to violaceous
firm
dome shaped
ulceration may occur
115
Q

How is MCC treated?

A

Surgery
Radiotherapy
Chemotherapy- anti-PD1 (pembrolizumab)/anti-PDL1 (avelumab)

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