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Year 2 - BRS > 7.5 - Skin cancer > Flashcards

7.5 - Skin cancer Flashcards

1
Q

What two investigation types are mainly used for neoplastic skin conditions?

A
  • imaging (internal organ involvement, vascular supply)
  • skin biopsy (microscopy)
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2
Q

Define melanoma

A

Malignant tumour arising from melanocytes

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3
Q

What cells do melanomas arise from?

A

Melanocytes

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4
Q

How deadly is melanoma?

A

Causes 75% of skin cancer deaths (despite not being the most common type of skin cancer)

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5
Q

Describe the incidence rates of melanoma worldwide.

A

Rising incidence rates observed worldwide (although mortality is stable)

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6
Q

Where on the body can melanoma arise?

A
  • mucosal surfaces (e.g. oral, conjunctival, vaginal) and within uveal tract of eye
  • internal organs can be affected (even by primary melanoma not just metastatic) - probably due to impaired melanocyte migration during embryogenesis
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7
Q

What are central depigmented parts of melanoma lesions due to?

A

Tumour regression

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8
Q

What are the genetic risk factors for melanoma? (4)

A
  • family history (CDKN2A mutations), MC1R variants
  • DNA repair defects (e.g. xeroderma pigmentosum)
  • lightly pigmented skin (fairer)
  • red hair
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9
Q

What are the environmental risk factors for melanoma? (3)

A
  • sun exposure - intense intermittent, or chronic
  • sunbeds
  • immunosuppression
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10
Q

What are the phenotypic risk factors for melanoma? (2)

A
  • > 100 melanocytic nevi (moles)
  • atypical melanocytic nevi (moles)
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11
Q

How is the molecular pathogenesis of melanoma important clinically? (2)

A
  • genetic mutations in this pathway can predispose to melanoma
  • these processes can be targeted therapeutically e.g. BRAF, MEK
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12
Q

Describe the epidemiology of melanoma.

A
  • increasing worldwide
  • develops predominantly in Caucasian populations
  • incidence low amongst darkly pigmented populations
  • 10-19/100k per year in Europe
  • 60/100k per year in Australia/NZ
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13
Q

What are the subtypes of melanoma? (5)

A
  • superficial spreading
  • nodular
  • lentigo maligna
  • acral lentiginous
  • unclassifiable
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14
Q

How common is superficial spreading melanoma?

A

60-70% of all melanomas

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15
Q

Which group of people is superficial spreading melanoma most common in?

A

Fair-skinned

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16
Q

Where is superficial spreading melanoma seen on the body most frequently?

A
  • trunk of men
  • legs of women
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17
Q

How can superficial spreading melanoma arise?

A

Can arise de novo (no previous moles) or in pre-existing nevus (previous mole)

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18
Q

How is regression seen in superficial spreading melanoma and why does it happen?

A
  • in 2/3 of tumours, regression is visible as grey or hypopigmentation/depigmentation
  • shows interaction of host immunity against tumour
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19
Q

Describe the growth pattern of superficial spreading melanoma.

A
  1. horizontal (or radial) growth phase where you see 4 characteristic features:
    • asymmetry (A)
    • border irregularity (B)
    • colour variation (C)
    • diameter increase (D)
  2. vertical growth phase - leads to appearance of nodule or bump
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20
Q

What is the ABCD rule that you see in superficial spreading melanoma (horizontal growth phase)?

A
  • Asymmetry
  • Border irregularity
  • Colour variation
  • increased Diameter
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21
Q

How common is nodular melanoma?

A

15-30% of all melanomas

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22
Q

Which groups of people is nodular melanoma common in? (2)

A
  • 2nd most common type of melanoma in fair-skinned individuals
  • more common in men than women
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23
Q

Which body parts is nodular melanoma most common in?

A

Trunk, head and neck

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24
Q

How does nodular melanoma present?

A
  • usually as blue-black, but sometimes pink-red nodule (= a pigmented nodule)
  • may be ulcerated, bleeding
  • develops rapidly

(Trunk, head, neck)

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25
Q

What does amelanotic mean?

A

When a nodule has no pigment - always consider nodules even if not brown

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26
Q

Describe the growth of nodular melanoma.

A
  • no horizontal/radial growth phase - features e.g. asymmetry, border irregularity, colour variation are not present/obvious
  • only vertical growth phase - invades earlier and tends to present at more advanced stage with worse prognosis (vs superficial spreading)
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27
Q

In nodular melanoma, what does only having a vertical growth phase mean clinically?

A

It invades earlier and tends to present at more advanced stage with worse prognosis (compared to superficial spreading melanoma)

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28
Q

How common is lentigo maligna?

A

10% (minority) of cutaneous melanomas

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29
Q

Which groups of people is lentigo maligna most commonly in? (2)

A
  • > 60 years old
  • occurs in chronically sun-damaged skin
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30
Q

Where is lentigo maligna most commonly seen on the body?

A

Most common on face

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31
Q

What does the term ‘lentigo maligna’ refer to?

A

Pre-invasive, slow growing, asymmetric brown/black macule with colour variation and an irregular indented border

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32
Q

When do we call it lentigo maligna and when do we call it lentigo maligna melanoma?

A
  • in situ - termed ‘lentigo maligna’
  • invasive - termed ‘lentigo maligna melanoma’
  • 5% of lentigo maligna progresses to invasive melanoma
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33
Q

How common is acral lentiginous melanoma?

A

Relatively uncommon - 5% of all melanomas

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34
Q

Which group is acral lentiginous melanoma diagnosed most frequently in?

A

7th decade of life (60s)

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35
Q

Where in the body does acral lentiginous melanoma occur?

A

Typically occurs on palms and soles OR in/around nail apparatus (melanonychia)

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36
Q

What is the incidence of acral lentiginous melanoma in different racial groups?

A
  • similar across all racial and ethnic groups
  • disproportionate % of melanomas diagnosed in Afro-Caribbean (up to 70%) or Asians (up to 45%) - as they do not typically develop sun-related melanomas
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37
Q

How are patients instructed to detect melanomas early?

A

Look for history of change in colour, shape or size of a pigmented skin lesion

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38
Q

What is the ABCDE public awareness campaign for melanomas?

A
  • Asymmetry - one half does not match
  • Border - uneven borders
  • Colour - variety of colours
  • Diameter - larger than a pencil eraser
  • Evolution - change in size, shape, colour etc (most important)
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39
Q

What is Garbe’s rule?

A

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

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40
Q

How do we diagnose melanoma?

A

Skin biopsy

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41
Q

What are the differential diagnoses for melanoma? (3)

A
  • basal cell carcinoma - can be pigmented
  • seborrheic keratosis - harmless skin lesions that increase in number with age
  • dermatofibroma - harmless benign skin tumour
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42
Q

What are poor prognostic features for melanoma? (6)

A
  • increased Breslow thickness >1mm (measured histologically from stratum granulosum downwards to bottom of tumour)
  • ulceration
  • age
  • male gender
  • anatomical site - trunk, head, neck
  • lymph node involvement
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43
Q

What are the survival rates for melanoma like?

A
  • stage 1A melanoma have 10 year survival of >95%
  • thick melanomas >4mm and ulceration (stage pT4b) have a 10 year survival of 50%
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44
Q

What technique do we use to investigate melanoma?

(Alongside biopsy)

A

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

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45
Q

What are the global features of melanoma seen on dermoscopy - not on slides, just be aware of? (11)

A
  • asymmetry
  • multiple colours
  • reticular, globular, reticular-globular, homogenous
  • starburst
  • atypical network
  • atypical dots or globules
  • irregular blood vessels
  • regression
  • structures
  • streaks
  • blue-white veil (sign of vertical growth phase)
46
Q

What else is important to consider other than dermoscopy when investigating melanoma?

A

Dermoscopic findings should not be considered in isolation - history and risk factor status are important

47
Q

What do we do if in doubt about melanoma?

A

If in doubt, take it out - excise lesion for histological assessment if in any doubt (clinical features are not specific, low threshold for excision)

48
Q

What are the stages of excision of a melanoma?

A
  • primary excision down to subcutaneous fat (2mm peripheral margin)
  • if melanoma confirmed, wide excision done
    • margin determined by Breslow depth
    • 5mm for in situ
    • 10mm for </=1mm
49
Q

What does melanoma excision prevent?

A

Local recurrence or persistent disease

50
Q

How do we stage melanoma?

A
  • pathological staging occurs then clinical exam
  • TNM staging happens in some instances

TNM staging T includes thickness + ulceration e.g.
pT1a <1mm no ulceration
pT4b >4mm with ulceration

51
Q

What is a sentinel lymph node?

A
  • initial node within a nodal basin that lymphatic drainage (of finite regions of skin) drains into (1st LN encountered)
  • most likely nodes to contain metastatic disease
52
Q

What types of TNM melanomas is sentinel lymphoma node biopsy available for?

A

Currently offered for pT1b and more advanced

53
Q

What would extracapsular spread on lymph node biopsy of melanoma require?

A

Lymph node dissection

54
Q

What two types of imaging are available for melanoma, and for what stages of melanoma are they available for?

A
  • PET-CT
  • MRI brain
  • available for:
    • stage IIc without SLNB (sentinel lymph node biopsy)
    • stage III
    • stage IV
55
Q

What is a major prognostic indicator in melanoma?

56
Q

What are two ways we can treat unresectable or metastatic melanomas?

A
  • immunotherapy
    • CTLA-4 inhibition - unresectable or metastatic BRAF -ve melanoma (e.g. Ipilimumab)
    • PD-L1 (programmed cell death ligand) inhibitors (e.g. Nivolumab)
  • mutated oncogene targeted therapy
    • combination of a BRAF inhibitor (e.g. encorafenib, vemurafenib, dabrafenib) and MEK inhibitor (e.g. trametinib)
57
Q

What groups of people do keratinocyte dysplasia/carcinoma mostly affect?

A

Predominantly pale skin types

58
Q

What is the mechanism of keratinocyte dysplasia/carcinoma?

A

Solar-induced UV damage

59
Q

What are the stages of development of keratinocyte dysplasia?

A
  • actinic keratoses - dysplastic + atypical keratinocytes
  • Bowen’s disease - squamous cell carcinoma in situ (full thickness)
  • squamous cell carcinoma - potential for metastasis/death (full thickness and invasion)
60
Q

What type of keratinocyte carcinoma does not metastasise?

A

Basal cell carcinoma - virtually never metastasises, locally invasive

61
Q

What are the two types of keratinocyte carcinomas?

A
  • squamous cell carcinoma
  • basal cell carcinoma
62
Q

What is the epidemiology of keratinocyte carcinoma (BCC vs SCC)?

A
  • basal cell carcinoma most common skin cancer
  • BCC:SCC = 4:1
  • both commoner in paler skin types
  • both more common in men than women (2/3 : 1)
  • median age at diagnosis of BCC is 68
63
Q

What are the risk factors for keratinocyte carcinomas? (9)

A
  • UV exposure e.g. PUVA
  • fair skin
  • genetic syndromes (xeroderma pigmentosum, oculocutaneous albinism, Muir Torre syndrome, naevoid basal cell carcinoma syndrome)
  • nevus sebaceous
  • porokeratosis
  • organ transplantation (immunosuppressive drugs)
  • chronic non-healing wounds
  • ionising radiation e.g. airline pilots
  • occupational toxic exposures e.g. tar, polycyclic aromatic hydrocarbons
64
Q

What is a significant risk factor for basal cell carcinoma?

A

UV radiation

65
Q

What happens between tumour cells and mesenchymal cells of stroma in basal cell carcinoma?

A
  • cross talk occurs, including with platelet-derived growth factor (PDGF)
  • receptors for PDGF are upregulated in stroma but PDGF is upregulated in tumour cells
66
Q

What kind of activity do basal cell carcinomas have and how does that help them?

A
  • proteolytic activity e.g. metalloproteinases and collagenases
  • degrade pre-existing dermal tissue and facilitate spread of tumour cells
67
Q

Loss of function of what genes can contribute to basal cell carcinoma progression and can be targeted for treatment? (2)

A
  • loss of function in chromosome 8q (PTCH gene)
  • p53 mutations also important - majority are missense mutations that carry UV signature
68
Q

What is a significant risk factor for squamous cell carcinoma?

A

UV radiation

69
Q

What causes squamous cell carcinoma to develop?

A
  • develops through a series of genetic alterations
  • alterations in p53 are most common
  • CDKN2A alterations also common
  • NOTCH1 or NOTCH2 (Wnt/b-catenin) signalling pathway also plays a role
70
Q

What are actinic keratoses?

A

Atypical dysplastic keratinocytes confined to the epidermis (not full thickness)

71
Q

Where do actinic keratoses develop?

A
  • develop on sun-damaged skin
  • usually head, neck, upper trunk and extremities
72
Q

How do actinic keratoses present? (3)

A
  • macules or papules
  • red or pink
  • usually some scale - may be thick scale
73
Q

When would a biopsy be needed for actinic keratoses?

A

The distinction of actinic keratoses from SCC is sometimes difficult so a biopsy is required

74
Q

What is there a risk of with actinic keratoses?

A

Progression to squamous cell carcinoma (0.025-16% per year for any single lesion)

75
Q

What is Bowen’s disease?

A

Squamous cell carcinoma in situ (full thickness)

76
Q

How does Bowen’s disease present?

A

Erythematous scaly patch, or slightly elevated plaque

77
Q

How may Bowen’s disease arise?

A

May arise de novo or from pre existing actinic keratoses

78
Q

What may Bowen’s disease resemble? (3)

A
  • actinic keratoses
  • psoriasis
  • chronic eczema
79
Q

What is the treatment for actinic keratoses and Bowen’s disease? (6)

A
  • 5-fluorouracil cream (topical chemo)
  • cryotherapy (freeze with liquid nitrogen)
  • imiquimod cream (stimulate immune system to kill)
  • photodynamic therapy (apply porphyrin and shine light to generate free radicals and cause apoptosis)
  • curettage and cautery (scrape under local anaesthetic)
  • excision
80
Q

What is squamous cell carcinoma?

A
  • invasive atypical keratinocytes
  • potential for metastasis/death
81
Q

What skin do squamous cell carcinomas arise in?

A

Arises within background of sun-damaged skin

82
Q

How can squamous cell carcinomas present? (6)

A
  • erythematous or skin-coloured
  • papule
  • plaque-like
  • exophytic
  • hyperkeratotic
  • ulceration
83
Q

What high risk clinical features of squamous cell carcinoma are there? (6)

A
  • localisation and size:
    • trunk and limbs >2cm
    • head/neck >1cm
    • periorificial zones
  • ill-defined margins
  • rapidly growing
  • immunosuppressed patients
  • previous radiotherapy or site of chronic inflammation
  • histology (do not need to know)
84
Q

What histological features are high-risk for squamous cell carcinoma? (5 - do not need to know for exam)

A
  • poorly differentiated
  • acantholytic, adenosquamous, demosplastic subtypes
  • tumour thickness - Clark level >6mm, Clark IV, V
  • invasion beyond subcutaneous fat
  • perineural, lymphatic or vascular invasion
85
Q

How do we investigate squamous cell carcinoma?

A
  • often clinical diagnosis is sufficient
  • diagnostic biopsy may be taken if diagnostic uncertainty
  • ultrasound of regional lymph nodes +/- fine needle aspiration, if concerns of regional lymph node metastasis
86
Q

What differentials are there for squamous cell carcinoma? (3 + 1)

A
  • basal cell carcinoma
  • viral wart
  • Merkel cell carcinoma
  • (keratoacanthoma)
87
Q

How do we treat squamous cell carcinoma? (5)

A
  • examination of rest of skin and regional lymph nodes
  • excision
  • radiotherapy if unresectable / high-risk features e.g. perineural invasion
  • Cemiplimab (PD1 inhibitor) for metastatic SCC
  • secondary prevention e.g. skin monitoring advice and sun protection advice (high risk of developing another SCC)
88
Q

What is a keratoacanthoma?

A

Rapidly enlarging papule that evolves into a sharply circumscribed, crateriform nodule with keratotic core

89
Q

How do we treat keratoacanthoma?

A

Resolves slowly over months

90
Q

Why is keratoacanthoma difficult to diagnose/classify?

A
  • difficult to distinguish clinically and histologically from SCC
  • can only tell it was keratoacanthoma if/when it resolves
91
Q

Where do keratoacanthomas occur on the body?

A

Most occur on head or neck / sun-exposed areas

92
Q

What are the 6 main subtypes of basal cell carcinoma?

A
  • nodular
  • superficial
  • morpheic
  • infiltrative
  • basisquamous
  • micronodular
93
Q

How does nodular basal cell carcinoma present?

A
  • typically presents as shiny, pearly papule or nodule
  • on dermoscopy you can see arborising (branching) blood vessels
94
Q

How common is nodular basal cell carcinoma?

A
  • most common subtype of BCC
  • accounts for approximately 50% of BCC
95
Q

How does superficial basal cell carcinoma present?

A
  • well-circumscribed, erythematous macule/patch or thin papule/plaque
  • can resemble actinic keratosis, Bowen’s disease, eczema
96
Q

How does morphoeic basal cell carcinoma present?

A
  • slightly elevated or depressed area of induration
  • usually light pink to white in colour
  • aggressive behaviour - extensive local tissue destruction
97
Q

How common is morphoeic basal cell carcinoma?

A

Less common than other subtypes

98
Q

What features does basisquamous basal cell carcinoma have?

A

Histological features of both basal cell carcinoma and squamous cell carcinoma, can metastasise

99
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
100
Q

How do we investigate basal cell carcinoma?

A
  • often clinical diagnosis sufficient
  • diagnostic biopsy may be taken
101
Q

What differentials are there for basal cell carcinoma? (3)

A
  • squamous cell carcinoma
  • adnexal (sebaceous) carcinoma
  • Merkel cell carcinoma
102
Q

What treatments are there for basal cell carcinoma? (7)

A
  • standard surgical excision
  • Moh’s micrographic surgery
  • topical therapy e.g. 5-fluorouracil, Imiquimod
  • photodynamic therapy (superficial BCC)
  • curettage (superficial BCC)
  • radiotherapy (>70yo)
  • Vismodegib - selectively inhibits abnormal signalling in Hedgehog pathway
103
Q

When is Moh’s micrographic surgery used? (3)

A
  • recurrent basal cell carcinoma
  • aggressive subtype (morpheic/infiltrative/micronodular)
  • critical site
104
Q

What is bread loafing?

A
  • when you send a histological specimen for analysis, it is sectioned using bread loafing technique
  • some areas of skin may be missed = falsely reassuring report, false-negative tumour margins
105
Q

How does Moh’s micrographic surgery avoid the problems of bread loafing?

A
  • you remove the tumour
  • you then take thin onion skin layers from the margin and examine them repeatedly until you see healthy tissue
  • helps us have healthy margins without removing excess skin
  • but this process takes hours and requires highly skilled surgeon
106
Q

What is Merkel cell carcinoma?

A

Malignant proliferation of highly anaplastic (lack identifiable features) cells which share features with neuroectodermally derived cells (including Merkel cells)

107
Q

Why is the name Merkel cell carcinoma misleading?

A

They are not actually derived from Merkel cells

108
Q

What are risk factors for Merkel cell carcinoma? (2)

A
  • 80% associated with polyomavirus
  • UV exposure is also an aetiological factor
109
Q

Where in the body does Merkel cell carcinoma tend to develop?

A

Predilection for head and neck region of older adults

110
Q

How does Merkel cell carcinoma present? (3)

A
  • solitary, rapidly growing nodule
  • pink-red to violaceous, firm, dome-shaped
  • ulceration can occur
111
Q

How does Merkel cell carcinoma behave?

A
  • aggressive, malignant behaviour (most aggressive type of skin cancer)
  • > 40% develop advanced disease (metastatic)

Year 2 - BRS (84 decks)

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