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BRS DERMATOLOGY > 1b// Skin cancer > Flashcards

1b// Skin cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

What do you have to consider to make a differential diagnosis with derm?

A
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2
Q

What are the investigations you can do for derm?

A

and tissue culture

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3
Q

What investigations are best for derm cancers?

A

imaging and skin biopsies

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4
Q

What are the derm cancers you need to know?

A

melanoma
squamous cell carcinoma (SCC)
basal cell carcinoma (BCC)
Merkel cell carcinoma

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5
Q

What is a melanoma?

A

a malignant tumour arising from melanocytes

leads to >75% of skin cancer deaths
Rising incidence rates observed worldwide

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6
Q

Where can a melanoma arise?

A

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

skin asw

these are just the ones that you wouldn’t expect

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7
Q

What happens when a melanoma is found in weird places such as the GI tract?

A

abnormal migration of melanocyte precursors

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8
Q

What is this?

A

An asymmetric, irregularly pigmented melanocytic lesion. The central depigmented zone is due to tumour regression.

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9
Q

What are the categories of the risk factors for melanoma?

A

genetic factors
environmental factors
phenotypic

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10
Q

What are the genetic risk factors for melanoma?

A
  • Family history (CDKN2A mutations), MC1R variants
  • DNA repair defects (e.g. xeroderma pigmentosum)
  • Lightly pigmented skin
  • Red hair
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11
Q

What are the environmental risk factors for melanoma?

A
  • Sun exposure – intense intermittent or chronic
  • Sunbeds
  • Immunosuppression
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12
Q

What are the phenotypic risk factors for melanomas?

A
  • > 100 Melanocytic nevi
  • Atypical melanocytic nevi

nevi= mole

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13
Q

What is the epidemiology of melanomas?

A
  • Increasing worldwide
  • Develops predominantly in Caucasian populations
  • Incidence low amongst darkly pigmented populations
  • 10-19/100,000 per year in Europe
  • 60/100,000 per year in Australia / NZ
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14
Q

What are the subtypes of melanomas? (5)

A

Superficial spreading

Nodular

Lentigo maligna

Acral lentiginous

Unclassifiable

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15
Q

How common are superficial spreading melanomas?

A

60-70% of all melanomas
- most common type in fair skin

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16
Q

Where are superficial spreading melanomas most frequently on?

A

trunk of men
legs of women

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17
Q

How can superficial spreading melanomas arise?

A

de novo or in pre-existing nevus

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18
Q

What happens in roughly 2/3 of tumours of superficial spreading melanomas?

A

In ~2/3 of tumours, regression (visible as grey, hypo-or depigmentation visible (host immunity against tumour)

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19
Q

What type of growth happens in superficial spreading melanomas?

A

horizontal growth and vertical growth

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20
Q

What happens in horizontal growth?

A

asymmetry
border irregularity
colour variation
diameter greater than 5/6mm

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21
Q

What happens in vertical growth?

A

grow downwards (and upwards)
nodule formed, raised

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22
Q

What is the 2nd most common type of melanoma in fair skinned individuals?

A

nodular melanoma

15-30% of all melanomas

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23
Q

What growth occurs with nodular melanoma?

A

no horizontal growth

just vertical

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24
Q

Where are the most common places for nodular melanomas?

A

most commonly trunk, head and neck

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25
Q

Is nodular melanoma more common in women or men?

A

men

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26
Q

How does nodular melanoma usually present?

A

Usually present as blue to black, but sometimes pink to red, nodule – may be ulcerated, bleeding

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27
Q

Do nodular melanomas develop rapidly or slowly?

A

rapidly

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28
Q

What melanoma makes up 10% (minority) of cutaneous melanomas?

A

lentigo maligna

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29
Q

In who is lentigo maligna most common?

A

Elderly over 60 y/o

  • chronically sun damaged skin
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30
Q

Where on the body is lentigo maligna most common?

A

on the face

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31
Q

How would you describe a lentigo maligna?

A

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

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32
Q

What are the 2 types of lentigo maligna melanomas?

A

in-situ=> lentigo maligna

invasive=> lentigo maligna melanoma

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33
Q

Is it common for lentigo maligna to progress to invasive melanoma?

A
  • 5% of lentigo maligna progresses to invasive melanoma
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34
Q

Which melanoma is most frequent in 7th decade of life?

A

acral lentiginous

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35
Q

Where is acral lentiginous most frequently found?

A

Typically palms and soles OR in / around nail apparatus

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36
Q

What is the incidence like of acral lentiginous?

A

Incidence similar across all racial and ethnic groups
- Disproportionate percentage of melanomas diagnosed in Afro-Caribbean (up to 70%) or Asians (up to 45%)

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37
Q

What is pigmentation in the nail called?

A

melanonychia

con happen with acral lentiginous
but also common in afro-carribean after trauma

(not necessarily a term to describe melanoma)

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38
Q

What is an amelanotic melanoma?

A

no pigment so pink

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39
Q

What is the method for self-detection of melanomas?

A
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40
Q

What are differential diagnoses of melanomas?

A

basal cell carcinoma
seborrhoeic keratosis
dermatofibroma

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41
Q

What are poor prognostic features of melanomas?

A

Increased Breslow thickness >1mm (increased thickness means a worse prognosis)

Ulceration

Age

Male gender

Anatomical site – trunk, nhead, neck

Lymph node involvement

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42
Q

What is survival llke comparing a stage 1a melanoma and a pT4b?

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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43
Q

Who gives you the measurements of the depth of a melanoma? And what is that thickness called

A

histologists

Breslow thickness

44
Q

How do you investigate for melanomas?

A

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

NB
Dermoscopic findings should not be considered in isolation
History and risk factor status are important
Excise lesion for histological assessment if in any doubt

“If in doubt, take it out”

45
Q

What is the management for resectable melanomas?

A

Primary excision down to subcutaneous fat
- 2mm peripheral margin

Wide excision (go beyond lesion)
- Margin determined by
Breslow depth
- 5mm for in situ
- 10mm for </=1mm
- Prevents local recurrence or persistent disease

Sentinel lymphoma node biopsy
- Lymphatic drainage of finite regions of skin drain specifically to an initial node within a given nodal basin - the ‘sentinel node’
- Most likely nodes to contain metastatic disease
- Currently offered for pT1b+
- Extracapsular spread on lymph node biopsy – needs lymph node dissection

46
Q

What is the staging for melanomas?

A
47
Q

What is the imaging done for melanomas?

A

Imaging
- Stage III, IV
And Stage IIc without SLNB

PET-CT
MRI Brain

48
Q

What is a major prognostic indicator in melanoma?

A

LDH
Lactate dehydrogenase

49
Q

What is the management of unresectable melanomas or metastatic melanomas?

A

Immunotherapy

Mutated oncogene targeted therapy:

50
Q

What is the immunotherapy for unresectable melanomas?

A

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

PD-L1 (Programmed cell death ligand) inhibitors (Nivolumab)

51
Q

What is the mutated oncogene targeted therapy for melanomas?

A

Combination of a BRAF inhibitor (e.g. encorafenib, vemurafenib, dabrafenib) and MEK inhibitor (e.g. trametinib)

52
Q

In who are Keratinocyte Dysplasia / Carcinomas most common in? And what type of damage is it?

A

predominantly pale skin types

solar induced UV damage

53
Q

What is a carcinoma?

A

cancer that forms in epithelial tissue

54
Q

What are the types of Keratinocyte Dysplasia / Carcinoma?

A

Actinic keratoses

Bowen’ s disease

Squamous cell carcinoma

Basal cell carcinoma

55
Q

What is actinic keratoses?

A

dysplastic keratinocytes

56
Q

What is Bowen’s disease?

A

squamous cell carcinoma in situ

57
Q

what is does squamous cell carcinoma have the potential for?

A

metastasis/ death

58
Q

What does basal cell carcinoma basically never do?

A

(virtually) never metastasises

locally invasive

59
Q

What is a significant risk factor for basal cell carcinoma?

A

UV radiation

60
Q

What is the pathogenesis of basal cell carcinoma?

A

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

Loss of function in chromosome 8q (PTCH gene)
- p53 mutations are also important – majority are missense mutations that carry a UV signature

61
Q

What is a significant risk factor of squamous cell carcinoma?

A

UV radiation

62
Q

What is the pathogenesis of SCC?

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

63
Q

What is epidemiology of keratinocyte carcinomas?

A
  • Basal cell carcinoma is most common skin cancer
  • BCC:SCC 4:1
  • Both commoner in pale skin types
    Systemic
  • Both more common in men vs women (2-3:1)
    disease
  • Median age at diagnosis of BCC is 68
64
Q

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

A

UV exposure - e.g., PUVA

Fair skin

Genetic syndromes

Nevus sebaceous

Porokeratosis

Organ transplantation (immunosuppressive drugs)

Chronic non-healing wounds

Ionising radiation
- Airline pilots

Occupational chemical exposures
- Tar, polycyclic aromatic hydrocarbons

65
Q

What are the genetic syndromes that are risk factors for keratinocyte carcinomas?

A
  • Xeroderma pigmentosum
  • Oculocutaneous albinism
  • Muir Torre syndrome
  • Nevoid basal cell carcinoma syndrome
66
Q

What are actinic keratoses?

A

Atypical keratinocytes confined to epidermis

67
Q

Where do actinic keratoses develop?

A

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

68
Q

What can actinic keratoses look like?

A

macules or papules

red or pink

Usually some scale – may be thick scale

69
Q

What type of carcinoma is it hard to make a distinction between it and actinic keratoses? And how do you make that distinction?

A

Distinction from squamous cell carcinoma sometimes difficult – requiring biopsy

70
Q

What can actinic keratoses progress to, and what are its chances of progressing?

A

Risk of progression to squamous cell carcinoma: 0.025–16% per year for any single lesion

71
Q

What is Bowen’s disease?

A

squamous cell carcinoma in situ

72
Q

What does Bowen’s disease look like?

A

Erythematous scaly patch or slightly elevated plaque

73
Q

How may Bowen’s disease arise?

A

de novo or from pre-existing Actinic keratosis

74
Q

What can Bowen’s disease resemble?

A

actinic keratoses, psoriasis, chronic eczema

75
Q

What is the treatment for actinic keratosis and Bowen’s disease?

A

5-fluorouracil cream

Cryotherapy (liquid nitrogen)

Imiquimod cream

Photodynamic therapy

Curettage and cautery

Excision

76
Q

What does squamous cell carcinoma arise within the background of?

A

of sun damaged skin

77
Q

What can squamous cell carcinoma look like?

A
  • Erythematous to skin coloured
  • Papule
  • Plaque-like
  • Exophytic
  • Hyperkeratotic
  • Ulceration
78
Q

What are high risk features of squamous cell carcinoma?

A

don’t need to know all of this esp the second box
but j in case

79
Q

What tumour mimics SCC?

A

Keratoacanthoma

Difficult to distinguish clinically and histologically from squamous cell carcinoma

80
Q

What is keratoacanthoma?

A

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

81
Q

How are keratoacanthomas resolved?

A

resolves itself slowly over time

but excisions occur often

82
Q

Where do most keratoacanthomas occur?

A

Most occur on head or neck / sun exposed areas

83
Q

What are the investigations for SCC?

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

84
Q

What are the differential diagnoses for SCC?

A

basal cell carcinoma
viral wart
merkel cell carcinoma

85
Q

What is the treatment for non-metastatic SCC?

A

Examination of rest of skin and regional lymph nodes

Excision

Radiotherapy
- Unresectable
- High risk features e.g. perineural invasion

86
Q

What is the secondary prevention for SCC?

A
  • Skin monitoring advice
  • Sun protection advice
87
Q

What do you give for metastatic SCC?

A

cemiplimab

88
Q

What are the main subtypes for basal cell carcinoma? (6)

A
  • Nodular
  • Superficial
  • Morpheic
  • Infiltrative
  • Basisquamous
  • Micronodular
89
Q

What is the most common subtype of BCC?

A

nodular

90
Q

How does nodular BCC present typically?

A

Typically presents as shiny, pearly papule or nodule

91
Q

How would you describe superficial BCC?

A

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

92
Q

What does a morphoeic BCC look like?

A

(looks like a scar and grows rapidly)

  • Less common
  • Slightly elevated or depressed area of induration
  • Usually light-pink to white in colour
  • More aggressive behaviour
  • Extensive local destruction
93
Q

What histological features does basisquamous have?

A

Histological features of both basal cell carcinoma and squamous cell carcinoma

94
Q

Describe micronodular BCC?

A
  • Resembles nodular basal cell carcinoma clinically
  • More destructive behaviour – high rates of recurrence and subclinical spread
95
Q

What are the investigations of BCC?

A

Often clinical diagnosis sufficient

Diagnostic biopsy may be taken

96
Q

What are the differential diagnoses for BCC?

A

SCC
adnexal (sebaceous) carcinoma
Merkel cell carcinoma

97
Q

What is the difference between SCC and BCC (google)?

A
98
Q

What is the treatment for BCC?

A

Standard surgical excision

Mohs micrographic surgery
- Recurrent basal cell carcinoma
- Aggressive subtype (morphoeic/ infiltrative / micronodular)
- Critical site

Other options:
- Topical therapy e.g. 5-Fluorouracil, Imiquimod
- Photodynamic therapy
- Curettage
- Radiotherapy
- Vismodegib

99
Q

What does vismodegib do?

A

selectively inhibits abnormal signalling in Hedgehog (Hh) pathway

100
Q

Types of surgery for BCC, which is better?

A

Bread loafing method

Mohs micrographic surgery

Mohs is better, but takes longer and you have to be very skilled
- 2nd image

101
Q

Why is merkel cell carcinoma named after merkel cell?

A

Origin cell not a Merkel cell –

are highly anaplastic cells which share features with neuroectodermally derived cells (including Merkel cells) (I don’t really get this part bu hey ho! its not a merkel cell cancer)

102
Q

What are most MCC associated with?

A

80% are associated with polyomavirus

103
Q

Where are MCC most common on the body?

A

head and neck region of older adults

104
Q

What is the growth and appearance of MCC?

A

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

105
Q

What is the behaviour like of MCC?

A

Aggressive, malignant behaviour

> 40% develop advanced disease/ metastasis

BRS DERMATOLOGY (8 decks)

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