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Dermatology > Skin Cancer > Flashcards

Skin Cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

Skin cancer (all types) are on the increase in Scotland, true or false

A

TRUE

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2
Q

What is the connection between the ageing population and skin cancer

A

There is a larger population of people with many years of UV exposure
Cumulative damage is a cause of the cancer

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3
Q

What is the most common cancer in 15-24 year olds

A

Melanoma

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4
Q

Which property of melanocytes makes melanoma so dangerous

A

They are motile cells that can migrate
This means melanoma is much more likely to spread
Once it has metastasised it is very hard to treat

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5
Q

What measurement is used to determine prognosis of melanoma

A

Breslow thickness
Measures how deep in the skin layer the melanoma has gone from the granular layer
Thicker = worse prognosis

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6
Q

What is the chance of survival once melanoma has metastasised

A

5%

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7
Q

What is the ugly duckling sign

A

Can be a sign of melanoma

A skin mole/lesion that does not look like any others on the body

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8
Q

Do BCC’s usually spread widely

A

No
Usually only invade locally and are very slow growing
Can be locally destructive though

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9
Q

How are BCC’s usually treated

A

Skin surgery - Standard excision or Mohs surgery

Non-surgical – Imiquimod (topical), PDT, cryotherapy

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10
Q

Name some different types of BCC

A

Superficial - looks like a scaly plaque, often multiple and on the trunk
Nodular - classic and most common
Infiltrative -ill-defined border (most dangerous)
Pigmented

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11
Q

What are some high risk sites for SCC

A 
Ear
Scalp 
Lip 
Hands 
Sun exposed sites
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12
Q

What is a cutaneous horn

A

A large deposit of keratin
Protrudes from skin
Well demarcated
Early SCC

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13
Q

Where can SCC spread to

A

First go to lymph nodes

Bone

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14
Q

What is the survival rate for metastatic SCC

A

25%

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15
Q

What must you consider in a leg ulcer that doesn’t heal

A

SCC

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16
Q

What is Bowen’s disease

A

Carcinoma in situ - intra-epidermal squamous cancer
Precursor to SCC - often more aggressive forms
Appears as a scaly patch/plaque with an irregular border
Most commonly lower legs elderly females

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17
Q

What gene is mutated in xeroderma pigmentosum

A

Nucleotide excision repair gene
Means sufferers cannot repair damaged DNA
Much higher cancer risk

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18
Q

What are some of the early symptoms of xeroderma pigmentosum

A 
Acute sunburn reaction on minimal exposure 
Hugely photosensitive 
Solar lentigines at early age 
Dryness 
Atrophy
Actinic keratoses
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19
Q

What does Type VII collagen deficiency increase your risk of

A

You get a lot of blistering as less collagen to anchor dermis and epidermis
High risk of SCC in wounded areas

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20
Q

What are some methods of skin cancer prevention

A

Behaviour - avoid midday, stay in shade
Clothing - cover up
Sunscreen
Check skin regularly

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21
Q

define cancer

A

An accumulation of Abnormal cells that multiply through uncontrolled cell division and spread to other parts of the body by invasion and/or distant metastasis via the blood and lymphatic system

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22
Q

how does cancer occur (generally)

A

Multi-step gene damage

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23
Q

what are the hallmarks of cancer

A 
Resisting cell death 
Inducing angiogenesis 
Enabling replicative immortality 
Invasions and metastasis 
evading growth suppressors
Sustaining proliferative signalling
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24
Q

What characteristics enable cancer

A

Deregulating cellular energetics - cancer needs more energy so changes metabolism
Genome instability and mutation
Avoiding immune destruction
Tumour-promoting inflammation

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25
Q

What is an oncogene

A

Over-active form of a gene that positively regulates cell division
Drives tumour formation

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26
Q

What is a protooncogene

A

the normal, not yet mutated,
form of an oncogene
In normal

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27
Q

What is a tumour suppressor

A

Inactive or non-functional form of a gene that negatively regulates cell division
When functioning it prevents tumour formation

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28
Q

What Is RAS signalling

A

RAS protein is in the cell membrane
When growth factors bind they switch on RAS which drives cell proliferation

If RAS gets mutated and stays on permenantly it can cause cancer

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29
Q

What scale is used to determine a persons skin type

A

The Fitzpatrick skin type scale

Goes from 1-6

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30
Q

What are the 2 ‘types’ of melanin

A

Eumelanin - black/brown pigment

Pheomelanin - yellowish pigment

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31
Q

What is the consequence of paler skin types producing pheomelanin

A

It doesn’t absorb UV as well as eumelanin so paler skin types are more likely to burn

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32
Q

What sun exposure pattern is SCC most associated with

A

Life-long cumulative exposure
Occurs in sun exposed areas
Outdoor workers
Elderly

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33
Q

What sun exposure pattern is BCC and melanoma most associated with

A

Intermittent bursts of sun exposure
Frequent holidays
Sunbeds

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34
Q

What causes a 4 fold increase in melanoma risk

A

childhood sunburn

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35
Q

What is the difference in the damage caused by UVA and UVB

A

UVA causes indirect damage to DNA

UVB causes direct

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36
Q

How is DNA usually repaired

A

NER detects and cleaves the damaged DNA
DNA polymerase fills the gap
DNA ligase joins edges

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37
Q

How is UV immunosuppressive

A

Keratinocytes will start to secrete immunosuppressive cytokines after UV exposure
Depletion of Langerhans cells in the skin and reduced ability to present antigens

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38
Q

Which mutation is associated with BCC formation

A

Mutations in PTCH1

Key part of hedgehog pathway

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39
Q

Which mutations are associated with melanoma

A

Mutations in the Ras/Raf/MAPK pathway

This signalling pathway leads to cell division and proliferation

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40
Q

Which gene targeted therapies are available for melanoma

A

Braf mutation inhibitor Vemurafenib

MEK inhibitors

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41
Q

Which components of the skin can skin tumours arise from

A 
epidermis 
melanocytes 
dermis
appendages 
lymphoid elements
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42
Q

what is the ration of melanocytes to basal keratinocytes

A

Somewhere between 1:5 and 1:10

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43
Q

Mutations in the MC1R gene increase your risk of melanoma - true or false

A

True

People with these mutations are freckly or red heads

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44
Q

Which people are ephilides most common in

A

Fair skinned
Red heads
ephilides are freckles!

45
Q

Where do actinic lentigines usually appear

A

Face, forearms and dorsal hands

46
Q

which naevi are at higher risk of becoming cancerous

A

More complex, larger naevi

More melanocytes involved

47
Q

How do naevi progress through stages of development

A

Start as junctional in childhood
May become compound in adolescence
Finally intradermal in adulthood
Melanocytes move down from DEJ into dermis

48
Q

Describe sporadic dysplastic naevi

A

Not inherited
One to several
Slightly increased risk of melanoma

49
Q

Describe familial dysplastic naevi

A

Will have lots of lesions
autosomal inherited condition
strong FH of melanoma
Risk is significantly increased

50
Q

Describe dysplastic naevi

A

Both architecture and cells are atypical
Get fibrosis and inflammation
Epidermis not affected

51
Q

What are halo naevi

A

Naevi with a peripheral halo of depigmentation - paler circle
Contain a lot of lymphocytes

52
Q

What are blue naevi

A 
Relatively uncommon 
Entirely dermal - deep 
Appear bluish in colour
Turn up in odd places
Contain pigment rich dendritic cells
53
Q

What are Spitz naevus

A

Occur in the under 20’s
Made of large spindle or epithelioid cells
Closely mimic melanoma but are usually benign

54
Q

How does most melanoma arise

A 
From de novo mutations 
Acquired rather than genetic 
Usually through UV exposure 
Fairer skin is higher risk 
May occur in existing mole
55
Q

Where does melanoma most commonly appear

A 
Sun exposed sites 
Scalp
Face
Neck 
Arm 
Trunk 
Leg
56
Q

Which factors would make you suspect melanoma

A 
Asymmetry 
Border - irregular 
Colour - Irregular pigmentation/ multiple colours
Diameter - >6mm
Elevation/ Evolution

Bleeding
Development of satellite nodules
Ulceration
New pigmented lesion develops in adulthood

57
Q

Where does acral/mucosal lentiginous melanoma occur

A

Palms and soles
Nailbeds
Mucosal surfaces

58
Q

Where does lentigo maligna melanoma occur

A

Face
Neck
Scalp
Sun damaged skin

59
Q

Which melanomas can metastasise

A

Only those that have entered vertical growth phase
All types can progress to this
Nodular will already be in this phase - start out in vertical

60
Q

Describe nodular melanoma

A

Will go straight into vertical growth phase
No evidence of radial growth phase
sometimes considered more aggressive

61
Q

What factors can indicate poor prognosis

A 
Presence of ulceration 
high Breslow thickness 
high mitotic rate 
lymph/vascular invasion 
satellites 
Node involvement
62
Q

Which paths can melanoma use to spread

A

Local dermal lymphatics - get satellite lesions
Mets to lymph nodes
Spread through the blood - can go anywhere in body

63
Q

How do you treat melanoma

A

Primary excision to give clear margins
Some also receive a sentinel node biopsy
If SN positive - regional lymphadenectomy

Mau also use chemo, immunotherapy or genetic therapy in advanced disease

64
Q

What causes seborrheic keratosis

A

A benign proliferation of epidermal keratinocytes

Get thickened skin, hyperkeratosis

65
Q

Palisading or picket fencing is a key histological sign of what condition

A

BCC

66
Q

Who is most likely to present with Bowen’s disease

A

Females

Mostly on lower leg

67
Q

What actinic keratosis

A

Common lesion which can be a precursor to invasive SCC
Occurs on sun exposed skin - scalp, face and hands
Appears as a hyperkeratotic area
Variable epidermal dysplasia - atypical lesions

68
Q

What are some viral precursors to skin cancer

A

Viral genital lesions are often dysplastic

HPV is often involved

69
Q

what are some adverse prognostic features of SCC

A

thickness greater than 4mm
Lymphatic/vascular space invasion
Some sites have a poorer - scalp. ear, nose

70
Q

What are the 5 main ways a skin disease could affect quality of life

A 
Physical comfort - itch 
Acceptability to self and others 
Emotional well being 
Social functioning 
Confidence
71
Q

What is a primary skin disease

A

One that is precipitated or exacerbated by emotional factors

72
Q

What is a secondary psychiatric illness

A

One that is arising from or exacerbated by primary skin disease

73
Q

What is the biopsychosocial model

A

That genetic, psychiatric and environmental factors overlap when causing a condition

74
Q

What is Morgellons syndrome

A

A psychiatric skin manifestation where people think they are infested with bugs etc

75
Q

How would you manage the psychological aspects of a skin disease

A 
Listen to the patient 
Empathise - be genuine 
Cover ICE 
Check for other social factors etc 
Carry out psych assessment if necessary
76
Q

What are the indications for skin biopsy

A

Rashes - to help diagnose

Tumours - help diagnose, remove malignancy or remove unwanted skin growths

77
Q

What is a dermatofibroma

A

Benign nodule on skin

Firm to touch

78
Q

why might biopsy of a rash not provide a diagnosis

A

Different conditions can have similar histology - e.g. different types of eczema
One condition can have several histology patterns

79
Q

What are some potential treatments for skin conditions/ lesions

A 
Drug therapy 
Cryotherapy 
Phototherapy 
Surgery 
Chemo/radiotherapy
80
Q

How is 5% imiquimod cream used

A

Can be used to treat skin cancer
Causes regression of the tumour
Not the first choice of treatment as it doesn’t always work

81
Q

How do you treat non-melanoma skin cancer

A

Traditionally surgery

Some new treatments becoming available - e.g. imiquimod cream

82
Q

How do you treat melanoma skin cancer

A

Initially surgical excision +/- sentinel node biopsy

May need further surgery, radiotherapy or chemo

83
Q

What are the 5 layers of the scalp

A 
Skin 
Connective tissue 
Aponeurosis 
Loose connective tissue 
Periosteum
84
Q

What are the different methods of local anaesthesia

A

Topical - takes some sensation away but doesn’t achieve complete numbness
Local infiltration
Nerve block
Field block

85
Q

What are some potential complications of skin biopsy

A 
bleeding
wound dehiscence
infection
scarring
motor or sensory nerve damage
loss of function
86
Q

List some basic skin surgery methods

A 
Electrosurgery 
Snip excision 
Curettage 
Shave excision 
Punch biopsy 
Elliptical excision 
Laser
Photodynamic
87
Q

What are the pros and cons of a punch biopsy

A

quick
produces good wound edges

Difficult to judge depth
Round holes don’t heal well
Sample may be too small

88
Q

What is a sentinel node biopsy

A

Inject dye to area and it allows you to track the first node that the cancer cells would get to
Determine area for node biopsy to check for spread

89
Q

Describe the typical appearance of a nodular BCC

A

Well defined nodule with
Shiny or pearly surface
Rolled edges
Telangiectasia - dilated surface capilliaries
Develops central ulceration and necrosis
May have flares - weepy, sore etc

90
Q

Describe the typical appearance of a SCC

A

Lesions are scaly, sometimes warty, poorly defined and can ulcerate and be tender
Will expand
Often arises on a background of sun damaged skin or precancerous lesion

91
Q

How does UV exposure cause cancer

A

The DNA in skin cells is damaged by UV radiation
This can lead to mutations is key genes - tumour supressor, oncogenes etc.
Solar UV also suppresses normal cell mediated immune response against tumour cells
Cancer able to develop

92
Q

SCC develops from which cell type

A

Keratinocytes - squamous cells in the epidermal layer

93
Q

List risk factors for BCC

A 
Fair skin type 
Male, older age 
Intermittent sunburn episodes 
Association between recreational sun exposure during childhood and adolescence
Immunosuppression
94
Q

List risk factors for SCC

A

Fair skin type
Cumulative exposure to sunlight ( esp. UVB)
Premalignant lesions:
- Actinic Keratoses (AK)
- Bowen`s disease -
Transplant patients on immunosuppressive therapy
Excess X-rays or other ionising radiation

95
Q

Describe a junctional naeuvus

A

Naevus is in the DEJ - made up of melanocytes
Tends to be flat or slightly elevated with smooth surface
Uniform pigmentation

96
Q

Describe a compound naeuvus

A

Naevus cells at DEJ and into dermis
Lesions slightly elevated or dome shaped, often pigmented,
Hairs may project from surface

97
Q

Describe a dermal naeuvus

A 
Naevus cells are purely in dermis 
Dome shaped, verrucous (warty), pedunculated or sessile
Often flesh-coloured
Occasionally hairy 
May display surface telangiectasia
98
Q

List features of a benign naevus

A

Well defined margin
Even pigmentation
Symmetrical
Not changing over time or changing very slowly

99
Q

List risk factors for melanoma

A 
Fair, freckled skin that doesn't tan.
Red or fair hair and light coloured eyes
Large number of moles (50-100)
Unusual, large, irregular, "dysplastic" moles
History of severe (blistering) sunburn as a child - key
Excess sun exposure 
Sunbed use 
Family history of malignant melanoma
Had previous malignant melanoma.
100
Q

What is the gold standard treatment for both BCC and SCC

A

Mohs surgery

Actually only used in specific cases - high risk or complex ares

101
Q

What are the indications for Mohs surgery

A

High-risk location - most important (face, hands, feet, genitals)
Large size
Poor border definition
Recurrent or previous incomplete resection
Immunosuppression
Aggressive histological subtype

102
Q

How is Mohs surgery performed

A

Excise lesion with small margin and examine the margin microscopically there and then
Repeat process until all margins are clear
Reduces the amount of tissue removed
Once all margins negative, the wound is closed over

103
Q

BCC arise from which cell type

A

Keratinocytes within the basal layer of

the epidermis

104
Q

How do you treat SCC

A

SSC in situ (Bowens) may be treated medically, with imiquimod/ 5-
fluorouracil creams or photodynamic therapy

Invasive = surgical excision

Mets = adjuvant radiotherapy + excision

105
Q

What is the most common type of melanoma

A

Superficial spreading

106
Q

Which skin cancer is most common in those post transplant

A

SCC

107
Q

Immunosuppression increases risk of skin cancer - true or false

A

True

108
Q

Which skin cancers can be treated non-surgically

A

Those which are superficial and non-life threatening
Superficial BCC
AK
Bowens

109
Q

What is the side effect of aldara or imiquimod

A

It triggers an inflammatory reaction so area may look worse before it gets better

Dermatology (14 decks)

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