Skin Cancer Flashcards
(109 cards)
1
Q
Skin cancer (all types) are on the increase in Scotland, true or false
A
TRUE
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
3
Q
What is the most common cancer in 15-24 year olds
A
Melanoma
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
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
6
Q
What is the chance of survival once melanoma has metastasised
A
5%
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
8
Q
Do BCC’s usually spread widely
A
No
Usually only invade locally and are very slow growing
Can be locally destructive though
9
Q
How are BCC’s usually treated
A
Skin surgery - Standard excision or Mohs surgery
Non-surgical – Imiquimod (topical), PDT, cryotherapy
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
11
Q
What are some high risk sites for SCC
A
Ear Scalp Lip Hands Sun exposed sites
12
Q
What is a cutaneous horn
A
A large deposit of keratin
Protrudes from skin
Well demarcated
Early SCC
13
Q
Where can SCC spread to
A
First go to lymph nodes
Bone
14
Q
What is the survival rate for metastatic SCC
A
25%
15
Q
What must you consider in a leg ulcer that doesn’t heal
A
SCC
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
17
Q
What gene is mutated in xeroderma pigmentosum
A
Nucleotide excision repair gene
Means sufferers cannot repair damaged DNA
Much higher cancer risk
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
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
20
Q
What are some methods of skin cancer prevention
A
Behaviour - avoid midday, stay in shade
Clothing - cover up
Sunscreen
Check skin regularly
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
22
Q
how does cancer occur (generally)
A
Multi-step gene damage
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
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
25
What is an oncogene
Over-active form of a gene that positively regulates cell division
Drives tumour formation
26
What is a protooncogene
the normal, not yet mutated,
form of an oncogene
In normal
27
What is a tumour suppressor
Inactive or non-functional form of a gene that negatively regulates cell division
When functioning it prevents tumour formation
28
What Is RAS signalling
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
29
What scale is used to determine a persons skin type
The Fitzpatrick skin type scale
| Goes from 1-6
30
What are the 2 'types' of melanin
Eumelanin - black/brown pigment
| Pheomelanin - yellowish pigment
31
What is the consequence of paler skin types producing pheomelanin
It doesn't absorb UV as well as eumelanin so paler skin types are more likely to burn
32
What sun exposure pattern is SCC most associated with
Life-long cumulative exposure
Occurs in sun exposed areas
Outdoor workers
Elderly
33
What sun exposure pattern is BCC and melanoma most associated with
Intermittent bursts of sun exposure
Frequent holidays
Sunbeds
34
What causes a 4 fold increase in melanoma risk
childhood sunburn
35
What is the difference in the damage caused by UVA and UVB
UVA causes indirect damage to DNA
| UVB causes direct
36
How is DNA usually repaired
NER detects and cleaves the damaged DNA
DNA polymerase fills the gap
DNA ligase joins edges
37
How is UV immunosuppressive
Keratinocytes will start to secrete immunosuppressive cytokines after UV exposure
Depletion of Langerhans cells in the skin and reduced ability to present antigens
38
Which mutation is associated with BCC formation
Mutations in PTCH1
| Key part of hedgehog pathway
39
Which mutations are associated with melanoma
Mutations in the Ras/Raf/MAPK pathway
| This signalling pathway leads to cell division and proliferation
40
Which gene targeted therapies are available for melanoma
Braf mutation inhibitor Vemurafenib
| MEK inhibitors
41
Which components of the skin can skin tumours arise from
```
epidermis
melanocytes
dermis
appendages
lymphoid elements
```
42
what is the ration of melanocytes to basal keratinocytes
Somewhere between 1:5 and 1:10
43
Mutations in the MC1R gene increase your risk of melanoma - true or false
True
| People with these mutations are freckly or red heads
44
Which people are ephilides most common in
Fair skinned
Red heads
ephilides are freckles!
45
Where do actinic lentigines usually appear
Face, forearms and dorsal hands
46
which naevi are at higher risk of becoming cancerous
More complex, larger naevi
| More melanocytes involved
47
How do naevi progress through stages of development
Start as junctional in childhood
May become compound in adolescence
Finally intradermal in adulthood
Melanocytes move down from DEJ into dermis
48
Describe sporadic dysplastic naevi
Not inherited
One to several
Slightly increased risk of melanoma
49
Describe familial dysplastic naevi
Will have lots of lesions
autosomal inherited condition
strong FH of melanoma
Risk is significantly increased
50
Describe dysplastic naevi
Both architecture and cells are atypical
Get fibrosis and inflammation
Epidermis not affected
51
What are halo naevi
Naevi with a peripheral halo of depigmentation - paler circle
Contain a lot of lymphocytes
52
What are blue naevi
```
Relatively uncommon
Entirely dermal - deep
Appear bluish in colour
Turn up in odd places
Contain pigment rich dendritic cells
```
53
What are Spitz naevus
Occur in the under 20's
Made of large spindle or epithelioid cells
Closely mimic melanoma but are usually benign
54
How does most melanoma arise
```
From de novo mutations
Acquired rather than genetic
Usually through UV exposure
Fairer skin is higher risk
May occur in existing mole
```
55
Where does melanoma most commonly appear
```
Sun exposed sites
Scalp
Face
Neck
Arm
Trunk
Leg
```
56
Which factors would make you suspect melanoma
```
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
Where does acral/mucosal lentiginous melanoma occur
Palms and soles
Nailbeds
Mucosal surfaces
58
Where does lentigo maligna melanoma occur
Face
Neck
Scalp
Sun damaged skin
59
Which melanomas can metastasise
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
Describe nodular melanoma
Will go straight into vertical growth phase
No evidence of radial growth phase
sometimes considered more aggressive
61
What factors can indicate poor prognosis
```
Presence of ulceration
high Breslow thickness
high mitotic rate
lymph/vascular invasion
satellites
Node involvement
```
62
Which paths can melanoma use to spread
Local dermal lymphatics - get satellite lesions
Mets to lymph nodes
Spread through the blood - can go anywhere in body
63
How do you treat melanoma
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
What causes seborrheic keratosis
A benign proliferation of epidermal keratinocytes
| Get thickened skin, hyperkeratosis
65
Palisading or picket fencing is a key histological sign of what condition
BCC
66
Who is most likely to present with Bowen's disease
Females
| Mostly on lower leg
67
What actinic keratosis
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
What are some viral precursors to skin cancer
Viral genital lesions are often dysplastic
| HPV is often involved
69
what are some adverse prognostic features of SCC
thickness greater than 4mm
Lymphatic/vascular space invasion
Some sites have a poorer - scalp. ear, nose
70
What are the 5 main ways a skin disease could affect quality of life
```
Physical comfort - itch
Acceptability to self and others
Emotional well being
Social functioning
Confidence
```
71
What is a primary skin disease
One that is precipitated or exacerbated by emotional factors
72
What is a secondary psychiatric illness
One that is arising from or exacerbated by primary skin disease
73
What is the biopsychosocial model
That genetic, psychiatric and environmental factors overlap when causing a condition
74
What is Morgellons syndrome
A psychiatric skin manifestation where people think they are infested with bugs etc
75
How would you manage the psychological aspects of a skin disease
```
Listen to the patient
Empathise - be genuine
Cover ICE
Check for other social factors etc
Carry out psych assessment if necessary
```
76
What are the indications for skin biopsy
Rashes - to help diagnose
| Tumours - help diagnose, remove malignancy or remove unwanted skin growths
77
What is a dermatofibroma
Benign nodule on skin
| Firm to touch
78
why might biopsy of a rash not provide a diagnosis
Different conditions can have similar histology - e.g. different types of eczema
One condition can have several histology patterns
79
What are some potential treatments for skin conditions/ lesions
```
Drug therapy
Cryotherapy
Phototherapy
Surgery
Chemo/radiotherapy
```
80
How is 5% imiquimod cream used
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
How do you treat non-melanoma skin cancer
Traditionally surgery
| Some new treatments becoming available - e.g. imiquimod cream
82
How do you treat melanoma skin cancer
Initially surgical excision +/- sentinel node biopsy
| May need further surgery, radiotherapy or chemo
83
What are the 5 layers of the scalp
```
Skin
Connective tissue
Aponeurosis
Loose connective tissue
Periosteum
```
84
What are the different methods of local anaesthesia
Topical - takes some sensation away but doesn't achieve complete numbness
Local infiltration
Nerve block
Field block
85
What are some potential complications of skin biopsy
```
bleeding
wound dehiscence
infection
scarring
motor or sensory nerve damage
loss of function
```
86
List some basic skin surgery methods
```
Electrosurgery
Snip excision
Curettage
Shave excision
Punch biopsy
Elliptical excision
Laser
Photodynamic
```
87
What are the pros and cons of a punch biopsy
quick
produces good wound edges
Difficult to judge depth
Round holes don't heal well
Sample may be too small
88
What is a sentinel node biopsy
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
Describe the typical appearance of a nodular BCC
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
Describe the typical appearance of a SCC
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
How does UV exposure cause cancer
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
SCC develops from which cell type
Keratinocytes - squamous cells in the epidermal layer
93
List risk factors for BCC
```
Fair skin type
Male, older age
Intermittent sunburn episodes
Association between recreational sun exposure during childhood and adolescence
Immunosuppression
```
94
List risk factors for SCC
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
Describe a junctional naeuvus
Naevus is in the DEJ - made up of melanocytes
Tends to be flat or slightly elevated with smooth surface
Uniform pigmentation
96
Describe a compound naeuvus
Naevus cells at DEJ and into dermis
Lesions slightly elevated or dome shaped, often pigmented,
Hairs may project from surface
97
Describe a dermal naeuvus
```
Naevus cells are purely in dermis
Dome shaped, verrucous (warty), pedunculated or sessile
Often flesh-coloured
Occasionally hairy
May display surface telangiectasia
```
98
List features of a benign naevus
Well defined margin
Even pigmentation
Symmetrical
Not changing over time or changing very slowly
99
List risk factors for melanoma
```
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
What is the gold standard treatment for both BCC and SCC
Mohs surgery
| Actually only used in specific cases - high risk or complex ares
101
What are the indications for Mohs surgery
High-risk location - most important (face, hands, feet, genitals)
Large size
Poor border definition
Recurrent or previous incomplete resection
Immunosuppression
Aggressive histological subtype
102
How is Mohs surgery performed
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
BCC arise from which cell type
Keratinocytes within the basal layer of
| the epidermis
104
How do you treat SCC
SSC in situ (Bowens) may be treated medically, with imiquimod/ 5-
fluorouracil creams or photodynamic therapy
Invasive = surgical excision
Mets = adjuvant radiotherapy + excision
105
What is the most common type of melanoma
Superficial spreading
106
Which skin cancer is most common in those post transplant
SCC
107
Immunosuppression increases risk of skin cancer - true or false
True
108
Which skin cancers can be treated non-surgically
Those which are superficial and non-life threatening
Superficial BCC
AK
Bowens
109
What is the side effect of aldara or imiquimod
It triggers an inflammatory reaction so area may look worse before it gets better
