Skin Cancer Flashcards

1
Q

2 main types of skin cancer

A

Keratinocyte skin cancer - basal cell carcinoma and squamous cell carcinoma
Melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why may the incidence of non-melanoma skin cancer in Scotland be increasing?

A

Cheap air travel
More leisure time
Sun-seeking behaviour
Ageing population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does melanoma arise from?

A

Melanocytes - pigment forming cells scattered along the basal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which skin cancer is most likely to spread - keratinocyte skin cancer or melanoma?

A

Melanoma as melanocytes migrate into the skin from the neural crest and move around

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does melanoma survival depend on?

A

Breslow thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Breslow thickness?

A

The measurement of depth of the melanoma from the surface of the skin to the deepest point of the tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

5 year survival of melanoma with:

  • Breslow thickness <1mm
  • Breslow thickness >4mm
  • Metastases
A
<1mm = 95-100%
>4mm = 50%
Metastases = 5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diagnosis of melanoma

A

ABCDE rule
“ugly duckling” sign
Dermoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ABCDE rule in diagnosis of melanoma

A
A = asymmetry
B = border
C = colour (change of colour or presence of 2/3 different)
D = diameter (>0.7mm is likely to be melanoma)
E = evolution (speed of change, changing over weeks/months)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

“Ugly duckling sign”

A

The mole suspected as being a melanoma looks very different to all other moles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is dermoscopy useful in the diagnosis of melanoma?

A

It allows us to see a magnified view showing pigment pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Atypical mole syndrome

A

Genetic condition where patients have multiple atypical moles. These patients are more likely to develop melanoma but are harder to monitor as they have so many moles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical presentation of basal cell carcinoma

A

Slow growing lumps or ulcers that are painless
‘Pearly’ or translucent
Visible, arborising blood vessels
Central ulceration
Locally invasive but rarely metastasise
Can look scar-like with ill-defined edges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Different types of basal cell carcinoma

A

May present as scaly plaque - superficial
Nodular or nodulystic
Infiltrative - “morphoeic”
Pigmented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical presentation of squamous cell carcinoma

A

Hyperkeratotic (crusty) lump or ulcer
Arises on sun damaged skin - often seen in elderly
Grow fairly fast
May be painful and/or bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Risk of metastases of squamous cell carcinoma

A

3-5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Common sites for squamous cell carcinoma (higher risk)

A

Ear, lip, scalp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Keratoacanthoma

A

Self resolving squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Precursor lesions for squamous cell carcinoma

A

Actinic keratosis

Bowen’s disease - carcinoma in situ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where to squamous cell carcinomas tend to spread to when they metastasise?

A

Lymph nodes and bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Rarer sites for squamous cell carcinoma

A

Chronic ulceration/wounds/scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Actinic keratoses

A

Pre-cancerous skin lesions. Precursors for non-melanoma skin cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What do actinic keratoses tell us about the skin?

A

That the skin is damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Actinic keratoses are highly associated with the risk of developing what?

A

Squamous cell carcinoma or basal cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is Bowen’s disease?

A

Carcinoma in situ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which type of cancer is Bowen’s disease related to?

A

Squamous cell carcinoma

27
Q

Risk factors for skin cancer

A

Sun exposure
Genetic predisposition
Immunosuppression
Other environmental

28
Q

Genetic predisposition conditions that can cause increased risk for skin cancer

A

DNA repair syndromes
Albinism
Naevoid basal cell carcinoma syndrome
Epidermolysis bullosa

29
Q

What is albinism?

A

A congenital absence of melanin.

There is absence or defect of tyrosinase

30
Q

Albinism is autosomal dominant/recessive

A

Recessive

31
Q

Other environmental factors that are risk factors for skin cancer

A
Coal tar
Smoking
Ionising radiation
Arsenic
Trauma
Chronic ulceration
32
Q

Skin cancer prevention

A

Behaviour
Clothing
Sunscreens
Regular self surveillance for early detection

33
Q

Things that fall under behaviour modification in skin cancer prevention

A

Avoid sun in its height (11am-3pm)
Use shade where possible
Particular care of babies/children
Avoid sunbeds

34
Q

Things that fall under clothing modification in skin cancer prevention

A

Tightly woven, loose fitting clothing (dark clothing)

Long sleeves, trousers, skirts, hat, sunglasses

35
Q

Information you should give about sunscreens in skin cancer prevention

A

The sunscreen should be broad spectrum (SPF 30+) with UVA protection
You usually only get a 1/3rd of the protection it says
Application is important - apply twice in sufficient quantities, re-apply after swimming or towelling

36
Q

Oncogene

A

An overactive form of a gene that regulates cell division and drives tumour formation when activity or copy number is increased

37
Q

Proto-oncogene

A

The normal, not yet mutated form of oncogene

38
Q

Tumour suppressor

A

Inactive or non functional form of a gene that negatively regulates cell division. It prevents the formation of a tumour when functioning normally

39
Q

Wavelength of UVB radiation

A

290-320nm

40
Q

What does UVB radiation cause direct damage to?

A

Causes direct DNA damage

41
Q

When is UVB radiation more damaging than UVA radiation?

A

It is 1000x more damaging than UVA when the sun is directly overhead

42
Q

Wavelength of UVA radiation

A

320-400nm

43
Q

What does UVA radiation cause indirect damage to?

A

Causes indirect oxidative damage

44
Q

True or false: UVB radiation penetrates more deeply into the skin than UVA

A

False - UVA penetrates more deeply into the skin than UVB

45
Q

Why are those with skin type I unable to tan?

A

Pheomelanin is produced instead of eumelanin, and pheomelanin absorbs UV less efficiently. Those with skin type I are unable to tan in a protective way

46
Q

Sun exposure patterns

A

> 90% on head, neck, ears, hands, forearms
Outdoor workers
Ageing population
Arises from lifetime cumulative UV exposure

47
Q

What is melanoma and basal cell carcinoma associated with, relating to UV exposure?

A

Associated with intermittent burning episodes

Also associated with subbed use

48
Q

When does up to 80% of sun damage occur?

A

In first 18 years of life

49
Q

Childhood sunburn increases the risk of melanoma by how much?

A

4-fold

50
Q

Pyrimidine dimers

A

UV induced DNA lesions

51
Q

2 types of pyrimidine dimers

A

Cyclobutane pyrimidine dimers and pyrimidine-pyrimidone photo-products

52
Q

Which type of pyrimidine dimer is more common and which is more mutagenic?

A

Cyclobutane pyrimidine dimers are more common

Pyrimidine-pyrimidone photo-products are more mutagenic

53
Q

How are pyrimidine dimers formed?

A

By covalent bonding between adjacent pyrimidines on the same DNA strand

54
Q

How are pyrimidine dimers removed?

A

Nucleotide excision repair

55
Q

Steps of nucleotide excision repair

A
  1. Recognition of the damaged DNA
  2. Cleavage of the damaged DNA on the other side of the photoproduct
  3. DNA polymerase fills the gap, using the undamaged strand as a template
  4. DNA ligase seals the end
56
Q

What happens in UV induced immunosuppression?

Regards to Langerhans cells, T cells and cytokines

A

Depletion of Langerhans cells in the skin and reduced ability to present antigen
Generation of UV induced regulatory T cells with immune suppressive activity
Secretion of anti-inflammatory cytokines by macrophages and keratinocytes

57
Q

Risk factors for UV induced immunosuppression

A

Inflammatory or autoimmune conditions
Immunosuppressants
Organ transplant recipients

58
Q

Which autoimmune conditions can increase risk of UV induced immunosuppression

A

UC - 23% higher risk of melanoma

Crohn’s - 80% higher risk of melanoma

59
Q

Immunosuppressants that can cause IV induced immunosuppression

A

Azathioprine
Cyclosporine
Adalimumab

60
Q

Exposure to which chemical materials can increase the risk of non-melanoma skin cancer?

A
Coal tar pitch
Soot
Creosote
Petroleum products
Shale oils
Arsenic
61
Q

Examples of drugs which are phototoxic

A

NSAIDs
Thiazide diuretics
Anti-TNF
Azathioprine

62
Q

Management of skin cancer

A

Sun protection
Surgery main treatment for skin cancers
Hedgehog inhibitors for BCC
Targeted responses for melanoma

63
Q

Examples of targeted therapies for melanoma

A

Vemurafenib, dabarefenib, MEK inhibitors

64
Q

What is the target for vemurafenib and dabarefinib?

A

Mutated form of B-raf