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J Derm > Skin cancer > Flashcards

Skin cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

what are the risk factors for skin cancer (4)

A

sun exposure
age
genetics
immunosuppression

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2
Q

how does UVA increase risk of skin cancer

A

indirect oxidative damage

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3
Q

how does UVB increase risk of skin cancer

A

direct DNA damage

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4
Q

what genetic influences are there on skin cancer (3)

A

albinism
xeroderma pigmentation
naevoid basal cell carcinoma syndrome

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5
Q

what is albinism

A

do not produce melanin

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6
Q

what function does melanin have in preventing skin cancer

A

protects DNA in the basal layer form sun exposure

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7
Q

what causes xeroderma pigmentation

A

abnormal XP genes

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8
Q

why are XP (xeroderma pigmentation) genes important in preventing skin cancer

A

XP (xeroderma pigmentation) genes are needed to repair DNA damaged by sunlight

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9
Q

what is naevoid basal cell carcinoma syndrome

A

familial increased likelihood of cancer

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10
Q

what causes of immunosuppression increase skin cancer risk (3)

A

immunosuppressive drugs
autoimmune conditions (eg crohns)
organ transplant

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11
Q

how does skin cancer present in post organ transplant (immunosuppressed) patients

A

‘transplant hands’ = changes to hands may be malignant

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12
Q

which type of skin cancer is malignant

A

melanoma

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13
Q

what are the 2 type of non-melanoma skin cancer

A

basal cell carcinoma (BCC)

squamous cell carcinoma (SCC)

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14
Q

what is an oncogene

A

an overactive form of a gene = regulates cell division, can be switched off but not switched off

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15
Q

what is the difference between a proto-oncogene and an oncogene

A

a proto-oncogene can be switched on and off, an oncogene can only be switched on

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16
Q

UVB causes direct DNA damage, what happens to the damaged DNA

what happens if this doesnt occur

A

NER (nucleotide excision repair) recognises damaged DNA and ‘fills it in’

if this doesnt occur = damaged DNA is replicated = mutations arise

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17
Q

what base change usually occurs in the damaging of DNA by UVB

A

TT to CC

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18
Q

UVA causes indirect damage via what mechanism

A

oxidation of DNA bases

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19
Q

how are oxidised DNA bases usually repaired

A

by base excision repair (BER)

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20
Q

which base change usually occurs in the damaging of DNA by UVA

A

C to A

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21
Q

are melanomas more or less common than non-melanoma skin cancers

A

less

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22
Q

are melanomas more or less serious than non-melanoma skin cancers

A

more

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23
Q

are melanomas more common in young or elderly

A

young

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24
Q

are melanomas more common in males or females

A

females

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25
Q

what skin types are a risk factor for melanoma

A

skin type I/II

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26
Q

what are the 4 types of melanoma

A

superficial melanoma (SSM)
acral/mucosal lentiginous melanoma (A/MLM)
lentigo maligna melanoma (LMN)
nodular melanoma

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27
Q

which type of melanoma is most common

A

superficial melanoma

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28
Q

where do superficial melanomas present

A

trunk/limbs

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29
Q

what is the general pathophysiology of melanomas (growth phases and presentation)

A

radial growth phase (RGP) = present as macules

vertical growth phase (VGP) = invade and mitose in the dermis = present as lumps

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30
Q

in which growth phase can melanomas metastasise

A

vertical growth phase

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31
Q

what differs in the pathophysiology of nodular melanomas to the other melanomas

A

there is no horizontal growth phase

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32
Q

what differs in the presentation of nodular melanomas to the other melanomas

A

they dont present as macules, just as nodules

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33
Q

what differentiates a melanoma from a non-melanoma skin cancer (BCC or SCC)

A 
ABCDE
Asymmetry 
Border (irregular) 
Colour (>2)
Diameter (>6mm) 
Evolution (changing)
34
Q

what is the treatment of malignant melanomas

A

elliptical excision biopsy followed by further surgery/radiotherapy/chemo

35
Q

what is the pharmacological treatment of malignant melanoma (eg if surgery is contraindicated)

A

drugs to prevent cell growth

drugs that activate T cells to enable tumour cell killing

36
Q

which drugs prevent cell growth in malignant melanomas

A

end in -nib

think - you want to ‘nip it in the bud’

37
Q

which drugs activate T cells to enable tumour cell killing in malignant melanomas

A

end in -umab

38
Q

what are the signs of poor prognosis in malignant melanomas (4)

A

ulceration
lymph involvement metastasis
tumour depth (Breslow thickness >4mm)

39
Q

how is Breslow thickness measured for the prognosis of malignant melanomas

A

granular layer to deepest part of tumour

40
Q

a Breslow thickness of

A

<1mm

41
Q

a Breslow thickness of >?mm in a malignant melanoma has a poor prognosis (50% 5 year survival)

A

> 4mm

42
Q

how long does it take a malignant melanoma to be >4mm deep (Breslow thickness)

A

6 months

43
Q

is a basal cell carcinoma malignant or not

A

no

44
Q

where does a basal cell carcinoma arise from

A

keratinocytes in the basal layer of the epidermis

45
Q

what % of non-melanoma skin cancers are basal cell carcinomas

A

75

46
Q

are basal cell carcinomas fast or slow growing

A

slow growing (take years)

47
Q

what genetic mutation causes basal cell carcinomas

A

PTCH1 mutation

48
Q

what signalling pathway does a PTCH1 cause in basal cell carcinomas

A

hedgehog signalling pathway = causes cell proliferation

49
Q

what are the 3 types of basal cell carcinoma

A

nodular
superficial
infiltrative

50
Q

how does a nodular basal cell carcinoma present (3+location)

A

pearly colour
raised lesion
rodent ulcer

location - usually on face, head, neck

51
Q

how does a superficial basal cell carcinoma present (+location)

A

pink/red patch ( looks like eczema but wont go away with cream!)
crusted

location - usually trunk, shoulders

52
Q

how would you differentiate between eczema and a superficial basal cell carcinoma

A

eczema will go away with cream (emollients etc)

53
Q

how would you treat a superficial basal cell carcinoma

A

extensive surgery

54
Q

how does a infiltrative basal cell carcinoma present (+location)

A

waxy, scaly plaque
thickened skin

location - usually in middle of face

55
Q

what is the treatment for basal cell carcinoma (4)

A

vismodegib (blocks hedgehog signalling pathway = prevents proliferation)
radiotherapy
5% imiquimod cream
mohs surgery - if superficial

56
Q

what is mohs surgery

A

when the skin is biopsied throughout the surgery so that only cancerous cells are being removed

57
Q

what is the prognosis for basal cell carcinoma (good/bad)

A

good if treated

58
Q

is squamous cell carcinoma a type of melanoma

A

no

59
Q

where does squamous cell carcinoma arise from

A

keratinocytes in the epidermis (anywhere in epidermis)

60
Q

are squamous cell carcinomas fast or slow growing

A

fast growing (take months)

61
Q

where do squamous cell carcinomas arise

A

sun damaged skin (eg face, ears, hands)

62
Q

what are the precancerous lesions associated with squamous cell carcinomas (not BCCs) (2)

A

actinic keratosis

bowens disease

63
Q

what is the treatment of precancerous squamous cell carcinoma lesions

A

cryotherapy

NOT surgery

64
Q

where do actinic keratosis typically present

A

head/neck

65
Q

how does actinic keratosis present (not the same as actinic lenitigines)

A

thick, crusty or scaly skin

red

66
Q

which precancerous squamous cell carcinoma lesion presents on the shins of females as a red and scaly plaque

A

bowens disease

67
Q

where does bowens disease usually present

A

on the skins of females

68
Q

how does bowens disease present

A

red and scaly plaque

non pigmented

69
Q

how does bowens disease look on histology

A

full thickness dysplasia of keratinocytes

70
Q

if a patient present with a ‘horn’, what type of skin cancer do they have

why

A

squamous cell carcinoma

a ‘horn’ is keratinised (not BCC as they only have keratinocytes from basal layer, SCC have keratinocytes from everywhere in epidermis)

71
Q

is it worrying if a squamous cell carcinoma bleeds

A

no, treated the same as any other squamous cell carcinoma, same prognosis

72
Q

how are squamous cell carcinomas treated (2)

A

elliptical excision biopsy

5% imiquimod cream

73
Q

are squamous cell carcinomas more or less likely to spread than basal cell carcinomas

where do they spread to/via

A

more likely - can spread along nerves and cause a new tumour growth just along from the original tumour site

74
Q

is the prognosis of non-melanoma skin cancers (SCC and BCC) better or worse than melanomas

A

much better, 0.5% death rate

75
Q

is a benign seborrheic keratosis (aka seborrheic wart, basal cell papilloma) benign or malignant

A

benign tumour, will not metastasise

76
Q

how does a benign seborrheic wart present (5)

A 
stuck on appearance 
warty surface 
well defined 
keratin pearls 
greasy appearance
77
Q

do benign seborrheic warts present in the young or elderly

A

elderly

78
Q

is a merkel cell carcinoma serious

A

yes, needs removal

79
Q

which type of non melanoma skin cancer presents as ‘picket fence’ around cells on histology

A

nodular basal cell carcinoma

80
Q

what is another name for a benign seborrheic wart

A

basal cell papilloma

81
Q

which type of cancer looks as if it is ‘stuck on’

A

basal cell papilloma (seborrheic wart)

82
Q

which type of cancer has ‘horn cysts’ on histology

A

basal cell papilloma (seborrheic wart)

J Derm (23 decks)

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