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Dermatology > Skin Cancer > Flashcards

Skin Cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

what are the majority of skin cancers- melanoma or non melanoma

A

non melanoma- esp basal cell

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2
Q

what do non melanoma skin cancers arise from

A

keratinocytes within the epidermis

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3
Q

what do basal cell skin carcinomas arise from

A

keratinocytes within the basal layer of the epidermis

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4
Q

where do squamous cell skin cancers arise form

A

suprabasal layer of the skin

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5
Q

where are melanocytes

A

scattered along the basal layer of the epidermis

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6
Q

what is the most serious form of melanoma

A

melanoma

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7
Q

why are skin cancers becoming more common

A

cheap air travel, more leisure time, sun-seeking behaviour, ageing population

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8
Q

what percentage of cancers in UK are skin

A

one third

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9
Q

what facts show melanoma is so serious

A

only 6% of skin cancers but 75% of skin cancer deaths

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10
Q

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

A

melanoma

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11
Q

why are malignant melanomas more likely to metastasise than keratinocyte skin cancers

A

as melanocytes migrate into the skin from the neural crest and are motile cells that move around (unlike keratinocytes)

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12
Q

what does melanoma survival depend on

A

tumour depth- breslow thickness

less than 1mm 5 year survival 95-100%
greater than 4mm 50%

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13
Q

what is the ABCDE rule for malignant melanomas

A 
Asymmetry
Border
Colour
Diameter
Evolution
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14
Q

a diameter of more than what is a high risk melanoma

A

6/7mm

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15
Q

how quickly will melanomas change

A

weeks and months

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16
Q

what is the ugly duckling sign

A

a lesion that looks different to all the others

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17
Q

why are moles important

A

genetic predisposition to getting skin cancer

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18
Q

name 2 types of non melanoma skin cancer

A

basal cell carcinoma

squamous cell carcinoma

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19
Q

describe basal cell carcinomas

A

slow growing lump or non healing ulcer (shiny lumps)
painless, often ignored
locally invasive, doesnt spread- treated with surgery

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20
Q

describe squamous cell carcinomas

A

warty/ crusty lump/ ulcer
arises from sun damaged skin
grow slower than basal, may be painful or bleed
if neglected may spread

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21
Q 
name the cancer:
pearly/ transulcent 
visible, arborising blood vessles
central (rodent) ulceration
locally invasive, rarely metastasise
A

basal cell carcinoma

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22
Q

how else can basal cell carcinomas present

A

scaly plaque, superficial
nodular or nodulocystic
inflitrative ‘morphoeic’ (hard to see and define outline)
pigmented

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23
Q 
name the cancer 
hyperkeratotic (crusted) lump/ulcer
arises on sun damaged skin 
grows relatively fast
may be painful/bleed
chance of metastasis low but poor prognosis if so
A

squamous cell carcinoma

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24
Q

what are the prescursors of squamous cell carcinoma

A

actinic keratoses and bowens disease (carcinoma-in-situ)

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25
Q

what is keratoacanthoma

A

self resolving from of SCC

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26
Q

what are where are cutaneous horns

A

squamous cell carcinoma, on top of ear

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27
Q

where is a high risk site for squamous cell carcinoma

A

ear, lip and scalp

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28
Q

where do squamous cell carcinomas metasasise to

A

lymph nodes and bone

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29
Q

what is the 5y survival rate for metastatic SCC

A

25%

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30
Q

how else can SCC present

A

chronic ulcer, scars, wounds

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31
Q

what are actinic keratoses

A

pre cancerous skin lesions

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32
Q

what are actinic keratoses associated with

A

risk of developing SCC or BCC

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33
Q

what does multiple actinic keratoses suggest

A

a field of abnormality

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34
Q

what does bowens disease look like

A

erythematous plaque

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35
Q

what are the risk factors for skin cancer

A

sun exposure
genetic predisposition (white and ginger)
immunosuprpesion
enviromental carcinogens

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36
Q

give 6 examples of environmental carcinogens

A

coal tar, smoking, radiation, aresenic, trauma, chronic ulceration

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37
Q

name 4 genetic syndromes that predispose to skin cancer

A

DNA repair syndromes (xeroderma pigmentosum)
albinism
Gorlins syndrome
epidermolysis bullosa

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38
Q

what is xeroderma pigmentosum

A

a photosensitivity disorder die to defective nucleotide excision repair
causes photodamage and neurological degeneration

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39
Q

what is gorlins syndrome

A

autosomal dominant familial cancer syndrome

early onset/ multiple BCCs

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40
Q

what defect do you get in recessive dystrophic epidermolysis bullosa

A

mitten defromities

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41
Q

what are causes of immunosupression (all immunosuppression leads in marked increase in skin cancers)

A

organ transplant treatments
haematological malignancies
immunosuppresant therapies for IBD, RA, vasculitis
HIV/AIDS

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42
Q

what is ‘transplant hands’

A

field cancerisation on the hands of transplant patients

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43
Q

what is clonal evolution

A

when a series of mutations accumulate in successive generations

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44
Q

what does field cancerisation result in

A

many different mutations and possible tumours arising from one tumour

45
Q

what are the 6 hallmarks of cancer

A

sustaining proliferation signalling

evading growth suppressors

activating invasion and metastases

enabling replicative immortality

inducing angiogenesis

resisting cell death

46
Q

what are the two emerging hallmarks of cancer

A

deregulating cellular energetics

avoiding immune destruction

47
Q

what are the enabling characteristics of cancer

A

tumour promoting inflammation

genome instability and mutation

48
Q

what is an oncogene

A

over active form of a gene that positively regulates cell division- drives tumour formation

49
Q

name two growth factors

A

RAS and RAF

50
Q

what is a proto-oncogene

A

the normal, not yet mutated, form of an oncogene

51
Q

what is a tumour suppressor

A

inactive or non functional form of a gene that negatively regulates cell division

52
Q

name two tumour suppressors

A

Rb, TP53

53
Q

what is a driver mutation

A

a mutation that drives the cancer e.g. increases mutation rate or prevents cell dying

54
Q

what does RAS do

A

growth factors bind to growth factr receptors which then activates RAS causing cell division and proliferation

turned off when no growth factors circulating

55
Q

describe oncogenic RAS

A

always activated- constantly initiating cell division and proliferation

56
Q

what is the role P53

A

tumour suppressor

  • binds to cell DNA
  • cell halts at G1 checkpoint
  • DNA repair activated
  • apoptosis triggered
57
Q

what happens if P53 is non functional

A

damaged DNA (mutations) are passed on

58
Q

what type of melanin is in yellow skin and why does it increase skin cancer risk

A

pheomelanin- doesnt absorb UV radiation, cant tan as a protective response. Freckles sign of damage

59
Q

what is the type of melanin in brown and black skin

A

eumelanin

60
Q

what happens to keratinocytes when you sunburn

A

they die, sheet of skin is replaced

61
Q

what type of UV exposure causes SCC

A

life long accumulative UV exposure

62
Q

what type of UV exposure causes BCC and MM

A

intermittant burning episodes as usually on lesser exposed sites (BCC 40% on lesser exposed, 60% MM)

63
Q

when does 80% of skin damage occur by

A

the age of 18

64
Q

when do you get UVB and UVA expsoure in scotland

A

UVB only midday summer

UVA daylight all year round

65
Q

describe how UVB and UVA and different mutagen

A

UVB direct mutagen

UVA indirect mutagen through oxidation

66
Q

what wavelength of UV is filtered by window glass

A

UVB

67
Q

can UV cause immunosuppression

A

yes

68
Q

what is the UV signature DNA damage

A

pyrimidine dimer - covalent bonds formed between adjacent bases on same DNA strand (CPDs and 6-4 photproducts) causing C-T or CC-TT mutations

69
Q

what usually removes CPDs and 6-4PP, how?

A

nucleotide excision repair

  1. Recognition of the damaged DNA
  2. Cleavage of the damaged DNA on either
    side of the photoproduct
  3. DNA polymerase fills in the gap, using
    the undamaged strand as a template
  4. DNA ligase seals the ends
70
Q

UVA causes indirect DNA damage by oxidation of DNA bases. what usually repairs oxidised bases

A

base excision repair

71
Q

what happens in oxidattive DNA damage

A

Oxidation of deoxyguanosine forming 8-oxo-deoxyguanosine

creates C to A point mutation

72
Q

how does UV exposure cause immunosuppression

A

causes secretion of immunosuppressant cytokines (IL-10) from keratinocytes and dermal DC cells (macrophages)

Lanngerhans cells depleted and loose antigen presenting ability

CD4 T cells predominate

73
Q

a mutation in what gene which is an important part of which signalling pathway is associated with BCC development

A

PTCH1

Hedgehog

74
Q

what mutations are important in melanomas

A

RAS, RAF, MAPK

75
Q

what is the treatment for actinic keratosis

A

topical treatment- aldara (immunomodulator/ efudix- cytotoxic)

76
Q

when do seborrheic keratosis develop and look lik

A

middle/ old

stuck on, warty surface, well defined

77
Q

what grows quicker BCC or SCC

A

SCC

78
Q

acantholysis + positive immunofluorescence =?

A

bullous pemphigus

79
Q

what are bowens and actinic keratosis precursors of

A

SCC

80
Q

what is a splitz naevi

A

red, usually in childre/ young adults

mostly benign

81
Q

why is a blue naevus blue

A

as melanocytes deep in dermis

82
Q

why are SCC scaly

A

have a lot of keratin

83
Q

what is a nodule in MM suggestive of

A

vertical growth phase

84
Q

what are dermatofibroma

A

very firm, common benign lesions
proliferation of dermal fibroblasts
common in middle aged/ older women, possible in response to trauma (insect bite)

85
Q

what are features of basal cell PAPILLOMAS

A

well defined, unchanging (seb keratosis)

86
Q

what is a halo naevi

A

depigmentation around the mole as immune system tries to get rid of it

87
Q

what is haemangioma

A

benign proliferation of blood vessels in the skin

88
Q

should all things removed from the skin be sent to pathology

A

YES

89
Q

what are the indications for skin biopsy

A

skin rash- to help in diagnosis

tumours- assist in diagnosis, remove malignancy, remove unwanted skin growth

90
Q

which cancer has a rolled edge

A

BCC

91
Q

do you remove dermatofibroma

A

no- benign

92
Q

how do you treat a MM

A

surgery
+ new therapies possibly
-photodynamic
- 5% imiquimod cream

further radiotherapy or chemotherapy may be needed

93
Q

what is the treatment for common pre cancers

A 
cryotherapy 
solaraze
5 FU
PDT
imiquimod
resurfacing
94
Q

what is an excision biopsy

A

when you remove the whole tumour

95
Q

how does smoking affect surgery patients

A

causes decreased wound healing

96
Q

what areas as are risky for skin surgery

A

tiger country (temples due to temporal artery)
eyelids, scalp, skin tension lines, in front of ear (facial nerve)
cosmetic effect- vermillion (lips), hairline

97
Q

what are the 5 layers of the scalp

A

skin, connective tissue, aponeurosis, loose connective tissue

98
Q

what facial nerves do shingles commonly affect

A

ophthalmic
maxillary
mandibular
(all from trigeminal nerve)

99
Q

what are the methods of local anaesthesia

A

topical cream or subcutaneous infection (nerve of field block)

100
Q

how does adrenaline help in surgery

A

prolongs anaesthesia and reduces bleeding

101
Q

how do you reduce pain during local anaesthesia

A

relax patent, topical local, fine needle, warm local, massage skin, slow injection

102
Q

what are the complications of skin biopsy

A

bleeding, wound dehiscence (wound break down), infection, scarring, motor or sensory nerve damage, loss of function

103
Q

what is electrosurgery used for

A

haemostasis and minor skin lesions e.g. skin tags

104
Q

what is a snip excision

A

cut across base of lesion with scissors as lesion grasped upwards with hook

105
Q

what are the negatives of a punch biopsy

A

difficult to judge depth

round holes do not often heal well pathology sample may be too small

106
Q

what are the breslow prognostic parameters

A

<1mm good
1-4mm moderate
>4mm poor

107
Q

what is a sentinel node biopsy

A

removal of the first lymph node that the tumour could spread to to asses metastasis

108
Q

where does melanoma commonly spread to

A

skin, lung, bran and liver

Dermatology (23 decks)

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