tumours/cancers Flashcards

1
Q

what is seborrhoea keratosis

A

benign feature which is very common in ageing skin

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2
Q

what is the appearance of seborrhoea keratosis

A

“stuck on”

greasy, hyperkeratotic surface

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3
Q

what causes a seborrhoea keratosis

A

benign proliferation of epidermal keratinocytes

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4
Q

what is Gorlin’s syndrome

A

autosomal dominant familial cancer syndrome

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5
Q

what is Gorlin’s syndrome also called

A

Naevoid basal cell carcinoma

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6
Q

what are the symptoms of Gorlin’s syndrome

A
early onset/multiple BCCs
palmar pits
jaw cysts
ectopic calcification flax
skeletal abnormality
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7
Q

what is xeroderma pigmentosum

A

defect in one of seven nucleotide excision repair (NER) genes which increases susceptibility to cancer

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8
Q

what are the symptoms of xeroderma pigmentosum

A

hugely photosensitive
early onset skin cancers
photo damage
neurological damage

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9
Q

what is Bowen’s disease

A

squamous cell carcinoma in situ

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10
Q

who gets Bowen’s disease

A

mostly females

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11
Q

what is the appearance of Bowen’s disease

A

scaly, erythematous plaque
irregular border
no dermal invasion

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12
Q

what is actinic keratosis

A

very common, precancerous skin lesions associated with SSC or BCC

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13
Q

what is the appearance of Actinic keratosis

A

located on sun-exposures areas
variable epidermal dysplasia
rough, scaly patch

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14
Q

what are the two main types of skin cancer

A

melanoma

non-melanoma

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15
Q

what are the two types of non-melanoma

A

basal cell carcinoma (BCC)

squamous cell carcinoma (SCC)

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16
Q

what is cancer

A

an accumulation of abnormal cells that multiply through uncontrolled division and spread via invasion and/or distant metastasis via the blood and lymphatic systems

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17
Q

how does cancer occur

A

multi-step gene damage via dynamic colonal diversification

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18
Q

what is colonal evolution

A

a series of mutations that accumulate in successive generations

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19
Q

what is a oncogene

A

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

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20
Q

give an example of a oncogene

A

RAS

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21
Q

what is a proto-oncogene

A

normal, not yet mutation form of a oncogene

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22
Q

what is a tumour suppress gene

A

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

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23
Q

give an example of a tumour suppressor gene

A

p53

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24
Q

what are the risk factors to skin cancer

A

sun exposure/UV radiation
genetic predisposition
immunosuppression
environmental carcinogens

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25
Q

what does UVB do

A

direct DNA damage

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26
Q

how does UVB cause DNA damage

A

causes a CC to TT mutation by damaging CPDs and pyrtomodone-pyrimidome

27
Q

how are CPDs and pyrtomodone-pyrimidome formed

A

covalent bonding between adjacent pyrimidines of the same DNA strand

28
Q

how is UVB damage repaired

A

nucleotide excision repair (NER) however this is error prone

29
Q

what does UVA do, why

A

indirect oxidative damage as it penetrates more deeply into the skin

30
Q

how does UVA cause damage

A

DNA bases are oxided especially deoxyguanosien to form 8-oxo-deoxyguanosine

this causes a GC to AT mutation

31
Q

how is UVA damage repaired

A

base excision repair (BER)

32
Q

give examples of genetic conditions which was predisposed you to skin cancer

A
albinism 
Gorlin's syndrome 
xeroderma pigmentosum
Bowen's disease
actinic keratosis 
epidermoylsis bullosa
33
Q

why would someone be immunosuppressed

A

genetic condition
UC and crohn’s
organ transplant
chronic UV exposure

34
Q

why does chronic UV exposure cause immunosuppression

A

langerhans cells are depleted and their ability to present antigens is reduced. there is a reduction in secretion of anti-inflammatory cytokines

35
Q

what is the most serious type of skin cancer

A

melanoma

36
Q

who gets melanoma

A

young-middle aged.

more common in females

37
Q

what cells cause melanoma

A

arises from melanocytes scattered along the basal layer

38
Q

what does survival depend on

A

tumour depth

ucleration

39
Q

what is breslow’s thickness

A

the deepest point a tumour is from the granular layer in mm

40
Q

what is the 5 yr survival rate for breslow thickness <1mm

A

95-100%

41
Q

what is the 5 yr survival rate for breslow thickness >4mm

A

50%

42
Q

what is the 5 yr survival rate for metastases

A

5%

43
Q

what are the 4 types of melanoma

A
  1. superficial
  2. acral/mucosal lentiginous
  3. lentigo meligna sun-damaged
  4. nodular
44
Q

how do all melanoma types develop (apart from nodular)

A

grow as macules before the cells invade the dermis forming expansile masses with mitoses

45
Q

how do nodular melanoma develop

A

they are simple tumours of nodular tissue

46
Q

what is the ABCDE of skin cancer

A
Asymmetry
irregular Border
dark and/or multiple Colours
large Diameter
Evolution
47
Q

what is the treatment of melanoma

A

primary excision
sentinel node biopsy
regional lymphadenectomy
targeted drugs

48
Q

what are the margins required if <1mm thick

A

1cm

49
Q

what are the margins required if >1mm thick

A

2cm

50
Q

when would you do a sentinel node biopsy

A

if >1mm thick or mitoses are present

51
Q

when would you do a regional lymphadenectomy

A

if sentinel node biopsy is positive

52
Q

what is the most common type of cancer

A

Basal cell carcinoma (BCC)

53
Q

where does BCC arise from

A

keratinocytes within the basal layer

54
Q

what mutation causes BCC

A

mutation of PCHT1

55
Q

what are the main subtypes of BCC

A

nodular
superficial
infiltrative (morphoeic)

56
Q

describe the appearance of a infiltrative BCC

A

poor margins which will make resection difficult

57
Q

describe the general appearance of BCC

A
located on sun-exposed sites
Slow growing lump or non-healing ulcer
May be shiny 
Central ulceration “rodent ulcer”
Translucent, pearly with visible blood vessels. 
Painless
58
Q

describe the appearance of a superficial BCC

A

scaly plaque

59
Q

what is the treatment for BCC, why?

A

excision as they almost never metastasise

60
Q

where does SSC arise from

A

suprabasal layer

61
Q

what are the precursors to SSC

A

bowen’s disease
actinic keratosis
viral lesions (HPV)

62
Q

describe the appearance of SSC

A
Warty/crusty lump or ulcer
Grows faster
Bleeding
Pain
Poorly differentiated (rare) = high risk 
Well differentiated (common) = low risk 
Ear, lip and scalp are high risk sites
63
Q

what is the treatment of SSC

A

removal then test to see if it’s spread