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Dermatology > Skin Cancer - Pathology > Flashcards

Skin Cancer - Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

what components of skin can give rise to tumours

A

all components

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2
Q

what type of immune cells are melanocytes

A

dendritic cells

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3
Q

where do melanocytes come from

A

melanoblasts migrate from the neural crest in early embryogenesis to skin, uveal tract and leptomeninges

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4
Q

what happens when melanoblasts settle in the skin

A

form melanocytes

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5
Q

where in skin are melanocytes

A

in the basal layer of the epidermis

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6
Q

do darker skinned people have more melanocytes

A

no, they just produce more pigment. same ration to basal keratinocyte (1:10) irregardless of race

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7
Q

where do melanocytes transfer their pigment to

A

keratinocytes

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8
Q

what does melanocortin 1 receptor gene do

A

encodes for MC1R protein which determines pigment of hair and skin

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9
Q

what pigments cause hair colour

A

eumelanin (everything but red hair)

phaeomelanin (red hair)

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10
Q

how does MC1R affect pigment

A

turns phaeomelanin into eumelanin

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11
Q

what do mutations in MC1R genes do

A 
one= freckles 
two= red hair and freckles
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12
Q

what are ephilides

A

freckles

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13
Q

what are freckles

A

patchy increase in melanin pigmentation occuring after UV exposure

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14
Q

what do freckles reflect in the skin

A

clumpy distrubution of melanocytes + sun damage

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15
Q

what are actinic or solar lentigines

A

age/ liver spots

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16
Q

where do you get actininc lentigines

A

face, forearms, dorsal hands

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17
Q

what is the pathology of actinic lentigines

A

epidermis elongated rete ridges

increase melanin and basal melanocytes

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18
Q

what are actinic lentigines due to

A

chronic sun exposure

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19
Q

when are most melanocystic naevi acquired

A

in 1st 2 decades of life

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20
Q

what are dysplastic melanocytic naevis

A

have atypical features but not melanomas

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21
Q

how many babies are born with a congenital naevus

A

1-2%

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22
Q

what do large melanocytic naevi (>20cm diameter) have increased risk of getting

A

melanoma

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23
Q

what allows for the formation of simple acquired naevi

A

during infancy the melanocyte:keratinocyte ratio breaks down at a number of cutaneous sites

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24
Q

what are simple naevi

A

very common benign lesions, average person has 20-30 naevi

low malignant potential

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25
Q

describe the stages of naevus development

A

childhood: junctional naevus- melanocytes proliferate creating clusters of cells ar DEJ

adolescence/ early adulthood: compound naevus- junctional clusters + groups of cells in dermis

adulthood: intradermal naevus- all activity has ceased, entirely dermal (flattened)

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26
Q

what are the features of dysplastic naevi

A

architectural atypia and cellular
generally >6mm in diameter
variegated pigment
border asymmetry

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27
Q

what are the two types of dysplastic naevi

A

sporadic and familial

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28
Q

describe sporadic dysplastic naevi

A

not inherited
one to several aytpical naevi
risk of MM slightly raised

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29
Q

describe familial dysplastic naevi

A 
strong FH of melanoma 
autosomal inheritance
high penetrance
aytpical naevi +++
lifetime risk melanoma up to 100%
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30
Q

severe dysplasia in dysplastic naevi may make it hard to distinguish from what

A

melanoma in situ

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31
Q

what is the main feature of halo naevi

A

have a peripheral halo of depigmentation

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32
Q

what makes up blue naevi

A

pigment rich dendritic spindle cells in the dermis

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33
Q

what is the spitz naevus

A

made of large spindle and/or epithelioid cells

may closely mimic melanoma

34
Q

who tends to get spitz neavus

A

children

35
Q

what is seen pathologically in the spitz naevus

A

epidermal hyperplasia

36
Q

what does a de novo MM mean

A

didn’t arise from underlying naevus

37
Q

are men or women more likely to get MM

A

women

38
Q

where are MM most common

A

sun exposed areas- scalp, face, neck, arm, trunk, leg

39
Q

when should you suspect melanoma has formed in a naevus

A

change in shape

irregular pigmentation

bleeding

development of satellite nodules

ulceration

new pigmented lesion develops in adulthood

40
Q

what are the four main types of melanoma

A

superficial spreading (commonest- trunk and limbs)

acral/mucosal lentiginous (acral and mucosal)

lentigo maligna (sun-damaged face/neck/scalp)

nodular (varied sites- often trunk

41
Q

what is the radial growth phase of malignant melanoma

A

grow as macules when either entirely in-situ or with dermal microinvasion

42
Q

what is vertical growth phase in MM

A

when melanoma cells invade the dermis forming an expansile mass with mitoses

43
Q

only what type of MM can metastasise

A

those in vertical growth phase (as only then can enter blood and lymph vessels)

44
Q

what is an in situ MM

A

one confined to the epidermis

45
Q

what happens to MM when it enters the dermis

A

grows a nodule, metastasises

46
Q

describe nodular melanoma

A

no pategoid radial growth phase- suddenly appear as lump on skin
more aggressive

47
Q

what is breslow thickness

A

depth of tumour from granular layer mm

48
Q

what are prognostic indicators of MM

A 
breslow thickness
ulceration (strong adverse indicator)
high mitotic rate 
lymphovascular invasion 
satellites 
sentinel lymph node involvement
49
Q

what are the suffixes for ulceration

A
  • a not ulcerated
  • b ulcerated

e.g. pT3b

50
Q

how do MMs spread

A

local dermal lymphatics (satellite deposits of MM)

regional lymph node metastases (nodes excised (radical lymphadenectomy))

blood spread (skin, soft tissue, heart, lungs, GI tract, liver, brain)

51
Q

how do you treat MM

A

primary excision to give clear margins

possible sentinel node biopsy

is SNB positive regional lymphadenectomy

if advanced
chemo, immunotherapy, genetic therapy

52
Q

what are the possible genetic treatments for MM

A

treatments for c-kit mutations (imatinib)

and BRAF mutation (dabrafenib and vemurafenib)

53
Q

how can BRAF mutations cause cancer

A

growth factors bind to GFR and activate RAF pathway which drives cells division

wild type BRAF is a proto-oncogene- if mutated drives cell proliferation by upregulating MEK and ERK

54
Q

name a benign epidermal tumour

A

seborrhoeic keratosis

55
Q

name three precancerous dysplasias

A

bowen disease
actinic keratosis
viral lesions

56
Q

name two non melanoma invasive malignancies

A

basal and squamous cell carcinomas

57
Q

what are seborrhoeic keratosis

A

benign proliferation of epidermal keratinocytes

58
Q

describe the presentation of seborrhoeic keratosis

A

very common in ageing skin on face and trunk

stuck on appearance- greasy hyperkeratotic surface

59
Q

what are three forms of seborrhoeic keratosis

A

epidermal acanthosis, hyperkeratosis, horn cysts

60
Q

what is leser trelat a sign of

A

eruptive lesion indicating internal malignancy

61
Q

what is seen histologically in seborrhoeic keratosis

A

raised epithelium due to increased proliferation of keratinocytes

62
Q

what are the three main subtypes of basal cell carcinomas

A

nodular, superficial, infiltrative (morphoeic)

63
Q

where and when do you get BCC

A

sun exposed sites- middle aged/ elderly

64
Q

where do BCC’s originate from

A

epidermis

65
Q

describe the pathophsyiology of BCC

A

sprouts from epidermis, groups of cells invade dermis, peripheral pallisading around tumour edge, mitosis and apoptosis very numerous
poorly defined margins

66
Q

do BCC grow fast or slow and metastasise or not

A

grow slowly, locally destructive

almost never metastasise

67
Q

how can BCC kill people

A

by invading eye to brain

can spread along nerves

68
Q

what type of tumour has telangiectatic vessels

A

basal CC

69
Q

what is a key feature of BCC histology

A

peripheral palisading

desmoplastic stroma (infiltrative)

70
Q

what do BCC often look like

A

eczema/ impetigo

71
Q

what do precursors of squamuous cell carcinomas show

A

dysplasia

72
Q

what is bowens disease

A

squamous cell carcinoma in situ

73
Q

what does bowens disease look like

A

scaly patch/ plaque, irregular border, no dermal invasion

74
Q

who mostly gets bowens disease

A

middle age and older women

75
Q

what is typical in histology of bowens disease

A

full thickness dysplasia

dyskeratosis- cells keratising in epidermis

76
Q

what is actinic keratosis

A

variable epidermal dysplasia

77
Q

what are actinic keratosis commonly precursors of

A

invasive SCC

78
Q

name a viral precursor of skin malignancy

A

viral genital lesion often dysplastic, associated with HPV

79
Q

how aggressive is SCC

A

locally invasive with low but definite risk of metastasis

80
Q

where other than sun exposed sites can SCC arise from

A

chronic leg ulcer, burn sites, chronic lupus vulgaris

81
Q

what are adverse prognosis features of SCC

A

thickness of >4mm and poor differentiation

lymphatic/ vascular space invasion

perineural and intraneural spread

specific sites- scalp, ear (increase lymphatic drainage), nose (columella)

82
Q

what is a histological sign of angiosarcoma

A

tumour forms vessels

Dermatology (23 decks)

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