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Dermatology > Skin Cancer - Pathology > Flashcards

Skin Cancer - Pathology Flashcards

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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
describe the stages of naevus development
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)
26
what are the features of dysplastic naevi
architectural atypia and cellular generally >6mm in diameter variegated pigment border asymmetry
27
what are the two types of dysplastic naevi
sporadic and familial
28
describe sporadic dysplastic naevi
not inherited one to several aytpical naevi risk of MM slightly raised
29
describe familial dysplastic naevi
``` strong FH of melanoma autosomal inheritance high penetrance aytpical naevi +++ lifetime risk melanoma up to 100% ```
30
severe dysplasia in dysplastic naevi may make it hard to distinguish from what
melanoma in situ
31
what is the main feature of halo naevi
have a peripheral halo of depigmentation
32
what makes up blue naevi
pigment rich dendritic spindle cells in the dermis
33
what is the spitz naevus
made of large spindle and/or epithelioid cells | may closely mimic melanoma
34
who tends to get spitz neavus
children
35
what is seen pathologically in the spitz naevus
epidermal hyperplasia
36
what does a de novo MM mean
didn't arise from underlying naevus
37
are men or women more likely to get MM
women
38
where are MM most common
sun exposed areas- scalp, face, neck, arm, trunk, leg
39
when should you suspect melanoma has formed in a naevus
change in shape irregular pigmentation bleeding development of satellite nodules ulceration new pigmented lesion develops in adulthood
40
what are the four main types of melanoma
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
what is the radial growth phase of malignant melanoma
grow as macules when either entirely in-situ or with dermal microinvasion
42
what is vertical growth phase in MM
when melanoma cells invade the dermis forming an expansile mass with mitoses
43
only what type of MM can metastasise
those in vertical growth phase (as only then can enter blood and lymph vessels)
44
what is an in situ MM
one confined to the epidermis
45
what happens to MM when it enters the dermis
grows a nodule, metastasises
46
describe nodular melanoma
no pategoid radial growth phase- suddenly appear as lump on skin more aggressive
47
what is breslow thickness
depth of tumour from granular layer mm
48
what are prognostic indicators of MM
``` breslow thickness ulceration (strong adverse indicator) high mitotic rate lymphovascular invasion satellites sentinel lymph node involvement ```
49
what are the suffixes for ulceration
- a not ulcerated - b ulcerated e.g. pT3b
50
how do MMs spread
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
how do you treat MM
primary excision to give clear margins possible sentinel node biopsy is SNB positive regional lymphadenectomy if advanced chemo, immunotherapy, genetic therapy
52
what are the possible genetic treatments for MM
treatments for c-kit mutations (imatinib) | and BRAF mutation (dabrafenib and vemurafenib)
53
how can BRAF mutations cause cancer
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
name a benign epidermal tumour
seborrhoeic keratosis
55
name three precancerous dysplasias
bowen disease actinic keratosis viral lesions
56
name two non melanoma invasive malignancies
basal and squamous cell carcinomas
57
what are seborrhoeic keratosis
benign proliferation of epidermal keratinocytes
58
describe the presentation of seborrhoeic keratosis
very common in ageing skin on face and trunk stuck on appearance- greasy hyperkeratotic surface
59
what are three forms of seborrhoeic keratosis
epidermal acanthosis, hyperkeratosis, horn cysts
60
what is leser trelat a sign of
eruptive lesion indicating internal malignancy
61
what is seen histologically in seborrhoeic keratosis
raised epithelium due to increased proliferation of keratinocytes
62
what are the three main subtypes of basal cell carcinomas
nodular, superficial, infiltrative (morphoeic)
63
where and when do you get BCC
sun exposed sites- middle aged/ elderly
64
where do BCC's originate from
epidermis
65
describe the pathophsyiology of BCC
sprouts from epidermis, groups of cells invade dermis, peripheral pallisading around tumour edge, mitosis and apoptosis very numerous poorly defined margins
66
do BCC grow fast or slow and metastasise or not
grow slowly, locally destructive almost never metastasise
67
how can BCC kill people
by invading eye to brain | can spread along nerves
68
what type of tumour has telangiectatic vessels
basal CC
69
what is a key feature of BCC histology
peripheral palisading desmoplastic stroma (infiltrative)
70
what do BCC often look like
eczema/ impetigo
71
what do precursors of squamuous cell carcinomas show
dysplasia
72
what is bowens disease
squamous cell carcinoma in situ
73
what does bowens disease look like
scaly patch/ plaque, irregular border, no dermal invasion
74
who mostly gets bowens disease
middle age and older women
75
what is typical in histology of bowens disease
full thickness dysplasia dyskeratosis- cells keratising in epidermis
76
what is actinic keratosis
variable epidermal dysplasia
77
what are actinic keratosis commonly precursors of
invasive SCC
78
name a viral precursor of skin malignancy
viral genital lesion often dysplastic, associated with HPV
79
how aggressive is SCC
locally invasive with low but definite risk of metastasis
80
where other than sun exposed sites can SCC arise from
chronic leg ulcer, burn sites, chronic lupus vulgaris
81
what are adverse prognosis features of SCC
thickness of >4mm and poor differentiation lymphatic/ vascular space invasion perineural and intraneural spread specific sites- scalp, ear (increase lymphatic drainage), nose (columella)
82
what is a histological sign of angiosarcoma
tumour forms vessels

Dermatology (23 decks)

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