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Skin cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

What are the two main types of skin cancer?

A
  • keratinocyte skin cancer

- melanoma

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2
Q

Where does melanoma arise from?

A

From melanocytes - the pigment forming cells scattered along the basal cells

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3
Q

Where do melanocytes migrate into the skin from

?

A

The neural crest and are motile cells that move around (unlike keratinocytes)

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4
Q

Which type of skin cancer is more likely to spread (metastasize) ?

A

Melanomas

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5
Q

Melanoma survival depends on what?

A

Tumour depth (breslow thickness)

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6
Q

Describe the ABCDE rule for diagnosing melanoma

A
  • A - asymmetry
  • B - border
  • C - colour
  • D - diameter
  • E - evolution
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7
Q

What are the two types of keratinocyte (non melanoma) skin cancer?

A
  • basal cell carcinoma

- squamous cell carcinoma

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8
Q

Describe the characteristics of basal cell carcinoma

A
  • very common
  • slow growing lump or ulcer
  • painless and often ignored
  • locally invasive, but doesn’t spread
  • most can be treated by skin surgery
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9
Q

Describe the characteristics of squamous cell carcinoma

A
  • wart or crusted lump or ulcer
  • arises on sun damaged skin
  • grows faster, may be painful a/o bleed
  • if neglected may spread
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10
Q

Describe clinical presentation of basal cell carcinoma

A
  • pearly or translucent
  • visible, arborising blood vessels
  • central ulceration - rodent ulcer
  • locally invasive, but rarely metastasize
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11
Q

Name different types of BCC

A
  • may present as scaly plaque - superficial
  • nodular or nodulocystic
  • infiltrative morphoeic
  • pigmented
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12
Q

Describe the clinical presentation of squamous cell carcinoma

A
  • hyperkeratotic (crusted) lump or ulcer
  • arises or sun damaged skin; elderly
  • grow fairly fast, may be painful a/o bleed
  • majority low risk SCC
  • risk of metastasis 3-5%
  • but poor prognosis once metastatic
  • precursor lesions; actinic keratoses and bowens bdisease
  • keratoacanthoma
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13
Q

Name some high risk sites for SCC

A
  • ear is a high risk site

- lip and scalp

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14
Q

Name some risk factors for skin cancer

A
  • sun exposure
  • genetic predisposition
  • immunosuppression
  • other environmental carcinogens
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15
Q

Describe xeroderma pigmentosum

A
  • nucleotide excision repair defective
  • neuron loss
  • photosensitivity
  • photodamage
  • neurological degeneration
  • increased risk all skin cancers and other cancers
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16
Q

Describe oculocutaneous albinism

A
  • congenital absence of melanin
  • autosomal recessive
  • absence or defect of tyrosinase
  • sun sensitivity and skin cancers
  • lack of pigment in retina results in visual problems
  • visual defects including; photophobia, nystagmus, amblyobia
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17
Q

Name some factors for skin cancer prevention

A
  • behaviour
  • clothing
  • sunscreens
  • regular (self) surveillance
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18
Q

Describe clothing in terms of cancer prevention

A
  • tightly woven, loose fitting clothing (dark)
  • long sleeves, trousers, skirts
  • broad brimmed hat
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19
Q

Define cancer

A

An accumulation of abnormal cells that multiply through uncontrolled cell division and spread to other parts of the body by invasion and or distant metastasis via the blood and lymphatic system

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20
Q

What is clonal evolution?

A

A series of mutations accumulate in successive generations

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21
Q

Name the hallmarks of cancer

A
  • sustaining proliferative signalling
  • evading growth suppressors
  • activating invasions and metastasis
  • enabling replicative immortality
  • inducing angiogenesis
  • resisting cell death
  • deregulating cellular energetics
  • avoiding immune destruction
  • tumour promoting inflammation
  • genome instability and mutation
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22
Q

What is an oncogene?

A

Over-active form of a gene that positively regulates cell division
- drives tumour formation when activity or copy number is increased

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23
Q

What is a proto-oncogene?

A

The normal, not yet mutated, form of an oncogene

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24
Q

What is a tumour suppressor?

A

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

  • prevents the formation of a tumour when functioning normally (brake) eg Rb, TP53
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25
Q

UV can drive the clonal expansion of what?

A

Mutant p53 cells

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26
Q

Name some skin cancer risk factors

A
  • UV radiation
  • genetics
  • age
  • chemical exposure
  • immune suppression
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27
Q

Describe the damage of UVB

A
  • causes direct DNA damage
  • 290-320nm
  • 1000 x more damaging than UVA when sun directly overhead
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28
Q

Describe the damage of UVA

A
  • 320-400nm
  • causes indirect oxidative damage
  • UVA penetrates more deeply into the skin than UVB
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29
Q

The amount and type of what dictates your skin type?

A

Melanin

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30
Q

How many different skin types are there according to fitzpatrick skin type

A

6

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31
Q

Describe the different skin types (fitzpatrick skin type)

A
  1. always burns, never tans
  2. usually burns, can tan
  3. can burn, but usually tans
  4. always tans, never burns
  5. ‘brown’ skin
  6. ‘black’ skin
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32
Q

Describe skin type 1

A
  • very fair skin / redheads . blondes
  • pheomelanin instead of eumelanin
  • pheomelanin absorbs UV less effectively
  • unable to tan in a protective way
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33
Q

SCC arises from what exposure?

A

Life-time cumulative UV exposure

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34
Q

Who typically gets SCC?

A
  • 90% on head, neck, hands, forearms
  • outdoor workers
  • ageing population
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35
Q

Describe sun exposure patterns with melanoma and BCC

A
  • associated with intermittent burning episodes of sun exposure
  • sunbed use also increases risk
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36
Q

How much sun damage occurs during the first 18 years of life?

A

up to 80%

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37
Q

Childhood sunburn increases melanoma risk by how much?

A

4 fold

38
Q

Name the two major types of UVB induced DNA lesion

A
  • cyclobutane pyrimidine dimers (CPDs)
  • pyrimidine-pyrimidone (6-4) photo products
  • both are formed by covalent bonding between adjcaent pyrimidines on the same DNA strand
39
Q

Describe the repair of UVB induced DNA lesions

A
  • CPDs and 6-4PPs are relatively stable structures and are removed by nucleotide excision repair
40
Q

Describe nucleotide excision repair

A
  • recognition of the damage DNA
  • cleavage of the damage DNA on either side of the photoproduct
  • DNA polymerase fills in the gap, using the undamaged strand as a template
  • DNA ligase seals the ends
41
Q

Describe error prone DNA repair

A
  • unrepaired UV induced photoproducts interfere with base pairing during DNA replication leading to mutations
  • in most cases, polymerase will insert the correct bases (A-A)
  • because polymerase is error prone, it may not correctly guess the structure of the lesion and insert G-G opposite the thymidine dimer
42
Q

Describe indirect DNA damage by UVA

A
  • UVA causes indirect DNA damage via oxidation of DNA bases, especially deoxyguanosine to form 8-oxo-deoxyguanosine
  • 8-oxo-dG can mispair with deoxyadenosine rather than forming a normal base pair with deoxycytosine
  • if 8-oxo-dG is not removed, when DNA is replicated, dA rather than dC can be incorporated causing GC >AT point mutations
43
Q

Describe the repair of 8-oxo-dG lesions

A
  • oxidised bases are mainly repaired by base excision repair (BER)
  • recognition of the chemically altered base causing slight helix distortion
  • cleavage of the altered base from the deoxyribose by DNA glycosylase
  • base - free deoxyribose cleaved away from endonuclease
  • single nuclrotide gap filled by DNA polymerase beta
  • DNA ligase seals then ends
44
Q

UVB leads to direct DNA damage in what ways?

A
  • cyclobutane pyrimidine dimers (CPDs)
  • pyrimidine - pyrimidone (6-4) photo products
  • repaired by nucleotide excision repair
  • CC>TT UV signature mutation
45
Q

UVA leads to indirect DNA damage in what ways?

A
  • oxidation of deoxyguanosine forming 8-oxo-deoxyguanosine
  • repaired by base excision repair
  • C > A point mutation
46
Q

UV induced DNA damage also leads to immunosuppression how?

A
  • depletion of langerhans cells in the skin and reduced ability to present antigens
  • generation of UV induced regulatory T (T reg) cells with immune suppressive activity
  • secretion of anti-inflammatory cytokines eg IL-10 by macrophages and keratinocytes
47
Q

Occupational exposure to certain chemicals can increase the risk of non melanoma skin cancer. Name some of these chemicals

A
  • coal tar pitch
  • soot
  • creosote
  • petroleum products such as mineral oil or motor oil
  • shale oils
  • arsenic
48
Q

Name some phototoxic drugs

A
  • voriconazole (antifungal agent)
  • thiazide diuretics
  • NSAIDs
  • anti-TNF
  • azathioprine
49
Q

Describe some of the important mutations in BCC

A
  • mutations in PTCH1 re associated with BCC development
  • PTCH1 - human homologue of the drosophila gene patched
  • key component of the hedgehog signalling pathway
  • hedgehog signalling activates the transcription factors Gli 1/2, leading to induction of cell proliferation genes (cyclins D/E) and angiogenesis activators
50
Q

Describe the drug vismodegib

A
  • binds to smoothened to block hedgehog signalling and prevent cell cycle activation and angiogenesis
51
Q

Name a targeted therapy for melanoma

A

Vemurafenib (target the mutated form of B-Raf)

52
Q

Where can tumours arise from?

A
  • epidermis
  • melanocytes
  • dermis
  • appendages (adnexae)
  • lymphoid elements
53
Q

Early in embryogenesis melanoblasts mirgrate from where to where?

A
  • neural crest to
  • skin
  • uveal tract
  • leptomeninges
54
Q

When do melanoblasts form melanocyte?

A

Once settled in the skin

55
Q

Describe MC1R genetics

A
  • melanocortin 1 receptor gene is central
  • encodes MC1r protein-sites on cell surface
  • determines balance of pigment in skin and hair
  • eumelanin hair colour other than red
  • phaeomelanin causes red hair
  • MC1R turns phaeomelanin into eumelanin
  • one defective copy of MC1R causes freckling
  • two defective copes - red hair and freckles
56
Q

Describe freckles (ephilides)

A
  • patchy increase in melanin pigmentation
  • occurs after UV exposure
  • most common in fair skinned and red heads
  • reflects clumpy distribution of melanocytes
  • islands with most melanocytes tan
  • pale intervening skin has fewer melanocytes
  • have one defective copy of MC1r gene
57
Q

Describe actinic lentigines

A
  • actinic or solar lentigines
  • also known as age or liver spots
  • related to UV exposure
  • face, forearms and dorsal hands
  • epidermis elongated rete bridges
  • increase melanin and basal melanocytes
58
Q

Describe melanocytic naevi

A
  • broad range of lesions
  • may be either congenital or acquired
  • 1% of babies born with a congenital naevus
  • however most naevi acquired 1st 2nd decades
  • usual type, dysplastic, spitz, blue etc
59
Q

Describe congenital melanocytic naevi

A
  • 1-2% babies born with a congenital naevus
  • small <2cm diameter
  • medium >2cm but <20cm diameter
  • giant garment type lesions
  • large lesions 10-15% risk of melanoma
  • may need staged surgical excision
60
Q

Describe usual type acquired naevi

A
  • during infancy the melanocytes : keratinocyte ratio breaks down at a number of cutaneous sites
  • allows formation of simple naevi; very common benign lesions
  • average person has 20-30 naevi
  • common naevi have low malignant potential
61
Q

Acquired naevi develop along a well-defined path, describe this path

A
  • childhood; junctional naevus
  • adolesence / early adulthood; compound naevus
  • adulthood; intradermal naevus
62
Q

Describe junctional naevi

A
  • melanocytes proliferate
  • clusters of cells at DEJ
  • nests of melanocytes attached to epidermis
63
Q

Describe compound naevi

A
  • junctional clusters and groups of cells in dermis
64
Q

Describe intradermal naevi

A
  • all junctional activity has ceased, entirely dermal
65
Q

Describe dysplastic naevi

A
  • generally >6mm diameter
  • variegated pigment
  • border asymmetry
  • architectural atypia AND cellular atypia
  • host reaction fibrosis and inflammation
  • unlike melanoma epidermis not effaced
  • severe dysplasia may be difficult to distinguish from melanoma in situ
66
Q

Describe the 2 clinical settings of dysplastic naevi

A
  • sporadic; not inherited, one to several atypical naevi, risk of MM slightly raised
  • familial; strong FH of melanoma, autosomal inheritance, high penetrance eg CDKN2A, atypical naevi, lifetime risk melanoma up to 100%
67
Q

Describe halo naevi

A
  • have a peripheral halo of depigmentation

- they show inflammatory regression and are overrun by lymphocytes

68
Q

Describe blue naevi

A
  • entirely dermal and consist of pigment rich dendritic spindle cells
  • the cellular variant may have mitoses and mimic melanoma
69
Q

Describe the spitz naevus

A
  • rare
  • used to be called benign juvenile melanoma
  • usually occur <20 yrs
  • consist of large spindle and or epithelioid cells
  • may closely mimic melanoma
  • most are entirely benign
  • difficult area as there is a malignant variant
  • pink colouration due to prominent vasculature
70
Q

Describe the incidence of malignant melanoma

A
  • commoner in females
  • may arise at any site
  • rare in childhood
  • incidence peaks in middle age
71
Q

Describe the aetiology of malignant melanoma

A
  • role of sun exposure especially in childhood (sunburn)
  • UV exposure important in skin and eye melanomas
  • multifactorial - also genetic risk - skin colour and or dysplastic naevi
  • melanoma most common on sun exposed sites scalp, face, neck, arm, trunk, leg
  • rarely occur in eye, meninges, oesophagus, biliary tract, anus
72
Q

What sorts of complaints would make you suspect melanoma?

A
  • change in shape
  • new pigmented lesion develops in adulthood
  • ulceration
  • development of satellite nodules
  • irregular pigmentation
  • bleeding
73
Q

Describe the growth of malignant melanoma

A
  • SSM, A/MLM and LMM all
  • grow as macules when either entirely in-situ or with dermal microinvasion - this is the radio growth phase
  • eventually the melanoma cells invade the dermis forming an expansile mass with mitoses - this is VGP
  • only VGP melanomas can metastasise
74
Q

Describe nodular melanoma

A
  • no clinical or microscopic evidence of RGP
  • simply a nodule of VGP tumour
  • some consider this more aggressive
75
Q

Name the lesions with RGP +/- VGP

A
  • superficial spreading melanoma
  • acral / mucosal lentiginous melanoma
  • lentigo maligna melanoma
76
Q

Name some adverse prognostic indicators for malignant melanoma

A
  • ulceration is a strong adverse indicator
  • suffix B indicated tumour ulceration
  • high mitotic rate, lymphovascular invasion, satellites, sentinel lymph node involvement
77
Q

Describe the spread of malignant melanoma

A
  • local dermal lymphatics > satellite deposits of MM
  • regional lymph node metastases - common pattern of disease progressed, nodes excised
  • blood spread; skin soft tissue, heart, lungs, GI tract, liver, brain
78
Q

Describe the treatment of melanoma

A
  • primary excision to give clear margins
  • some also receive a sentinel node biopsy
  • if SN positive - regional lymphadenopathy
  • treatment of advanced disease difficult
  • chemo, immunotherapy, genetic therapies
79
Q

Name some epidermal tumours

A
  • benign seborrhoeic keratosis
  • precancerous dysplasias; bowens disease, actinic keratosis and viral lesions
  • invasive malinancies; basal and squamous cell carcinoma
80
Q

Describe seborrhoeic keratosis

A
  • very common in ageing skin
  • benign proliferation of epidermal keratinocytes
  • common face and trunk
  • stuck on appearance greasy hyperkeratotic surface
  • epidermal acanthosis, hyperkeratosis, horn cysts
  • eruptive appearance of many lesions may indicate internal malignancy - leser trelat sign
81
Q

Describe who gets BCC

A
  • sun exposed sites
  • UK; middle aged and elderly
  • australia; younger age groups
82
Q

Name the three main subtypes of BCC

A
  • nodular
  • superficial
  • infiltrative (morphoeic)
83
Q

Describe the progression of BCC

A
  • basal cells sprout from epidermis
  • groups of cells invade dermis
  • peripheral palisading
  • mitoses and apoptoses very numerous
  • slow growing, locally destructive
  • almost never metastases
  • may kill by invading eye > brain
84
Q

What is the most important type of BCC?

A

Infiltrative type

85
Q

Name some precursors of SCC

A
  • bowens disease; especially on legs
  • actinic keratosis; especially on head and neck
  • viral lesions; especially on anogenital skin
  • precursors show squamous dysplasia
86
Q

Describe bowens disease

A
  • squamous cell carcinoma in situ
  • female excess mostly on lower leg
  • scaly patch / plaque
  • irregular border
  • no dermal invasion
  • may mimic inflammatory conditions
87
Q

Describe actinic keratosis

A
  • very common
  • sun exposed skin esp scalp, face, hands
  • variable epidermal dysplasia
  • severely atypical lesions are bowenoid
  • common precursor of invasive SCC
88
Q

Describe viral precursors

A
  • viral genital lesions often dysplastic
  • erythroplasia ofqueryat-penile bowens
  • associated with HPV
89
Q

Where does SCC arise on the skin?

A
  • commonly; elderly, sun exposed sites (face, ears, dorsal hands), UV implicated

occasionally; chronic leg ulcers, sites of burns, chronic lupus vulgaris

rare; zeroderma pigmentosum; dystrophic variant epidermyolysis bullosa

90
Q

Describe the behaviour of SCC-

A
  • generally good prognosis
  • locally invasive
  • low but definite risk of metastasis
91
Q

Describe adverse prognostic features of SCC

A
  • thickness >4mm and poor differentiation
  • lymphatic / vascular space invasion
  • perineural spread
  • specific sites poorer prognosis; scalp, ear, nose

Dermatology (10 decks)

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