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Dermatology > Skin Cancer > Flashcards

Skin Cancer Flashcards

1
Q

State five factors that portray the impact of skin cancer on the population

A
  • size of problem
  • demographic/behavioural
  • cost of the problem
  • morbidity & mortality
  • lack of effective therapy
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2
Q

Name three types of skin cancer

A

Melanoma, squamous cell carcinoma, basal cell carcinoma

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3
Q

State four key risk factors for skin cancer

A
  1. Sun exposure
  2. Genetic susceptibility
  3. Immunosuppression
  4. Environmental factors
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4
Q

What conditions make a person more susceptible to skin cancer?

A
  • DNA repair syndromes
  • Albinism
  • Naevoid basal cell carcinoma (Gorlin’s)
  • Epidermolysis Bullosa (butterfly disease)
  • Collagen deficiency
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5
Q

Give an example of a DNA repair syndrome that is a risk factor for skin cancer

A

Xeroderma Pigmentosum

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6
Q

What patient groups are at increased risk of skin cancer?

A

Organ transplant recipients
Haematological malignancy
Specific drugs
HIV/AIDs

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7
Q

What environmental factors lead to an increased risk of skin cancer?

A

Ionising radiation
Arsenic, coal tar
Trauma, chronic wound

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8
Q

How does a skin cancer arise due to genetics?

A

Cancers originate from a single cell, genetic mutations contribute to the emergence of a cancer cell. A series of mutations accumulate in successive generations, eventually there are enough mutations for the cell to become cancerous

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9
Q

What are a series of mutations accumulating in successive generations known as?

A

Clonal evolution

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10
Q

What is an oncogene?

A

over-active form of a gene positively regulates cell division

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11
Q

Give an example of an oncogene

A

Ras, Raf

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12
Q

What is a proto-oncogene?

A

Normal not yet mutated form of an oncogene

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13
Q

What is a tumour suppressor?

A

Inactive/non-functional form of a gene that negatively regulated cell division

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14
Q

Give an example of a tumour suppressor

A

Rb, p53

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15
Q

Describe the impact of p53 on sun exposure

A

Tp53 prevents cancer by ‘fixing problems’ but damage by sun exposure results in p53 mutations leading to lack of cancer control

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16
Q

Describe the mechanism by which p53 mutations arise

A 
Cancer cell 
UVB specific damage 
Residual lesion 
Evasion of apoptosis by mutant p53 
UV driven clonal expansion leads to further mutations & thus proliferation  
Tumour formation
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17
Q

Describe how different doses/patterns of exposure often lead to different cancers

A

Chronic/long term = SCC
Recreational/burning = Melanoma/BCC
Artificial UV = SCC/BCC/Melanoma

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18
Q

What type of skin cancer does chemical exposure increase your risk for?

A

Non-melanoma

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19
Q

Describe the damage caused by UVB and what it looks like

A

Direct DNA damage to the epidermis leading to sunburn

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20
Q

Describe the damage caused by UVA and what it looks like

A

Indirect oxidative damage of DNA bases in collagen leading to ageing

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21
Q

What happens when UBV is absorbed by DNA? How does this occur?

A

Absorbed to the double helix it causes
- CPDs
- 6-4 photo-products
Both occur by the formation of coolant bonds between adjacent pyrimidines on the same DNA strand

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22
Q

How does DNA repair itself after UVB forming CPDs and 6-4PPs?

A
  1. Recognition of damaged DNA
  2. Cleavage of damaged DNA on either side of photoproduct
  3. DNA polymerase fills in the gap
  4. DNA ligase seals the end
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23
Q

What happens when UVA causes oxidative damage?

A

8 oxo dG mispairs form leading to a GC to AT point mutation

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24
Q

How does DNA repair itself when bases are oxidised?

A
  1. Recognition and cleavage by DNA glycosylase
  2. Cleavage of deoxyribose by endonuclease
  3. DNA polymerase fills gap
  4. DNA ligase seals the ends
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25
Q

How does UV cause immunosuppression?

A
  • depletion of langerhans
  • generation of UV induced T cells with immune suppressive activity
  • secretion of anti-inflammatory cytokines
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26
Q

What mutations are associated with BCC development?

A

PTCH1 mutations active hedgehog signalling to cause cell proliferation & angiogenesis

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27
Q

Name the drug that targets the hedgehog signalling pathway and can be used to treat BCC

A

Vismodegib

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28
Q

Mutations in what genes predispose to melanoma?

A

CDKN2A - prevents cells with damaged DNA replicating

CDK4 - permits cell cycle acting mutations to accelerate cell cycle

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29
Q

Where are melanocytes derived from?

A

Neural crest

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30
Q

What is the purpose of the MC1R protein?

A

Sits on cell surface and determines the balance of pigment in the skin and hair

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31
Q

Name the two main types of melanin

A

Eumelanin

Phaeomelanin

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32
Q

What is eumelanin responsible for?

A

Hair colour other than red

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33
Q

What is phaeomelanin responsible for?

A

Red hair

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34
Q

Name the portion that turns phaeomelanin to eumelanin

A

MCR1

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35
Q

What will on defective copy in MCR1 result in?

A

Freckles

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36
Q

What will two defective copies of MCR1 result in?`

A

Freckles and red hair

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37
Q

State another name for freckles

A

Ephilides

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38
Q

What are freckles?

A

Patchy increase in melanin - melanosomes produce increased melanin in response to sun exposure.

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39
Q

What are letingines?

A

Small pigmented macules as a result of increased melanocytes in the basal layer but does not darker after sun exposure - often found on sun exposed skin

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40
Q

Describe the histological finding of lentigines

A

Elongated rete pegs

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41
Q

What are the three common types of acquired melanocytic nave?

A
  • Junctional
  • Compound
  • Intradermal
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42
Q

What type of melanocytes give a navei their colour?

A

Junctional melanocytes

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43
Q

What type of melanocyte cause a naevi to be raised?

A

Dermal melanocytes

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44
Q

Describe a junctional naevus

A

Melanocytes are at DEJ only so appear dark but flat, appear in childhood

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45
Q

Describe a compound naevus

A

Melanocytes at DEJ and in dermis so appears dark and raised, appear in adolescence

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46
Q

Describe a intradermal naevus

A

Melanocytes are in the dermis only so appears raised but not dark

47
Q

Can melanocytic naevi be congenital?

A

Yes in 1% of babies usually large lesions which have up to 15% risk of melanoma therefore may need excised

48
Q

What are dysplastic naevi?

A

> 6mm diameter, variegated pigment, asymmetrical

49
Q

State two causes of dysplastic naevi

A

sporadic or familial

50
Q

Describe sporadic dysplastic naevi

A

Not inherited, risk of melanoma increased, number of atypical naevi

51
Q

Describe familial dysplastic naevi

A

Family history of melanoma, autosomal inheritance, high penetrance, 100% risk of melanoma

52
Q

State the histological appearance of dysplastic naevi

A

Architectural and cellular atypia
Fibrosis and inflammation
Epidermis not effaced

53
Q

Name three rare types of naevi

A
  • halo naevi
  • blue naevi
  • spitz naevi
54
Q

Describe a halo naevi

A

Peripheral halo of depigmentation due to lymphocytes & inflammatory regression

55
Q

Describe blue naevi

A

Entirely dermal, consists of melanin producing dendritic cells

56
Q

Describe spitz naevi

A

<20 year olds, most are benign but mimic melanoma with large spindle/epitheloid cells presents as a small red bump on face

57
Q

What are the signs of a malignant melanoma?

A

Change in shape, bleeding, ulceration, new lesion, irregular pigmentation, satellite nodules

58
Q

What do each of the letters in ABCD stand for in skin cancer diagnosis?

A

Asymmetry
Border
Colours
Diameter >6mm

59
Q

Name the instrument used to inspect a mole more closely

A

Dermatoscope

60
Q

Name four types of melanoma

A
  1. superficial spreading melanoma (trunk and limbs)
  2. Acral/mucosal lentiginous melanoma
  3. Letting maligna melanoma (sun exposed sites)
  4. Nodular melanoma
61
Q

What are the two growth phases of an melanoma?

A

Radial Growth Phase

Vertical Growth Phase

62
Q

What is the radial growth phase?

A

Macule, entirely in situ/dermal micro-invasion, no lymphatic involvement and curable

63
Q

What is the vertical growth phase?

A

Invasion of dermis to form an expansile mass, can metastasise.

64
Q

What type of melanoma only goes through VGP?

A

Nodular

65
Q

Define satellite nodules

A

Group of tumour cells near primary tumour

66
Q

What is used to predict the prognosis for a melanoma?

A

Breslow Depth

67
Q

What is Breslow depth?

A

Depth of tumour from granular layer

68
Q

State the categories and corresponding percentage survival of melanoma prognosis

A 
pTis - in situ 100% 
pT1 <1mm 90%
pT2 1-2mm 80%
pT3 2-4mm 55%
pT4 >4mm 20%
'b' added if ulceration occurs
69
Q

How will melanomas appear on histological stain?

A

Pagetoid (upward spread)
Mitosis
Melanin pigments
Melanocytes with nuclear atypia

70
Q

How will melanomas spread?

A

Local - satellite nodules
Lymphatic - lymph nodes
Blood - heart, lungs, GI tract, liver, brain

71
Q

How does melanomas be initially managed?

A

Primary excision with 2mm margin followed by wide local excision to reduce recurrence, sample should be sent for biopsy

72
Q

If lymph node spread has occurred due to melanoma what treatment is indicated?

A

Sentinel Node Biopsy

73
Q

What can be done in advanced malignant melanoma?

A

BRAF/MEK inhibitors
Systemic treatments (chemo/radiotherapy)
Immunotherapy

74
Q

Name the monoclonal antibody that can increase survival in patients with advanced melanoma

A

Ipilimumab

75
Q

What are seborrhoeic keratoses also known as?

A

Basal cell papilloma

Warts

76
Q

Who are where are seborrhoeic keratosis found?

A

Elderly patients on their trunk

77
Q

How do seborrhoeic keratosis present?

A

Superficial lesions appear greasy & stuck on, usually asymptomatic but can be itchy/inflamed/irritated after trauma

78
Q

Describe the histology of seborrhoeic keratosis

A

Proliferation of keratinocytes, acanthosis, hyperkeratosis

79
Q

What is done to manage seborrhoeic keratosis?

A

Reassurance

80
Q

What is the name given to a SCC in situ?

A

Bowen’s Disease

81
Q

Describe the appearance of Bowen’s Disease

A

Well defined inflamed scaly patch on lower limbs, irregular border looks like eczema

82
Q

What does bowen’s look like histologically?

A

Full thickness dysplasia but no dermal invasion

83
Q

How is Bownen’s disease treated?

A

Surgery if SCC suspected
Liquid nitrogen cryotherapy
Topical 5-fluorouracil
Imiquimod

84
Q

Describe actinic keratosis

A

Pre-Malignant lesions occurring on chronic light exposed skin common in fair skin individuals

85
Q

How can actinic keratosis present?

A

Usually asymptomatic but may cause an itch on be present as a cutaneous horn

86
Q

What does actinic keratosis look like and why?

A

Crumbly yellow-white scaly crusts due to dysplastic epidermal proliferation of atypical keratinocytes

87
Q

How is actinic keratosis managed?

A

Any chance in size or inflammation warrants biopsy
Surgery if SSC suspected
Cryotherpay
Topical - fluorouracil, diclofenac, imiquimod
Most commonly left and sun protection advised

88
Q

Describe viral precursors of skin cancer

A

Viral genital lesions are often dysplastic and associated with HPV
Type 1-4 common warts
Type 16 associated with dysplasia

89
Q

How can viral skin cancer precursors be treated?

A

Cryotherapy or imiquimod cream

90
Q

What is a dermatofibroma?

A

Proliferation of fibroblasts in the dermis often due to an insect bite

91
Q

How does a dermatofibroma present?

A

Firm hard nodule - may be itchy dimples when pressure exerted laterally

92
Q

Which gender is dermatofibroma more common in?

A

Females

93
Q

What is a epidermoid cyst?

A

Cysts derived from the pilar unit. Epidermal wall surrounding a core of keratin common in young to middle aged adults usually asymptomatic

94
Q

When to epidermoid cysts require treatment?

A

If they become inflamed or infected - often found on scalp

95
Q

Where are basal cell carcinomas generally found?

A

Sun-exposed sites (head and neck)

96
Q

What are the three main subtypes of basal cell carcinoma?

A
  • nodular
  • superficial
  • infiltrative/morphoeic
97
Q

Describe a nodular BCC

A

Most common type, pearly translucent papule/nodule with telangiectasia and rolled edge. Ulceration, bleeding and crusting may occur. May be pigmented causing confusion with melanoma.

98
Q

Describe a superficial BCC

A

Usually found on trunk, scaly pink - red/brown patches/papules with a pearly border

99
Q

Describe a infiltrative/morphoeic BCC

A

Scar-like waxy plaque/papule, ill defined edges. May spread along nerves with tumour extension beyond the observed clinical margins. Usually occur on the face and can have ulceration bleeding and crusting.

100
Q

What is the histological appearance of basal cell carcinomas?

A

Basal cells sprout from epidermis, groups of cells invade dermis. More dense at the periphery (palisading).

101
Q

Describe the progression of a BCC

A

Slow growing and locally destructive rarely metastases unless they invade eye and into the brain

102
Q

How is a BCC diagnosed?

A

Usually clinical diagnosis is sufficient but if doubt a biopsy is required - superficial shave is best

103
Q

What is the treatment pathway for a BCC?

A

Surgical excision is the most appropriate may require a skin graft or flap
Low risk sites can be treated by curettage or cautery
Radiotherapy for larger tumour’s
Topical therapy - cryotherapy, imiquimod or fluorouracil
Photodynamic therapy

104
Q

What surgery is indicated in morpheoic BCC?

A

Moh’s micrographic surgery

105
Q

State the risk factors for squamous cell carcinoma

A

Long term skin exposure, age (old), having fair skin

106
Q

What autoimmune condition can be associated with squamous cell carcinoma?

A

Lupus

107
Q

Where do SCCs occur?

A

Ear, lip, hands and scalp

108
Q

What do SCCs look like?

A

> 4mm indurated crusted or nodular ulcerated lesions

109
Q

Describe the histology of SCC

A

Irregular nests of epidermal cells with normal and atypical dysplastic squamous cells, keratinisation, perituoral inflammation

110
Q

How are SCCs managed?

A

Excision with 3-5mm margin or 1mm in larger lesions
Low risk can be treated with curettage or cautery
Radio or cryotherapy may also be used
Moh’s surgery may be required in high risk lesions

111
Q

What is the prognosis for SCC?

A

No mets - 30% risk of second primary SCC in 5 years
Regional lymphadenopathy <20% 10 year survival
Distant mets <10% 10 year survival

112
Q

State six complications of biopsy

A
  1. Bleeding
  2. Wound dehiscence
  3. Infection
  4. Scarring
  5. Motor/Sensory nerve damage
  6. Loss of function
113
Q

What is Moh’s micrographic surgery ?

A

Bulk of tumour is removed by curettage to create a saucer like defect, a further margin is removed from sides and base to work out if there is further excision required

Dermatology (13 decks)

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