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Dermatology Block > Cancer > Flashcards

Cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

UVB causes - - - and is

- more damaging that UVA when sun directly overhead

A

direct DNA damage

1000x

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2
Q

UVA causes - - -

UVA does what compared to UVB?

A

indirect oxidative damage

Penetrates more deeply into skin

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3
Q

UVC is blocked by ozone layer t/f

A

t

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4
Q

What can block UVB?

A

Sunscreen and window glass

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5
Q

What can block UVA?

A

Sunscreen

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6
Q

Both UVB and UVA can cause sunburn t/f

A

UVB only

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7
Q

What is the UV signature DNA damage pattern?

A

Pyrimidine dimer, covalent bonding between adjacent pyrimidines on the same DNA strand

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8
Q

Only UVB can cause pigmentation, but both uva and uvb cause skin cancer and ageing

A

both types cause pigmentation, skin cancer and ageing

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9
Q

Cells can be morphologically normal but still have abnormal genetic mutations t/f

A

T

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10
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 (accelerator) e.g. Ras, Raf, growth factor receptors

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11
Q

What is a tumor supressor gene?

A

Inactive or non-functional form of
a gene that negatively regulates cell division
Prevents the formation of a tumour when functioning normally (brake) e.g. Rb, TP53

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12
Q

Most skin cancers are melanomas t/f

A

f

mostly non melanomas

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13
Q

Melanoma most serious type of skin cancer t/f

A

t

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14
Q

skin cancer risk factors

A

UV radiation

Genetics

Age

Chemical exposure

Immune suppression

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15
Q

Chronic or long term sun exposure likely to cause which typer of cancer?

A

Squamous cell carcinoma

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16
Q

Intense intermittent
and
recreational likely to cause which typer of cancer?

A

Melanoma, Basal cell carcinoma

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17
Q

Artificial UV is likely to cause BCC t/f

A

f

all three tyes

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18
Q

What is Xeroderma pigmentosum?

A

rare autosomal recessive genetic disorder of DNA repair in which the ability to repair damage caused by ultraviolet (UV) light is deficient.

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19
Q

What is the signature DNA mutation caused by UV exposure?

A

Pyrimidine Dimer: covalent bonding between adjacent pyrimidines on the same DNA strand

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20
Q

What are the effects of UV induced immunosupression?

A

Depletion of Langerhans cells in the skin and reduced ability to present antigens

induction of regulatory T cells

Secretion of anti-inflammatory cytokines

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21
Q

What are the three stages of acquired naevi development?

A

Childhood - JUNCTIONAL NAEVUS: clusters of melanocytes at EDJ

Adolescence - COMPOUND NAEVUS: clusters as EDJ and dermis

Adult - INTRADERMAL NAEVUS: all EDJ activity ceases, entirely dermal

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22
Q

What is the gene that determines balance of pigment in skin and hair?

A

Melanocortin 1 receptor

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23
Q

Defective melanocortin 1 receptor gene causes freckles and red hair t/f

A

ONE copy = FRECKLES

TWO copies = FRECKLES & RED HAIR

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24
Q

What are ephilides?

A

freckles

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25
Q

What are actinic lentignes?

A

‘liver spots’ related to UV exposure

Inc. Melanin and melanocytes

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26
Q

Congenital naevi are always bening t/f

A

F

large lesions have a 10-15% risk of melanoma, may need surgical excision

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27
Q

How are aqcuired naevi induced in infancy?

A

Breakdown in melanocytes : keratinocyte ratio

the process is thought to be immune regulated

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28
Q

It is easy to tell the difference between dysplastic naevi and melanomas t/f

A

F

Both have variable pigment and border assymetry

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29
Q

Features of dysplastic naevi?

A

> 6mm
precursor to malignant malinoma
variable pigment
border assymetry

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30
Q

Features of halo naevi?

A
  • peripheral halo of depigmentation due to damage by inflammatory cells. Pigmented centre
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31
Q

Features of blue naevi?

A
  • entirely dermal
  • consist of pigment rich dendritic spindle cells
  • The cellular variant may have mitoses and mimic melanoma
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32
Q

Spitz naevus is always malignant

A

F
MOST ARE ENTIRELY BENIGN
there is a malignant variant

33
Q

Features of Spitz naevus?

A
  • occurs in <20yrs
  • closely mimics melanoma
  • epidermal hyperplasia (cells become spindle shaped)
34
Q

Melanoma

ABCDE?

A 
Assymetry
Border (irregular)
Colour variation
Diameter (tend to be bigger)
Evolution (fast)
35
Q

What are the four main types of melanoma?

A

Superficial spreading-commonest-trunk and limbs

Acral (peripheral body parts such as toes or fingers) or mucosal lentiginous (spread basally)

Lentigo maligna-sun-damaged face/neck/scalp

Nodular-varied sites but often trunk

36
Q

What are the two growth patterns of melanoma?

A

Radial- grows as macule, can be in sity or with dermal microinvasion

Vertical - invasion dermis forming expansile mass with mitoses. ONly this type can metastasize.

37
Q

Melanoma lesions with RGP +/- VGP include?

A

Superficial spreading
accral/mucosal
Lentigo malina

38
Q

Melanoma that are VGp only?

A

Nodular

39
Q

Prognosis melanoma largely related to?

A

Breslow thickness
Ulceration
High mitotic rate (satellites, invasion, sentinel lymph node involvement)

40
Q 
Breslow thickness
PT1?
PT2?
3?
4?
A
  1. <1mm 90%
    2, 1-2mm 80%
  2. 2-4mm 55%
  3. 4mm 20%
41
Q

Clearance and excision of melanoma:

If in-situ then clear by circa by?

A

5mm

42
Q

Clearance and excision of melanoma: If invasive but <1mm thick ?

A

1cm clearance

43
Q

Clearance and excision of melanoma: >1mm thick ?

A

2cm clearance

44
Q

What do you do if there is sentinel node involvement?

A

regional lymphadenectomy

45
Q

Some acral melanomas have - mutations and may be treated with -

A

c-kit

imatinib

46
Q

What is BRAF?

A

a cytoplasmic oncogene associated with melanomas on intermittently exposed skin.

47
Q

What are some new drugs developed to interfere with the BRAF pathway?

A

dabrafenib and vemurafenib

48
Q

seborrhoeic keratosis is very common in - skin. It is common on the - and - areas.

A

ageing, trunk, face

49
Q

What are some features of seborrhoeic keratosis?

A

Horn cysts
Acanthosis - thick skin due to hyperkeratosis
Benign
Stuck on cookie appearance - greasy hyperkeratotic surface.

50
Q

What are the histological features of seborrhoeic keratosis?

A

Horn cysts - circular things in epidermis, quite large

Acanthosis (diffuse epidermal hyperplasia and pigmentation)

Hyperkeratosis (cornlike surface of skin), flaky bits of keratosis on surface

51
Q

What are the three main subtypes of BCC?

A

Nodular
Superficial
Infiltrative (morphoeic)

52
Q

BCC is - growing, groups of cells sprout from the - and invade the -. BCC is locally - and metastsis occurs -

A

slow, epidermis, dermis, destructive, almost never

53
Q

Features of rodent ulcer?

A

it is a nodular BCC
rolled edge
ulcerated centre
pearly/shiny

54
Q

An isolated patch of “eczema” that does not respond to treatment should raise suspiscion of?

A

superficial BCC

55
Q

Infilitrativ type BCC is the most - type of BCC. It’s margins are -, it may spread a long - and resection is -. There is usually - , this where there are - blood vessels near the surface of skin.

A

aggressive, poorly defined, nerves, challenging, teleangiectasis (small dilated blood vessels near the surface of the skin)

56
Q

Infiltrative type BCC appearance?

A
  • ivory-white appearance

- scar tissue like appearnce due to desmoplasia (growth of fibrous tissue)

57
Q

Histology BCC nodular?

A

Palisading large basophilic cells (cluster together like cauliflower heads in epidermis)

58
Q

Histology BCC superficial?

A

Sprouting of dermis into epidermis

Multifocal distribution with normalised dermis - can be missed at biopsy

59
Q

Histology BCC infiltrative?

A

Little pods embedded in fibrous stroma – tumor nests in middle of strong fibrous reaction against tumor. This is called desmpolastic stroma

60
Q

What are precursors of SCC?

A

Types of dysplasia:

  • Bowen’s disease-especially on legs
  • Actinic keratosis-especially on head/neck
  • Viral lesions-especially on anogenital skin
61
Q

Clinical features of Bowen’s disease?

A
  • Discrete
  • slowly enlarging
  • pink-erythematous -
  • thin plaque/patch
  • well demarcated irregular border
  • overlying scale or crust
62
Q

Histopathology of Bowen’s disease?

A
  • Epidermis full thickness atypia
  • Basal layer present but can’t distinguish other layers
  • Huge crowded jumbled immature cells
  • No dermal invasion
63
Q

Histopathology of actinic keratosis?

A
  • parakeratosis
  • moderate squamous dysplasia
  • Atypia in upper part of epidermis
64
Q

Actinic keratosis presentation?

A

Variable epidermal dysplasia

Sun damaged skin with scaly areas

65
Q

Actinic keratosis lesions and bowenoid lesions are always different

A

F

Severely atypical lesions in AK are Bowenoid (similar to bowens disease)

66
Q

Actinic keratosis is associated with ?

A

Sun exposed skin (scalp,face,hands)

67
Q

Human papilloma virus type - is associated with dysplasia

A

16

68
Q

Viral precursors to SCC are associated with the - - virus. Lesions in the - area are often dysplastic

A

human papilloma, genital

69
Q

What is Erythroplasia of Queryat? Histological feature?

A

associated with human papillomavirus 16 and is a precursor for invasive squamous-cell carcinoma
Penile viral infection

Elevated atypical mitosis

70
Q

Squamous cell carcinoma can somtimes arise fron?

A
  • chronic leg ulcers e.g. stasis ulcers
  • sites of burns; sinuses e.g chronic osteomyelitis
  • chronic lupus vulgaris
71
Q

What are adverse prognostic features of SCC?

A

perineural spread
lymph/vasc invasion
thick >4mm
Site: eye ear nose

72
Q

Histopathology of SCC?

A

Keratinous pearls
Atypical mitosis
inflammatory infiltrate (locally destructive)

73
Q

Dermatofibrosarcoma

A

Due to genetic translocation

74
Q

Angiosarcoma

A

Bruise like

highly malignant and fatalwithin 2 yrs

75
Q

Merkel cell carcinoma

A

PRESSURE RECEPTOR BENEATH BASEMENT MEMBRANE

Neuroendocrine cell

76
Q

WHy do congenital melanocytic naevi sometimes need surgical excision?

A

If they are lare - may cause malignant/dysplastic melanoma

77
Q

What are the two types od dysplastic naevi?

A

Sporadic - risk of MM slightly raised

Familial - FH melanoma, VERY high risk

78
Q

Where does melanoma commonly occur?

A

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

79
Q

Hx melanoma?

A

Sun exposure - esp in childhood
genetic risk?
Skin colour
SUnbeds

Dermatology Block (8 decks)

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