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Dermatology Block > Cancer > Flashcards

Cancer 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
What are actinic lentignes?
'liver spots' related to UV exposure | Inc. Melanin and melanocytes
26
Congenital naevi are always bening t/f
F | large lesions have a 10-15% risk of melanoma, may need surgical excision
27
How are aqcuired naevi induced in infancy?
Breakdown in melanocytes : keratinocyte ratio | the process is thought to be immune regulated
28
It is easy to tell the difference between dysplastic naevi and melanomas t/f
F | Both have variable pigment and border assymetry
29
Features of dysplastic naevi?
>6mm precursor to malignant malinoma variable pigment border assymetry
30
Features of halo naevi?
- peripheral halo of depigmentation due to damage by inflammatory cells. Pigmented centre
31
Features of blue naevi?
- entirely dermal - consist of pigment rich dendritic spindle cells - The cellular variant may have mitoses and mimic melanoma
32
Spitz naevus is always malignant
F MOST ARE ENTIRELY BENIGN there is a malignant variant
33
Features of Spitz naevus?
- occurs in <20yrs - closely mimics melanoma - epidermal hyperplasia (cells become spindle shaped)
34
Melanoma | ABCDE?
``` Assymetry Border (irregular) Colour variation Diameter (tend to be bigger) Evolution (fast) ```
35
What are the four main types of melanoma?
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
What are the two growth patterns of melanoma?
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
Melanoma lesions with RGP +/- VGP include?
Superficial spreading accral/mucosal Lentigo malina
38
Melanoma that are VGp only?
Nodular
39
Prognosis melanoma largely related to?
Breslow thickness Ulceration High mitotic rate (satellites, invasion, sentinel lymph node involvement)
40
``` Breslow thickness PT1? PT2? 3? 4? ```
1. <1mm 90% 2, 1-2mm 80% 3. 2-4mm 55% 4. 4mm 20%
41
Clearance and excision of melanoma: | If in-situ then clear by circa by?
5mm
42
Clearance and excision of melanoma: If invasive but <1mm thick ?
1cm clearance
43
Clearance and excision of melanoma: >1mm thick ?
2cm clearance
44
What do you do if there is sentinel node involvement?
regional lymphadenectomy
45
Some acral melanomas have - mutations and may be treated with -
c-kit | imatinib
46
What is BRAF?
a cytoplasmic oncogene associated with melanomas on intermittently exposed skin.
47
What are some new drugs developed to interfere with the BRAF pathway?
dabrafenib and vemurafenib
48
seborrhoeic keratosis is very common in - skin. It is common on the - and - areas.
ageing, trunk, face
49
What are some features of seborrhoeic keratosis?
Horn cysts Acanthosis - thick skin due to hyperkeratosis Benign Stuck on cookie appearance - greasy hyperkeratotic surface.
50
What are the histological features of seborrhoeic keratosis?
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
What are the three main subtypes of BCC?
Nodular Superficial Infiltrative (morphoeic)
52
BCC is - growing, groups of cells sprout from the - and invade the -. BCC is locally - and metastsis occurs -
slow, epidermis, dermis, destructive, almost never
53
Features of rodent ulcer?
it is a nodular BCC rolled edge ulcerated centre pearly/shiny
54
An isolated patch of "eczema" that does not respond to treatment should raise suspiscion of?
superficial BCC
55
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.
aggressive, poorly defined, nerves, challenging, teleangiectasis (small dilated blood vessels near the surface of the skin)
56
Infiltrative type BCC appearance?
- ivory-white appearance | - scar tissue like appearnce due to desmoplasia (growth of fibrous tissue)
57
Histology BCC nodular?
Palisading large basophilic cells (cluster together like cauliflower heads in epidermis)
58
Histology BCC superficial?
Sprouting of dermis into epidermis | Multifocal distribution with normalised dermis - can be missed at biopsy
59
Histology BCC infiltrative?
Little pods embedded in fibrous stroma – tumor nests in middle of strong fibrous reaction against tumor. This is called desmpolastic stroma
60
What are precursors of SCC?
Types of dysplasia: - Bowen’s disease-especially on legs - Actinic keratosis-especially on head/neck - Viral lesions-especially on anogenital skin
61
Clinical features of Bowen's disease?
- Discrete - slowly enlarging - pink-erythematous - - thin plaque/patch - well demarcated irregular border - overlying scale or crust
62
Histopathology of Bowen's disease?
- Epidermis full thickness atypia - Basal layer present but can't distinguish other layers - Huge crowded jumbled immature cells - No dermal invasion
63
Histopathology of actinic keratosis?
- parakeratosis - moderate squamous dysplasia - Atypia in upper part of epidermis
64
Actinic keratosis presentation?
Variable epidermal dysplasia | Sun damaged skin with scaly areas
65
Actinic keratosis lesions and bowenoid lesions are always different
F | Severely atypical lesions in AK are Bowenoid (similar to bowens disease)
66
Actinic keratosis is associated with ?
Sun exposed skin (scalp,face,hands)
67
Human papilloma virus type - is associated with dysplasia
16
68
Viral precursors to SCC are associated with the - - virus. Lesions in the - area are often dysplastic
human papilloma, genital
69
What is Erythroplasia of Queryat? Histological feature?
associated with human papillomavirus 16 and is a precursor for invasive squamous-cell carcinoma Penile viral infection Elevated atypical mitosis
70
Squamous cell carcinoma can somtimes arise fron?
- chronic leg ulcers e.g. stasis ulcers - sites of burns; sinuses e.g chronic osteomyelitis - chronic lupus vulgaris
71
What are adverse prognostic features of SCC?
perineural spread lymph/vasc invasion thick >4mm Site: eye ear nose
72
Histopathology of SCC?
Keratinous pearls Atypical mitosis inflammatory infiltrate (locally destructive)
73
Dermatofibrosarcoma
Due to genetic translocation
74
Angiosarcoma
Bruise like | highly malignant and fatalwithin 2 yrs
75
Merkel cell carcinoma
PRESSURE RECEPTOR BENEATH BASEMENT MEMBRANE | Neuroendocrine cell
76
WHy do congenital melanocytic naevi sometimes need surgical excision?
If they are lare - may cause malignant/dysplastic melanoma
77
What are the two types od dysplastic naevi?
Sporadic - risk of MM slightly raised | Familial - FH melanoma, VERY high risk
78
Where does melanoma commonly occur?
sun-exposed sites scalp, face, neck, arm, trunk, leg
79
Hx melanoma?
Sun exposure - esp in childhood genetic risk? Skin colour SUnbeds

Dermatology Block (8 decks)

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