cancer 15: skin cancer Flashcards

1
Q

Where does most skin cancer rise (describe microanatomy)

A

Epidermis
4 cell types-keratynocytes, melanocytes, (most important for cancer)
Dendritic cells and merkey cells

differentiate up from basale-(where melabocytes are) and flatten/lose nucleus as reach top
Very close to UV

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2
Q

What cells can lead to skin cancer?

A

Keratinocye derives-basal cell or squamous
Melanocyte dervied
vasculature derived
Lymphocte derived

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3
Q

What are some causes of skin cancer?

A

genetic syndromes-predisposition
eg: Gorlins syndrome-basal cell
Xeroderma Pigmentosum-cant repair DNA-multiple skin cancer

Viral infections-HHV* (herpes)0=-kaposi
HPV-sqamous cell cancer

UV radiation-BCC/SCC/malignant melanomas

immunosupressants-drugs, HIV, old age, leukemia

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4
Q

Epidiemology of malignant melanoma?

A

In white skin people-increases since 1975

In other skinned people-pretty stable and very low

higher incidence in UK in south coast-high sun exposure

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5
Q

What does basal cell carcinoma look like?

A

Glistens, pinky/greyish/reddish with dilated small vessels-can see

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6
Q

What does malignant melaboma look like?

A

Dark, uneven borders, lumpy, new

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7
Q

What form of UV exist and why is it an issue?

A

UVC is blocked by atmospthere
UVB more importan wavelength in skin carcinogenesis
UVA-100 more abundant on earth-also contributes

UVB-causes cross linking of C and T bases with same or each other
normally repaured with excision repair

If damage happens in DNA repair gens-can cause evn more damage

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8
Q

What is xeroderma pigmentosum?

A

No DNA repair mechanism-genetic mutation
very early and agressive skin cancer (before even 5)

only treatment is complete sun protection

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9
Q

What 3 types of mutation cause skin cancer?

A

Mutation that stimulate cell prolferation
Mutation that alter response to growth stimuli/repression
Mutations that affect apoptosis

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10
Q

Describe what are the 3 fates of cell after being sun damaged?

A

Either repair
Either damage too serious-apoptose
Or if mutation in repair DNA-can become cancerous

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11
Q

Whta is the relation between sun, immunology and cancer?

A

Sun depletes langerhans cells in the epidermis-cause immunosupression-> cancer can rise easier, and less cells are cleared

also used for therapy-like psoriasis-supress resposne but can increase skin cancer incidence

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12
Q

What are the 6 skin types accodring to fitzpatrick phototypes

A
1-always burns, never tan
2-usually, sometimes
3-sometimes-usually tans
IV-never burns-always tans
V-Moderate constititive tan
VI-marked constitutive tan (african)

1-2 highest chances of damage

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13
Q

What is melanin

A

Produce by melanocytes and causes skincolor
skin color is dependent on amount baseline made, NOT number of cells
melanocytes site on basal membrane of epidermis
melanin produced from tyrosin via series of enzymes

after UV, melanocytes are stimulated-melanin produced more-taken up by keratinocytes-melanin placed around nucleus giving it UV protection
ratio usually 1:6 (melano:keratino)

2 types of melanin-eumelanin and phaemelanin
eu-brown
phaeo-yellowish/reddish (what red hairs produce most of)
variation of ratio of each produces causes variation of skin color/eye/hair

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14
Q

What is a malignant melanoma? What types are there

A

Malignant tumour of melanocytes
atrypical cells and architecture
causes by UV and genetic factors
risk of metastases

nodular – melanocytes tend to spread upwards-hallmark of melanoma -risk of metastasis (high risk)
lentigo melanoma Before breach epidermis-in situ–quite common in elderly patient-flat dark patches-excise + skin graft
often irregular edges
lateral spreading malignant melanoma-invasive (less than upward)

Acral lentiginous-on wird places
Amelanomic melanoma-no pigment but is melanoma

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15
Q

What the ABCD(E) rule of malignant melanoma?

A

asymterym border irregulaty
color varyation, diamter (growing/7mm
Erythrema

ABCDE

can lose/not be pigmented-amleranomic
on feet-always flat plques-acral lentiginous

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16
Q

What does regression of malignant melanoma mean?

A

that immune system has fought back-sounds good
BUT it means that it was more agressive at this place and had a reaction–become pink/faint grey
usually means it already metastases

17
Q

What determines the prognosis for a melanoma?

A

breslow thickness-Depth of progession of the invasion
less then 1mm-thin
more than 4mm-high

18
Q

What are the main risk factors of melanoma?

A

SELF histyory of disease
family history
Inermittet burning, sunburn in child, skin type I/II

19
Q

What is keratoacanthoma?

A

types of sqaumous cell carcninoma-from keratinocyes at top of epidermis
grows very very fast-
makes keratin if well differentiated-inside crater-can go away on its own or excised

causes by UV, HPV, immunosupression, scards/scarrin

low risk of metastasis

can progress to squamous cell cacrinoma-> usualy has a horn of keratin of the top of a lump
common sites-lower lips (smoking), ears, women legs

20
Q

What are basal cell carcninomas

A

types of sqaumous cell carcninoma-from keratinocyes at bottom of epidermis
fast growing, can invade tissues but dont metastases
causes by UV, immunosupression

DOES NOT METASTASE
usually pink, rolled edge at the edge, glistening surface. see a lot of suface blood vessels that branch (arboresing)-unique to BCC

common around eye/eyelids, nose

21
Q

What is mycosis fungoides?

A

Thought it was fungus a long time ago (200 years ago)
T cell lymphoma of the skin–can look like eczema/psoriasis
red plaque likes lesion

very slow disease-can take years and be controlled

22
Q

What is kaposi’s sarcomas?

A

Endothelial of lymphatics tumour
relatied to HIV and HHV8
purple nodules, plaques/flat lesion

go alon skin lines usually

treat undelying cause, excise. chemo, radio

23
Q

What is epidermadysplacia veruciformis?

A

genetic predisposed to HPV worts all over body
rare autosomal recessive condition
predisposed to HPV warts that become SCC