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cancer - year 2 > skin cancer > Flashcards

skin cancer Flashcards

1
Q

describe the skin microanatomy

A

have the epidermis

dermis

hypodermis - has subcutaneous fat

bm

muscle

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2
Q

describe the structure of the epidermis `

A

have keratinocytes, melanocytes, DC - langerhans cells, merkle cells

keratinocytes start at the bm, mature and differentiate and move up through layers - get exposed to UV = mutatations

melanocytes are by the bm - can get exposed to UV = mutations

layers are:

  • stratum corneum
  • startum lucidum
  • stratum granulosum
  • stratum spinosum
  • stratum basale
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3
Q

what are the different types of skin cancer *

A

keratinocyte derived - basal cell carcinoma, squamous cell carcinoma (aka non melanoma skin cancer)

melanocyte derived - malignant melanoma

vascular derived - kaposi sarcoma (common in AIDS), angiosarcoma

lymphocyte derived - mycosis fungiodes

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4
Q

general cause of skin cancer *

A

accumulation of mutations in key genes lead to uncontrolled cellular differentiation

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5
Q

causes of skin cancer *

A

genetic syndromes - give predisposition to cancer

  • Gorlin’s syndrome - tendancy for basal cell carcinoma - defect in ORC1 gene
  • xeroderma pigmentosum - defect in DNA repair by UV - develop multiple skin cancers

viral infections

  • HHV8 in kaposi sarcoma
  • HPV in SCC - particularly in the immunosuppressed

uv light - main cause

  • BCC, SCC, malignant melanoma

immunosuppression

  • drugs
  • old age = immunosuppression
  • HIV
  • leukaemia
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6
Q

characteristics of malignant melanoma *

A

dark

irregular border

lumpy

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7
Q

incidence of malignant melanoma *

A

increasing in whit people

pale skin - suseptible to UV damage

increasing because people are living longer, more sun and behaviour change

higher incidence where higher exposure eg cornwall and norfolk

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8
Q

characteristics of basal cell carcinoma (BCC) *

A

pearly

grey/shiny

glistens

have telangiectasia - dilated small capillary blood vessels that look like they are branching

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9
Q

incidence of BCC *

A

increasing

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10
Q

describe how UV light contributes to skin cancer *

A

3 types UVA UVB UVC

UVC is blocked by the stratosphere

UVB and UVA hit the surface and contribute to mutations

UV damage to DNA leads to mutations in specific genes - cell division, DNA repair, cell cycle arrest - if these accumulate = cancer

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11
Q

why is sunlight essential

A

for photosynthesis

infrarred spectrum provides warmth

effect ion human mood

stimulates the production of vitamin D in the skin

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12
Q

describe how UVB causes skin cancer *

A

most important wavelength in carcinogenesis

directly induces mutations

induces photoproducts - these are cross links between bases - affects pyrimidines (C and T) - forming cyclobutane pyrimidine dimers eg T=T, T=C, C=C (ie thymine dimers etc)

this is usually repaired by nucelar exision repair

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13
Q

describe role of UVA in skin cancer *

A

100x more penetrates to surface than UVB

major cause of skin aging - penetrates deeper and effects collagen in dermis

contributes to carcinogenesis - causes cyclobutane pyrimidine dimers but less effectively than UVB

also forms free radicals whcih damage DNA and cell mmebrane

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14
Q

therapeutic use of UVA

A

in PUVA therapy for psoriasis

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15
Q

how is UV damage usually repaired *

A

DNA nucleotide excision

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16
Q

describe xeroderma pigmentosum *

A

genetic defect with nucleotide excision repair

means get skin cancer early with minimal exposure

ie <10yrs age, freckles and photosensitivity

sublings need to be tested

treated by removing the skin cancer and strict sun protection ie completely covered in sun including wearing a visor over face

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17
Q

what are the mutations that can cause cancer *

A

stimulate uncontrolled cell proliferation - mutations in p53 gene

alter responses to growth stimulating/repressive factors

inhibit programmed cell death - apoptosis

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18
Q

describe sunburn

A

the keratinocytes undergo apoptosis because of UV

this removes UV damaged cells that might otherwise form cancer cells

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19
Q

summarise photocarcinogenesis *

A

UV causes DNA damage

DNA can be repaired = normal cells

or if damage too severe - apoptosis

or if mutation accumulate = cell will transform = skin cancer

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20
Q

describe the immunomodulatory effects of UV *

A

UVA and B effect expression of genes in immunity - depletes the langerhans cells in the epidermis = immune suppression

there is reduced skin immunocompetence and immunosurveillance

further increases cancer causing potential of sun - normally langerhans cells (APC) cause cell death of cells exposed to UV

(basis for treatment of psoriasis - exposure to UV improves psoriasis)

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21
Q

what determines the host response to UV *

A

genetic influences - especially phototype

22
Q

what are the fitzpatrick phototypes *

A

1 - always burns never tans

2 - usually burns, sometimes tans

3 - sometimes burns, usually tans

4 - never burns always tans

5 - moderate constitutive pigmentation - asian

6 - marked constituitive pigmentation - afro-carribean

23
Q

describe melanin *

A

melanin pigmentation is responsible for skin colour

produced by melanocytes within the basal layer of the epidermis

skin colour depends on the amount of melanin produced as baseline, not the number of melanocytes (number of cells is constant)

24
Q

describe melanocytes and production of melanin *

A

they are DC on the BM in epidermis that interdigitate and communicate with the keratinocytes - 1 melanocyte for 5 keratinocytes

they produce a baseline level of melanin

after UV exposure - keratinocytes send paracrine signal (MSH) that activates the melanocytes to make more melanin

melanin is taken up by keratinocytes and packaged around their nucleus to protect DNA

25
Q

what are the types of melanin and what determines them *

A

eumelanin - brown/black - in later skin types

phaeomelanin - yellowish/reddish brown - red hair and pale skin

melanin is produced from tyrosine by a series of enzymes

MCR1 gene has >20 polymorphisms - the variation of melanin ratio produced depends on the polymorphism

this explains the different hair and skin coulour types

melanin detects skin sensitivity to UV damage

26
Q

describe malignant melanoma *

A

tumour of the melanocytes - they become abnormal and have abnormal architecture

caused by UV exposure and genetic factors

there is a risk of metastasis leading to death

27
Q

describe lentigo maligna *

A

it is melanoma in situ

there is proliferation of malignant (atypical) melanocytes in the epidermis

pagetoid spread - ie the melanocytes spread upwards, they should be at the bm

no risk of metastisis because they havent breached the epidermis

28
Q

characteristics of lentigo maligna *

A

irregular shape

flaty

light and dark brown colours

>2cm usually

common in elderly at sites of skin exposure

29
Q

treatment of lentigo maligna

A

excision

and skin graft

30
Q

descrive lentigo maligna melanoma *

A

means there is invasion

dark patch

31
Q

describe superficial spreading malignant melanoma *

A

lateal proliferation of malignant melanocytes

invade the bm

risk of metastasis

pagetoid spread - melanocytes in epidermis and dermis

also spread out and downwards - when head out = radial growth phase, when down = vertical growth phase

32
Q

characteristics of superficial spreading MM *

A

dark - blue colour

irregular

33
Q

how do you diagnose a superficial spreading MM *

A

ABCDE rule

asymettry

border irregular

colour variation - dark brown/black

diameter >7mm and increasing

erythma

34
Q

what is the significance of a superficial spreading MM being pale in middle *

A

means middle has regressed - immune response against tumour

bad prognosis because means thicker and more invasive and perhaps already metastised

35
Q

describe nodular malignant melanoma *

A

vertical proliferation of melanocytes - grows up and down

no previous horizontal growth

risk of metastasis

can arise from a mole/de novo

36
Q

characteristics of nodular MM *

A

black and lumpy

37
Q

describe nodular melanoma arising within a superficial spreading melanoma *

A

downward proliferation of malignant melanocytes

previous horizontal growth

nodule develops within an irregular plaque

prognosis is worse

can lose pigmentation

can have erythma - superficial reddening, these are amelanotic areas of the melanoma

38
Q

describe acral lentiginous melanoma *

A

on soles or palms

lumps/flat pigmented plaques

common in darker skin types

39
Q

describe amelanotic melanoma *

A

not pigmented

40
Q

how do you determine the prognosis of melanoma

A

breslow thickness - depth of invasion of tumour cells in the skin

measurement from granular layer (just under the stratum corneum) to bottom of tumour

<1mm = thin

4= thick

1-4 = intermediate

41
Q

what are the risk factors for the development of melanoma *

A

FH of dysplastic nevi or melanoma

UV irradiation

sunburns during childhood

intermittent burning exposure in unacclimitised fair skin - most important

atypical/dysplastic nevus syndrome

personal history of melanomas - if you have one you’re likely to have another

skin type 1/2

genetic markers - CDKN2A mutation

cingenital nevi

number of atypical nevi >5

high socioaconomic status

1equatoral latitudes

dna repair defects eg xeroderma pigmentosum

immunosuppression

42
Q

describe kertaocanthoma *

A

grow rapidly then involutes

type of SCC

from keratinocyte - if well differentiated it produces keratin

43
Q

describe SCC *

A

malignant tumour of kertainocytes

caused by UV, HPV, immunosuppression, may occur in scars/scarring process eg burns scar/disease with scar/long term ulcer

risk of metastasis if poorly differentaited is 10% - this is less than for malignant melanomas

well differentiated produces keratin - can see horns

can occur on lower lip from sun adn smoking

occur on ears of men and leg of women - exposed to sun

44
Q

describe BCC *

A

malignant tumour from basal cell layer of epidermis

caused by sun exposure, genetics

slow growing - 3-4mm yr (can be faster)

invades tissue but doesnt metastise

common on face

common around eye - has telangiectasia - lost eyelash so destructive process

arborising telangiectasia - branching capillary bvs

45
Q

describe nodular BCC *

A

glistening

telangiectasia

46
Q

describe superficial BCC *

A

have rolled edge

glistening surface

crusty

47
Q

describe mycosis fungoides *

A

look like psoriasis/eczema

pink scaly patch that progresses to plaque like lesion then tumour, then disseminates then die

it is a T cell lymphoma of skin

also called cutaneous T cell lymphoma

48
Q

describe kaposi’s sarcoma *

A

HIV and HHV8 associated - HHV8 in AIDs and not

purplish nodules, plaques, flat legions

arise from the endothelial cells in lymphatics

orientation of plaque goes along the skin line

on palate, sole of foot, skin

treatment - excision, chemo/radio and treatment of HIV

49
Q

describe epidermodysplasia veruciformis *

A

rare autosomal recessive condition

predisposition ot HPV induced warts and SCCs

50
Q

role of immunomodulation in cancer

A

people with good immune systems resolve early cancers before they are detected

in immunocomprised people there is an increased occurrence of keratinocyte-derived skin tumours on sun-exposed sites.

51
Q

role of p53 in skin cancer *

A

normally mutations in DNA = activation of p53 = expression of Bax gene = apoptosis

if you have p53 mutation - DNA with mutations might survive = more likely to get heratinocyte cancers

cancer - year 2 (18 decks)

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