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Year 2 Collin > Cancer 14 - Skin Cancer > Flashcards

Cancer 14 - Skin Cancer Flashcards

1
Q

Most skin cancers arise from cells in the?

A

Epidermis

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2
Q

Describe the structure of the epidermis

A

Keratinocytes above Basement membrane —> differentiate as they move up.

Layers of epidermis =Stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, stratum basale

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3
Q 
Blood = leukaemia
Tissue = ?

(for lymphocyte derived carcinomas)

A

Lymphomas

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4
Q

What are the different types of skin cancer

A
  1. Keratinocyte derived - basal cell carcinoma, squamous cell carcinoma
  2. Melanocyte derived - malignant melanoma
  3. Vasculature derived - Kaposi’s sarcoma, angiosarcoma
  4. Lymphocyte derived - mycosis fungoides
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5
Q

What is the cause of skin cancer

A

Accumulation of genetic mutations leading to uncontrolled cell proliferation

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6
Q

Give examples of causes of skin cancer

A
  1. Genetic syndromes - e.g. Gorlins syndrome, xeroderma pigmentosum (problem with DNA repair mechanism)
  2. Viral infections - HHV8 in Kaposis sarcoma, HPV in Squamous cell carcinoma
  3. UV light - BCC, SCC, malignant melanomas
  4. Immunosuppression - Drugs, HIV, old age, leukaemia
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7
Q

Why is the incidence of basal cell carcinomas increasing

A

More sun exposure, behavioural changes e.g. not wearing hats

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8
Q

UV light is separated into 3 wavebands

A 
UVA = 310-400nm (most penetrative - major cause of skin aging) 
UVB = 280-310nm (most important wavelength in skin carcinogenesis)
UVC = 100-280nm (blocked out by ozone layer)
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9
Q

How do UVB (and UVA) cause DNA damage

UVB does it more than UVA

A

They induce photoproducts (mutations) in DNA by causing cross linking of pyrimidines - may cause 6-4 pyrimidine pyrimidine photoproduct

Normally, these mutations are repaired via nucleotide excision repair

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10
Q

How may UV induce skin carcinogenesis

A

UV damage to DNA –> mutations in specific genes. If these genes are genes for cell division, DNA repair, cell cycle arrest, could lead to skin carcinogenesis

e.g. xeroderma pigmentosum, genetic condition with defective nucleotide excision repair

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11
Q

Which mutations can cause cancer

A
  1. Mutations stimulating uncontrolled cell proliferation (e.g. P53 gene)
  2. Mutations altering responses to growth stimulating/repressing factors
  3. Mutations inhibiting apoptosis
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12
Q

Describe sunburn

A

UV exposure –> leads to keratinocyte apoptosis

Sunburn cells = apoptotic cells in UV overexposed skin

Apoptosis removes UV damaged cells in skin - which might otherwise become cancer cells

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13
Q

Explain the processes that may occur regarding photocarcinogenesis

A
  1. Keratinocyte exposed to UV

Either:

  • skin cancer occurs as UV mutates p53
  • DNA damage occurs but DNA repaired
  • DNA damaged beyond repair –> apoptosis
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14
Q

What are the immunomodulatory effects of UV light

A
  1. UVA and UVB affect expression of genes involved in skin immunity - depletes Langerhans cells in the epidermis
  2. Reduced skin immunocompetence and immunosurveillance - basis for IV phototherapy e.g. for psoriasis
  3. Further increases cancer causing potential of sun exposure
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15
Q

How many Fitzpatrick phototypes are there

A

6

1-6, gradually getting darker. Reflects melanin levels

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16
Q

Where is melanin produced?

What does skin colour depend on?

A

Melanin produced by melanocytes within basal layer of epidermis

Skin colour - depends on amount and type of melanin produced - not density of melanocytes (fairly constant)

17
Q

How does melanin production work

A

After sun exposure, keratinocytes produce MSH. Melanocytes produce melanin, packaged in melanosomes and sent via dendritic processes into keratinocytes

18
Q

What are the 2 types of melanin formed

A
  1. Eumelanin = brown/black
  2. Phaeomelanin - yellowish/reddish brown

Melanin = formed from tyrosine via series of enzymes

The variation in eumelanin : phaeomelanin is coded by MCR1 gene

Melanin = dictates skin sensitivity to UV damage

19
Q

Describe malignant melanoma

A

Malignant tumour of melanocytes - melanocytes become abnormal - atypical cells and architecture

Caused by UV exposure and genetic factors. Risk of metastasis

20
Q

Describe the types of melanoma

A
  1. Lentigo maligna (melanoma in situ) - proliferation of malignant melanocytes within epidermis - no risk of metastasis. (Lentigo maligna melanoma (if INVASIVE)
  2. Superficial spreading malignant melanoma - lateral proliferation of malignant melanocytes + invade basement membrane, risk of metastasis
  3. Nodular melanoma - vertical proliferation of malignant melanocytes (no previous horizontal growth) - risk of metastasis. (THERE IS ALSO NODULAR MELANOMA ARISING FROM SUPERFICIAL SPREADING MELANOMA)
  4. Acral lentiginous melanoma
  5. Amelanotic melanoma - no melanin produced, difficult to diagnose
21
Q

What is the ABCD(E) rule of diagnosing superficial spreading malignant melanoma

A
  1. Asymmetry
  2. Irregular border
  3. Colour variation
  4. Diameter >0.7mm and increasing
  5. Erythema
22
Q

Nodular malignant melanoma may arise from?

A

Superficial spreading melanoma

This is the case if:
Downward proliferation of malignant melanocytes, following previous horizontal growth

23
Q

Describe acral lentiginous melanoma

A

May occur in palms/soles (more likely in darker skin types)

24
Q

What does melanoma prognosis depend on?

A

The thickness/how deep the melanoma goes, aka Breslow thickness (mm from top to bottom of melanoma)

25
Q

What are the risk factors for melanoma development

A
  1. Family history of dysplastic nevi/melanoma
  2. UV radition
  3. Sunburns during childhood
  4. Intermittent burning exposure in unacclimatised fair skin
  5. Atypical/dysplastic nevus syndrome
  6. Personal history of melanoma
  7. Skin type 1/2
26
Q

Squamous cell carcinomas are bad - they also happen to look like?

A

Keratoacanthomas (benign)

27
Q

Describe squamous cell carcinoma

A
  1. Malignant tumour of keratinocytes

Caused by:
UV exposure, HPV, Immunosuppression, may occur in scars or scarring process

Risk of metastasis/spreading

Growing a horn = well differentiated - SCC

(no horn = poorly differentiated)

28
Q

SCC on the lip has a high risk of metastasis. Why?

A

Lips have rich blood supply

High risk of SCC = ears, lips and genital region

29
Q

Describe basal cell carcinomas

A

Malignant tumour arising from Basal layer of epidermis

Caused by sun exposure and genetics

SLOW GROWING, invades tissue but does not metastasise

Common on face

Dont make keratin so not rough and horny (unlike SCC)

Seeing tree-like blood vessels (aborising) = giveaway for BCC

30
Q

Flat appearance of basal cell carcinoma is aka

A

Superficial BCC

31
Q

Describe mycosis fungoides

A

Lymphoma - lymphocyte derived.

Plaques/patches of erythematous scaly skin. Can metastasise slowly.

Patches —> plaques –> tumour

32
Q

Describe Kaposis sarcoma

A

Tumour of endothelial cells of lymphatics

HIV and HHV8 associated - moley, purpley plaques on skin

33
Q

Describe epidermodysplasia veruciformis

A

Rare, autosomal recessive condition

Predisposition to HPV induced warts and SCCs

Year 2 Collin (114 decks)

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