Cancer as a disease-skin caner Flashcards

1
Q

What is it the name given to a large area of lentigo maligna that has a smaller area within it that has become invasive?

A

Lentigo maligna melanoma

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2
Q

WHat melanoma is represented

A

Lentingo maligna

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3
Q

What are the main cell types in the epidermis?

A

Keratinocytes Melanocyts Langerhans Cells Merkel Cells

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4
Q

Name a disease that predisposes to SCCs and HPV induced warts (that can become incredibly keratotic).

A

Epidermodysplasia Veruciformis

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5
Q

What are the consequences of UV therapy for psoriasis?

A

Increased risk of skin cancer UV can act on keratinocytes and cause DNA damage If the Langerhans cells have been depleted then they will be unable to knock out the damaged cells so they could persist and become cancerous

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6
Q

What is it called when you get a vertical proliferation of malignant melanocytes?

A

Nodular malignant melanoma

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7
Q

Describe the appearance of BCCs and their development

A

They are pearly, have a rolled edge and often have arborising telangiectasia, develop slowly, inavde tissue but do not metastasise and they are common on the face

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8
Q

Features of genes that are affected by UV damage and how

A

UV damage to DNA leads to mutations in specific genes involved in :

  • cell division
  • DNA repair
  • cell cycle arrest
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9
Q

WHat is this image showing

A

Lentingo maligna melanoma

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10
Q

State the types of skin cancer that come under each of the following types: a. Keratinocyte derived b. Melanocyte derived c. Vasculature derived d. Lymphocyte derived

A

a. Keratinocyte derived Basal Cell Carcinoma Squamous Cell Carcinoma b. Melanocyte derived Malignant Melanoma c. Vasculature derived Kaposi Sarcoma – endothelium of lymphatics Angiosarcoma – endothelium of blood vessels d. Lymphocyte derived Mycosis fungoides(lymphoma in the skin)

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11
Q

WHAt is the coomon genetic change and consequence that occur between cancers like skin cancer

A

Accumulation of genetic mutations uncontrolled cell proliferation

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12
Q

What type of melanoma produced no melanin?

A

Amelanotic melanoma

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13
Q

State two examples of genetic syndromes that massively increase the risk of getting skin cancer.

A

Gorlin’s Syndrome – regular BCCs Xeroderma Pigmentosum – increased risk of BCC, SCC and malignant melanoma

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14
Q

How can UVA promote skin carcinogenesis?

A

Forms cyclobutane pyrimidine dimers (but less effectively than UVB) Also generates free radicals that can damage DNA

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15
Q

What is a keratoacanthoma?

A

It is either a benign lesion or a benign version of an SCC It grows rapidly but then disappears There is no risk of metastasis

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16
Q

Which viruses are associated with Kaposi sarcoma?

A

HHV8 HIV

17
Q

What is a superficial spreading malignant melanoma?

A

Lateral proliferation of malignant melanocytes They invade the basement membrane so there is a risk of metastasis

18
Q

What is the prognosis of melanoma based on?

A

Breslow thickness – thickness from the top of the tumour to the bottom, measured in mm

19
Q

Give two examples of viruses that can lead to skin cancer?

A

HHV8 HIV

20
Q

Label

A
21
Q

What happens to keratinocytes in sunburn?

A

The UV damage leads to keratinocyte apoptosis The apoptotic cells in UV overexposed skin are called sun burn cells

22
Q

What is a basal cell carcinoma (BCC) and what are itheir two main causes

A

Malignant tumour arising from keratinocytes in the basal layer of theepidermis, sun exposure and genetics

23
Q

Which system is used to categorise people based on their skin type and sensitivity to UV?

A

Fitzpatrick Phenotypes

24
Q

Name a condition that is caused by a defect in nucleotide excision repair.

A

Xeroderma pigementosum

25
Q

How can you tell whether an SCC is well differentiated?

A

If the lesion has a keratin horn then it shows that the keratinocytes can still produce keratin and so they are well differentiated

26
Q

WHat melanoma is represented

A

superficial spreading malignant melanoma

27
Q

List features of Mutations that cause cancer

A

1.Mutations that stimulate uncontrolled cell proliferation

Eg abolishing control of the normal cell cycle (p53 gene)

2.Mutations that alter responses to growth stimulating / repressing factors

3.Mutations that inhibit programmed cell death (apoptosis)

c