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Year 2 - MCD Cancer > CasaD - Skin Cancer > Flashcards

CasaD - Skin Cancer Flashcards

1
Q

3 main leys of the skin and explain what one of the layers is made up of

A

3 main layers:
• epidermis
• dermis
• hypodermis (fat layer)

Epidermis is compromised of (superficial --> deep) :
 o	Stratum corneum
  – dead keratinocytes
o	Stratum lucidum
o	Stratum granulosum
o	Stratum spinosum
 – dendritic cells.
o	Stratum basale 
 – melanocytes, merkel cells, dividing cells
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2
Q

What are the different types of skin cancers?

A

 Keratinocyte derived
• e.g. BCC (Basal Cell Carcinoma), SCC (Squamous Cell Carcinoma)
• aka – Non-Melanoma Skin Cancer (NMSC)

 Melanocyte derived
• e.g. Malignant melanoma

 Vasculature derived
• e.g. Kaposi’s sarcoma,
angiosarcoma

 Lymphocyte (lymphoma) derived
• e.g. Mycosis fungoides

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3
Q

What is the main cause of skin cancer?

A

Accumulation of genetic proliferation

• uncontrolled cell proliferation

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4
Q

Example of causes of skin cancer

A

o Genetic syndromes
• Gorlin’s syndrome, Xeroderma pigmentosum

o Viral infections
• HHV8 (Kaposi’s sarcoma), HPV (SCC)

o UV light
• BCC, SCC, malignant melanoma

o Immunosuppression
• drugs, age, HIV, leukaemia

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5
Q

Explain what MM looks like and its epidemiology

A

Malignant Melanoma:
• has an irregular margin
• dark-coloured

Epidemiology:
• incidence highest in WHITE and lowest in BLACK
• incidence highest in SW England

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6
Q

Explain what B-C C looks like and its epidemiology

A

Basal-Cell Carcinoma:
• pearly appearance
• dilated vessels on surface

Epidemiology:
• incidence increasing in men & women (due to increasing ages and more exposure)

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7
Q

What is the different parts that makes up the UV Spectrum?

A

UVA
• 310-400nm
• penetrates to deep sea level

UVB
• 280 - 310nm
• penetrates to ground level

UVC
• 100-280nm
• does NOT penetrate ozone

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8
Q

Which is the most important UV that contributes to skin cacrinogenesis?

A

UVB

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9
Q

Explain how UVB contributes to skin carcinogenesis?

A

Most important in skin carcinogenesis:
• Induces direct abnormalities in skin DNA – e.g. mutations.
• Induces photoproducts – affects PYRIMIDINES (C, T) bases, e.g :
o Cyclobutane pyrimidine dimers (e.g. T=T, T=C, C=C).
o 6-4 pyrimidine pyrimidone photoproducts.

 Photoproducts are usually repaired quickly by nucleotide excision repair.

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10
Q

Explain how UVA contributes to skin carcinogenesis

A

 100x more penetrating than UVB

 Major cause of skin AGEING and contributes to skin carcinogenesis.
• Also forms Cyclobutane pyrimidine dimers BUT less efficiently than UVB
• Forms free radicals to damage DNA and cell membranes

 Used therapeutically in PUVA therapy – treats psoriasis etc.

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11
Q

How is UV damage repaired?

A

Nucleotide Excision Repair
• photoproducts removed

Xeroderma Pigmentosum
• genetic condition with defective Nucleotide Excision Repair

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12
Q

Mutations that cause cancer?

A

Mutations that:
(1) stimulate uncontrolled cell proliferation (e.g. abolishing control of normal cell cycle via. p53 gene)

(2) alter responses to growth stimulating/repressing factors
(3) inhibit programmed cell death (apoptosis)

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13
Q

What happens in sun burn?

A

UV light –>
• leads to keratinocyte apoptosis

• apoptosis removes UV damaged cells in skin which might otherwise become cancerous

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14
Q

Explain the immunomodulatory effects of UV light

A

UVA/B effect expression of genes:

  • deplete Langerhans cells in the epidermis
  • = decreased skin immunocompetance & immunosurveillance
  • = basis for using UV phototherapy to treat psoriasis BUT also further increases cancer chances
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15
Q

Explain photocarcinogenesis

A

Leads to DNA damage in kerainocytes
• can REPAIR or if damage to severe then can enter APOPTOSIS

BUT if also have
p53 mutations
CAN lead to skin cancer

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16
Q

What determines host reponse to UV?

A

By genetic influences especially SKIN PHOTOTYPE

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17
Q

What are the different skin phototypes?

A 
Fitzpatrick Phototypes:
 o	1 – always burns, never tans.
 o	2 – usually burns, sometimes tans.
 o	3 – sometimes burns, usually tans.
 o	4 – never burns, always tans.

o 5 – moderate
constitutive pigmentation – Asian.
o 6 – moderate constitutive pigmentation – Afrocaribean.

18
Q

Where is melanin produced and where does it go?

A

 Melanin:
• produced by melanocyte (from tyrosine)
• within the BASAL LAYER of the EPIDERMIS
• packed into melanosomes

It is then:
• transported UP SPINES to the keratinocytes where it passes into the cells
• here it then COATS the nuclei within the cells to protects from UV damage.

19
Q

What does skin colour depend on?

A

Skin colour depends upon AMOUNT and TYPE of melanin produced

NOT density

20
Q

What are the different types of melanin?

A

Types – encoded by MCR1 gene has that has >20 polymorphisms and describes the variations in melanin

Variation in eumelanin:phaeomelanin produced:
 Eumelanin – brown or black.
 Phaeomelanin – yellowish or reddish.

21
Q

How is melanin produced?

A 
1• Tyrosine 
2• DOPA 
3• Dopaquinone 
4• Eumelanin or Phaeomelanin 
5• Melanin
22
Q

What does melanin dictate?

A

Skin sensitivity to UV damage

23
Q

Explain what MM is and what causes it

A

Malignant Melanoma
• malignant tumours of melanocytes

Melanocytes become:
• abnormal
• & have atypical cells & atypical architecture

Caused by:
• UV exposure
• Genetic factors

Risk of METASTASIS
• so skin cancer with HIGHEST MORTALITY

24
Q

Summary of the Types of MM?

A

(1) Lentigo MM (in situ)
(2) Superficial Spreading MM
(3) Nodular MM
(4) Nodular MM arising within SSMM
(5) Acral Lantiginous MM
(6) Amelanotic MM

25
Q

Explain (1) L MM

A

Lentigo MM:
• melanoma in situ

 Proliferation of malignant melanocytes within the EPIDERMIS.
 No risk of metastasis.

Features:
o Considered premelanoma state
o Irregular shape.
o Light & dark colours.
o Size usually >2.0cm.
26
Q

Explain (2) SS MM

A

(2) Superficial Spreading MM

 Lateral proliferation of malignant melanocytes.
 Invasion of the BM (= grows outwards)
 Risk of metastasis.

Diagnosis rule of SSMMs – ABCD:
o	A – Asymmetry.
o	B – Border irregularity.
o	C – Colour variation.
o	D – Diameter >0.7mm and increasing.
o	(E – Erythema).
27
Q

Explain (3) N MM

A

(3) Nodular MM

 VERTICAL proliferation of MMs with no previous horizontal growth.
 Risk of metastasis (as growing downwards)
 Usually much darker in appearance.

28
Q

Explain (4) N MM arising within SSMM

A

(4) N MM arising within SSMM

 Downward proliferation of MMs FOLLOWING previous horizontal growth.
 Prognosis will become worse (as nodule growing within an irregular plaque).

 Some may have areas of ERYTHEMA
• usually when the tumour has lost ability to produce melanin so instead starts to looka erythematous

29
Q

Explain (5) AL MM

A

(5) Acral Lentiginous MM

 A malignant melanoma affecting the palms and soles of the feet.
 Occur in darker skinned people more often than lighter coloured skin people.

30
Q

Explain (6) A MM

A

(6) Amelanotic MM

 A melanoma where the cancer cells have lost the ability to create melanin.

31
Q

What is the prognosis of Melanoma determined by?

A

Breslow thickness!

Measured from granular layer to bottom of tumour
• states that the deeper the melanoma (>1mm), the worse the prognosis.

32
Q

Risk factors for the development of Melanoma?

A

 Family history  Intermittent burning exposure
 Skin types 1, 2.
 UV light exposure
 Atypical nevus syndrome
 Sunburns during childhood  Personal melanoma history

33
Q

Dysplastic nevi?

A

Moles that are a little atypical but are NOT melanomas

34
Q

What are keratoacanthomas?

A

Either a benign lesion OR version of an SCC
 grows rapidly but then DISAPPEARS
 NO RISK of metastasis

35
Q

Explain SCC

A

Squamous Cell Carcinoma:

 Malignant tumour of keratinocytes.

Caused by:
 • UV
 • HPV
 • immunosuppression
 • scarring processes

 Risk of metastasis (but not as high as in MMs)
 “Horny” descriptors indicate well differentiation and the cell has retained the ability to create keratin.

36
Q

Explain BCC

A

Basal Cell Carcinoma:

 Malignant tumour arising from the basal layer of the epidermis.

Caused by:
• sun exposure
• genetics

Features:
o Slow growing.
o Invades tissues but does NOT metastasise.
o Common on the face.

 Can be nodular (has a telangiectasia) or superficial

37
Q

Telangiectasia?

A

Localised collection of distended blood capillary vessels

It is a KEY FEATURE of BCC

38
Q

Explain MF

A

Mycosis Fungoides:

 Not a fungal condition – miss-classified.
 This is a lymphoma that affects the skin-resident T-lymphocytes
• red patches make it look like psoriasis BUT is not

 This can be fatal and has internal organ involvement.

39
Q

Explain KS

A

Kaposi’s Sarcoma:

 HIV and HHV8 associated.
 A tumour of the endothelial cells of the lymphatics.
 Can occur in non-HIV patients and can occur internally.

40
Q

Explain EV

A

Epidermodysplasia Verruciformis:

 Rare autosomal condition.
 Gives a predisposition to HPV-induced warts and SCCs.

41
Q

What is the treatment for many of these skin cancers?

A

SURGICAL

Year 2 - MCD Cancer (14 decks)

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