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Y3 IWB > PATHOLOGY- Common skin cancers > Flashcards

PATHOLOGY- Common skin cancers Flashcards

1
Q

Name some common skin cancers

A
  1. Basal cell carcinoma a
  2. Squamous cell carcinoma
  3. Melanocytic tumours
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2
Q

Name the different layers of the epidermis

A
  1. Basil cell layer
  2. Prickle cell layer
  3. Granule cell layer
  4. Keratinsed squames
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3
Q

Name the 3 main parts of the skin

A
  1. Epidermis
  2. Dermis
  3. Subcutaneous layer
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4
Q

Name some specialised cells in the epidermis

A
  1. Melanocytes
  2. Merkel cell
  3. Dividing cell
  4. Langerhan cell (immune cell)
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5
Q

What do melanocytes do?

A

They produce melanin

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6
Q

Name some cancers that can form in the epidermis of the skin

A
  1. Squamous cell carcinoma
  2. Basal cell carcinoma
  3. Melanoma
  4. Merkel cell carcinoma (quite rare)
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7
Q

What are benign glandular tumours called

A

Adenomas

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8
Q

What are malignant glandular tumours called

A

Carcinomas

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9
Q

Name some elements of the skin where skin tumours can arise from

A
  1. Epidermis
  2. Melanocytes
  3. Merkel cell tumours (Rare but dangerous)
  4. Adnexal structures (like sweat glands and hair follicles)
  5. Nerves and blood vessels
  6. Connective tissue
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10
Q

Where do basal cell carcinomas usually form

A

On EXPOSED hair bearing skin such as on the face and lips (apart from hands)

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11
Q

Name the most common malignant tumour humans can develop

A

Basal cell carcinomas (BCC)

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12
Q

Define metastases

A

the development of secondary malignant growths at a distance from a primary site of cancer.

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13
Q

How often do metastases form in basal cell carcinomas

A

Very rarely (1 in 10,000)

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14
Q

Why are basal cell carcinomas problematic?

A

As they can be locally aggressive and spread from the epidermas down to subcutaneous fat and the nerve and bone area

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15
Q

List the key risk factors for developing basal cell carcinomas

A
  1. UV light exposure (especially in pale individuals)
  2. Immunocompromised patients
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16
Q

Talk through the aetiology of basal cell carcinomas

A
  1. Prominently form on sun exposed sites, especially the face
  2. Pale skinned individuals who burn easily are at greater risk
  3. Immunosuppression
  4. Rare genetic predisposition (goblin syndrome and bazex)
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17
Q

What is gorlins syndrome

A

An autosomal dominant syndrome where the tumour suppressor genes are mutated

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18
Q

List some characteristics of goblin syndrome

A
  1. Palmar pits
  2. Odontogenic keratocytes
  3. Skeletal abnormalities
  4. Mental retardation
  5. Brain tumours
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19
Q

What do early lesions of basal cell carcinomas look like?

A

Nodules on the skin

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20
Q

If nodules on the skin (caused by BCCs) are neglected and left untreated what can happen?

A

They can begin to ulcerate with rolled edges

this is called a rodent ulcer

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21
Q

Why is the histology of basal cells carcinomas split into different types and name the 2 types of BCC histology

A

They are split as there’s a lot of variants

  1. Low risk types
  2. High risk types
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22
Q

What are basal cell carcinoma tumours made up of

A

Tumours composed of islands of basaloid cells with peripheral palisade

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23
Q

Describe the low risk histology of basal cell carcinomas

A

Superficial and nodular

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24
Q

Describe the high risk histology of basal cell carcinomas

A

Infiltrative, micro-nodular and morphoeic

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25
Q

Name the second most common skin cancer

A

Squamous cell carcinoma

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26
Q

Which is more aggressive Basal cell carcinomas or squamous cell carcinomas

A

squamous cell carcinomas

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27
Q

Name the high risk sites where squamous cell carcinomas are more likely to form

A

Lip
Ear
Perineum

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28
Q

How often do metastases form in squamous cell carcinomas

A

0.5-5%

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29
Q

List the risk factors associated with developing squamous cell carcinomas

A
  1. UV exposure
  2. Immunosuppressed individuals
  3. Patients with chronic ulcers
  4. Radiation burns
  5. Chemotherapy drugs
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30
Q

Describe the aetiology of squamous cell carcinomas

A
  1. UV radiation
  2. Radiotherapy
  3. Chronic scars/ ulcers
  4. Immunosuppression
  5. Drugs for melanoma
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31
Q

Describe the clinical presentation of early squamous cell carcinomas

A

Nodules ulcerated with a crusty surface

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32
Q

Describe how squamous cell carcinomas look under a microscope

A

They look like invasive islands and trabecular of squamous cells showing cytological atypia

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33
Q

What are carcinomas

A

Malignant glandular tumours

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34
Q

What are adenomas

A

Benign glandular tumours

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35
Q

Where do squamous cell carcinomas usually metastasise to?

A

Lymph nodes first

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36
Q

Name the pre invasive stage that occurs before a squamous cell carcinoma forms?

A

Actinic keratosis

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37
Q

What is actinic keratosis

A

A pre malignant change seen due to prolonged UV exposure

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38
Q

Describe actinic keratosis

A
  1. Dysplasia to squamous epithelium
  2. Can lead to the formation of a scaly lesion with erythematous base
  3. Rarely progresses to invasive disease
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39
Q

Where do actinic keratosis usually form?

A

Very common on chronic sun exposed sites

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40
Q

Where are melanocytes derived from

A

Derived from neural crest cells

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41
Q

What is the function of melanocytes?

A

To form melanin which is transferred to epidermal cells to protect the nucleus from UV radiation

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42
Q

Name the tumours melanocytes can give rise to?

A

Naevi (benign moles)

Melanoma (malignant)

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43
Q

Describe naevi

A

They are local benign collections of melanocytes

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44
Q

Name the different types of naevi

A
  1. Superficial
  2. Deep blue naevi
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45
Q

Name some types of deep blue naevi

A
  1. Mongolion spot
  2. Naevi of Ota, Ito and Hori
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46
Q

How are superficial naevi classified?

A

By their location

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47
Q

Name some different classifications of superficial naevi

A
  1. Junctional naevi
  2. Intra dermal naevi
  3. Compound naevi
48
Q

Where are junctional naevi found

A

At the base of the epidermis at the junction

49
Q

Where are intra dermal naevi found?

A

Found entirely in the dermis

50
Q

Where are compound naevi found

A

The naevi has nests in both the dermis and the junction

51
Q

How do deep blue naevi form

A

Melanocytes that have been migrating from the neural crest to the epidermis haven’t made it and sometimes form masses Called naevi

52
Q

How do we name deep naevi

A

By their morphological, macroscopic description

53
Q

In whom might you see deep naevi

A

Mainly in children but they often resolve over time

54
Q

What are the main problems associated with giant congenital naevi?

A

Aesthetics is the major problem especially if the naevi covers a large area
(very rarely do these naevi turn malignant)

55
Q

What is atypical mole syndrome

A

People with a large number of clinically atypical moles

56
Q

Describe atypical moles

A

Moles with irregular margins and that are greater than 1cm in diameter
Variations in colour

57
Q

What are people with atypical mole syndrome more likely to develop

A

Increased risk of developing melanomas

58
Q

What can atypical mole syndrome sometimes me caused by?

A

Due to mutations in gene CDKN21 (p16)

59
Q

What is the significance of the p16 gene

A

It is a key tumour suppressor gene

60
Q

Which tumour is the rarest:

  1. Basal cell carcinoma
  2. Squamous cell carcinoma
  3. Melanomas
A

Melanomas

61
Q

Why are melanomas dangerous

A

As they can metastasize widely

62
Q

What are naevi?

A

Benign moles that arise from melanocytes

63
Q

What are melanomas

A

Malignant tumours that arise from melanocytes

64
Q

Why are the instances of melanomas rising?

A

More foreign travel

65
Q

List some the risk factors for melanomas

A
  1. UV exposire
  2. Tend to arise in people with pale skin
  3. Personal or family history of malignant melanomas
  4. Giant congenital naevi
66
Q

Describe the aetiology of melanomas

A
  1. Sun exposure (especially short intermittent severe exposure)
  2. Race (fair complexion red hair etc)
  3. Family history of atypical mole syndrome and multiple large atypical moles
  4. Giant congenital naevi have. small risk in turning malignant (<5%)
67
Q

What is the probability that a giant congenital naevi will turn malignant?

A

less than 5%

68
Q

In terms of sun exposure and the risk of developing melanomas which is worse:

  1. Long periods of exposure
  2. Short rare periods of intense sun burn
A

short intermittent severe exposure especially sun burning

69
Q

Describe a benign naevus

A
  1. Symmetrical
  2. Even borders
  3. Uniform colour
  4. Diameter of less than 6mm
70
Q

Describe a malignant melanoma mole

A
  1. Asymmetrical
  2. Borders uneven
  3. Colour variation
  4. Diameter greater than 6mm
  5. Lesion has changed recently
71
Q

Name the most common type of melanoma in Britain

A

Superficial spreading melanoma

72
Q

Describe early superficial spreading melanoma lesions

A

Flat macule

73
Q

Describe late superficial spreading melanoma lesions

A

Blue / black nodules

74
Q

Describe how superficial spreading melanomas look macroscopically

A

Proliferation of atypical melanocytes which invade epidermis and dermis

75
Q

Describe the genetics of superficial spreading melanomas

A

Often BRAF mutations occur

76
Q

How do we treat superficial spreading melanomas

A

By using anticancer agents

77
Q

Name some different subtypes of melanomas

A
  1. Superficial spreading melanomas
  2. Nodular melanoma
  3. Lentigo maligna
78
Q

What is the difference between a superficial melanoma and a nodular melanoma

A

In nodular melanomas microscopically you don’t see extensions of the tumour within the dermis

79
Q

Describe nodular melanomas

A

They start as a pigmented nodule that can ulcerate

80
Q

What is the prognosis like for nodular melanomas

A

Poor prognosis

81
Q

Describe how nodular melanomas look microscopically

A

Invasive atypical melanocytes invade the dermis to produce nodules of tumour cells

82
Q

Who are more likely to see lentigo malinga on?

A

Seen on chronically sun exposed sites in ELDERLY patients

eg face

83
Q

Describe lentigo malinga lesions

A

They tend to be very big flat pigmented areas of the skin

They grow via disk adhesive single cells along the dermo epidermis junction

84
Q

Why are lentigo malinga tumours hard to get rid of?

A

They usually form at difficult to operate sites

They are ill defined

85
Q

How do we treat lentigo malinga lesions

A

We can use local therapies such as creams

86
Q

As lentigo malinga lesions progress what happens

A

Melanocytes may invade the dermis (forming a lentigo malignant melanoma)
This has the potential to metastasise)

87
Q

What are the problems associated with lentigo malinga melanomas

A

They have the potential to metastasise

88
Q

Which mutations are common in lentigo malingas

A

KIT mutations are more common

89
Q

Which mutations don’t usually occur in lentigo malingas and what problems does this cause

A

BRAF mutations are less common

This means the Vemurafenib drug tends not to work

90
Q

Name 2 subtype of lentigo melanomas

A
  1. Acral lentiginous melanoma
  2. Mucosal melanomas
91
Q

Where are Acral lentiginous melanomas formed

A

On the palms and soles (occasionally sublingual)

92
Q

In whom are Acral lentiginous melanoma common

A

Afro carribeans

93
Q

How do Acral lentiginous melanoma look like

A

They form enlarging pigmented patches

94
Q

What type of mutations do Acral lentiginous melanoma exhibit

A

KIT mutations

95
Q

How common are mucosal melanomas

A

Rare and they often have a poor prognosis

96
Q

Where do mucosal melanomas usually form?

A

Oral cavity
Nasal cavity
Genitourinary
GI tract

97
Q

Describe how mucosal melanomas present clinically

A

Clinically may be a pigmented patch

98
Q

Describe how mucosal melanomas look under a microscope

A

They have an early lentiginous growth pattern

99
Q

What causes mucosal membranes

A

KIT mutation
GNAQ mutation

100
Q

How do we determine the prognosis of a tumour

A
  1. Breslow thickness
  2. Site of tumour
  3. If the tumour ulcerates
  4. Satellites/ in transit
  5. If lymph nodes are affected
101
Q

What is breslows thickness

A

It is a measure through a microscope from the granular later of the epidermis to the base of the tumour

102
Q

According to breslows thickness if a tumours is less than 1mm what is the 5 year survival percentage of a patient

A

91-95%

103
Q

According to breslows thickness if a tumours is between 1-2mm what is the 5 year survival percentage of a patient

A

75-90%

104
Q

According to breslows thickness if a tumours is between 2-4mm what is the 5 year survival percentage of a patient

A

60-75%

105
Q

According to breslows thickness if a tumours is greater than 4 what is the 5 year survival percentage of a patient

A

45-60%

106
Q

A melanoma on which sites in the body have a poor prognosis

A

Back
Arms
Neck
Scalp

107
Q

If a tumour ulcerates does that mean it have a poorer or Better prognosis?

A

If the tumour has ulcerated it has a POORER prognosis

108
Q

What do advanced melanomas sometimes form?

A

Satellites/ transits

109
Q

What are satellites in terms of tumours

A

They are cutaneous deposits that occur before lymph nodes are affected

110
Q

In patients with thick or ulcerated tumours what do we usually take

A

A sentinel node biopsy

111
Q

What is the significance of the sentinel node?

A

It is the lymph node which drain from melanomas first so if we remove it and it tests positive it indicates that most lilt the rest of the lymph nodes in that anatomic areas are affected

112
Q

If a sentinel node biopsy come back positive what should we do?

A

Remove all the lymph nodes in that autonomic areas to try and halt disease progression

113
Q

What are the problems associated with removing all the lymph nodes from a certain area?

A

Can lead to lymphedema which ultimately harms the patent

114
Q

How can we treat melanomas?

A
  1. Surgery
  2. BRAF inhibitors
  3. Immunotherapy
115
Q

How many melanomas are caused by the BRAF gene?

A

60%

116
Q

What is immunotherapy

A

Drugs which prevent tumour cells from deactivating T cells which may kill them

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