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Dermatology > Pathology of Skin Cancer > Flashcards

Pathology of Skin Cancer Flashcards

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Dermatology Board Prep flashcards
1
Q

During embryonic development, melanoblasts migrate from the neural crest to where?

A

skin
uveal tract (gives pigment in eye)
leptomeninges (in the brain)

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2
Q

Where do melanocytes usually sit and where do they transfer their pigment to?

A

Sit on basement membrane

Transfer pigment to keratinocytes (can often be seen histologically)

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3
Q

What gene determines balance of pigment in skin and hair?

A

Melanocortin 1 receptor gene
MC1R
Turns phaeomelanin into eumelanin

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4
Q

What compound is responsible for giving people red hair?

A

Phaeomelanin causes red hair

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5
Q

What compound causes any hair colour other than red?

A

Eumelanin

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6
Q

How many faulty copies of the MC1R gene do you need to have freckles?

A

1

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7
Q

If you have red hair and freckles, how many mutated copies of the MC1R gene do you have?

A

2

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8
Q

What are freckles (ephilides) ?

A

Patchy increase in melanin pigmentation
Occurs after UV exposure
Reflects clumpy distribution of melanocytes

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9
Q

What are solar letigines?

A

age’ or ‘liver’ spots

Related to UV exposure

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10
Q

Where are solar letigines usually found?

A

Face, forearms and dorsal hands

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11
Q

How do patients get melanocytic naevi?

A

congenital or acquired

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12
Q

How are congenital naevi classified?

A

Small <2cm diameter
Medium >2cm but <20cm diameter
Giant-garment type lesions

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13
Q

What is the risk associated with large congenital melanocytic naevi ?

A

10-15% risk of melanoma

May need staged surgical excision

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14
Q

How are melanocytic naevi usually acquired?

A

During infancy the melanocytes : keratinocyte ratio breaks down at a number of cutaneous sites
=> formation of SIMPLE NAEVI

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15
Q

What is thought to contribute to acquired naevi?

A

Immunosuppresion

- immunosuppressed leukaemic children have more naevi

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16
Q

How many simple melanocytic naevi does an average person usually posses? And are they dangerous?

A

average person has 20 - 30 naevi

common naevi have low malignant potential

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17
Q

Describe the path of acquired naevi development from childhood to adulthood

A

CHILDHOOD =Junctional naevus
=> clusters of cells at DEJ

ADOLESCENCE = Compound naevus
=> junctional clusters + groups of cells in dermis

ADULTHOOD = Intradermal naevus
=> all junctional activity has ceased; entirely dermal

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18
Q

Give 3 examples of less common types of naevi

A

dysplastic, Spitz, blue

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19
Q

Describe the general appearance of a dysplastic naevi?

A

> 6mm diameter
Variegated pigment
Border asymmetry

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20
Q

Dysplastic naevi can either be sporadic or familial. Describe the difference between the two

A

SPORADIC
not inherited
1+ atypical naevi
risk of MM slightly raised

FAMILIAL
strong FH of melanoma
autosomal inheritance
high penetrance eg CDKN2A
lots of atypical naevi
lifetime risk melanoma up to 100%
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21
Q

What diagnosis is often confused with severe dysplastic naevi?

A

Severe dysplasia may be difficult to distinguish form melanoma in-situ

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22
Q

What is indicated by a “Halo” naevi?

A

peripheral halo of depigmentation

  • show inflammatory regression
  • overrun by lymphocytes
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23
Q

Where are Blue naevi found and what do they contain?

A

entirely dermal

consist of pigment rich dendritic spindle cells

24
Q

At what age is a Spitz naevus common?

A

Usually occur <20 years

25
Q

What do Spitz lesions contain?

A

Consist of large spindle and/or epithelioid cells

**May closely mimic melanoma
BUT Most are entirely benign

26
Q

Why do many Spitz naevi display a pink discolouration?

A

Prominent surface vasculature

27
Q

What sites does melanoma commonly affect?

A

sun-exposed sites scalp, face, neck, arm, trunk, leg

28
Q

What sites are rarely affected by melanoma?

A

eye, meninges, oesophagus, biliary tract, anus

29
Q

What factors can make you more likely to suspect melanoma?

A 
Change in shape
Irregular pigmentation
Bleeding
Development of satellite nodules
Ulceration
New pigmented lesion develops in adulthood
30
Q

What are the four main types of melanoma?

A

Superficial spreading
Acral/mucosal lentiginous
Lentigo maligna
Nodular

31
Q

Where are superficial spreading melanomas most commonly seen?

A

trunk and limbs

32
Q

Where are lentigo maligna melanomas often seen?

A

sun-damaged face/neck/scalp

33
Q

Where are nodular melanomas often seen?

A

varied sites but often trunk

34
Q

What factors determine melanoma prognosis?

A

Breslow Thickness and Ulceration

35
Q

What is Breslow Thickness?

A

Measurement from the granular layer to the deepest tumour cell

36
Q

What is the difference in survival rate between a melanoma of Breslow thickness <1mm and a tumour >4mm?

A

pT1-tumour < 1mm-90% survival

pT4-tumour > 4mm thick-20% survival

37
Q

How is melanoma usually treated?

A

Primary excision to give clear margins
Some also receive a sentinel node biopsy
If SN positive - regional lymphadenectomy

advanced disease = difficult
Chemo, immunotherapy, genetic therapies

38
Q

What mutation is common in acral melanomas and what treatment can be used for this?

A

c-kit mutations

treated with imatinib

39
Q

What is seborrhoeic keratosis and where does it usually occur?

A

Benign proliferation of epidermal keratinocytes

Common on face and trunk in ageing skin

40
Q

Describe the morphology of lesions in seborrhoeic keratosis

A

Stuck on appearance-greasy hyperkeratotic surface

41
Q

What is Leser-Trelat’s sign?

A

Eruptive appearance of many lesions indicating internal malignancy

42
Q

What age groups usually get Basal Cell Carcinoma?

A

middle aged and elderly people in the UK
on Sun-exposed sites

younger people more likely to develop BCC in Australia

43
Q

What are the three categories of Basal Cell Carcinoma?

A

Nodular
Superficial
Infiltrative (morphoeic)

44
Q

Do basal cell carcinomas usually grow quickly or slowly?

A

Slowly

45
Q

DO basal cell carcinomas metastasize?

A

Almost never metastasises

May kill by invading eye/brain

46
Q

What factors make resection of basal cell carcinomas difficult?

A

Margins are poorly defined

May spread along nerves

47
Q

Give examples of precursors for squamous cell carcinoma

A

Bowen’s disease - on legs
Actinic keratosis - on head/neck
Viral lesions - on anogenital skin

48
Q

What do precursors of squamous cell carcinoma show?

A

squamous DYSPLASIA

49
Q

Describe the morphology of a Bowen’s disease lesion

A

Scaly patch/plaque
Irregular border
No dermal invasion

**Squamous cell carcinoma in –situ*

50
Q

Where does actinic keratosis usually present?

A

Sun-exposed skin esp. scalp, face, hands

51
Q

How is Actinic Keratosis usually defined and what is it a precursor of?

A

Variable epidermal dysplasia

Precursor for INVASIVE SCC

52
Q

What variation of HPV is involved in dysplasia?

A

HPV Type 16

**HPV in almost 100% penile dysplasia

53
Q

In what percentage of invasive penile SCC is HPV involved?

A

50%

54
Q

Give some examples of common, less common and rare cases in which SCC would arise

A

COMMON:
- sun exposed sites in the elderly

LESS COMMON

  • chronic leg ulcers
  • burns

RARE

  • xeroderma pigmentosum
  • epidermolysis bullosa
55
Q

Give examples of tissues and other types of cell (NOT melanocyte/basal cell/ squamous cell) from which dermatological tumours can arise

A 
Langerhans cells
Merkel cells
subcutaneous fat
smooth muscle of arrector pili
lymphoid tissue

Dermatology (18 decks)

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