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year 2 clinical > Pigmented Skin Lesions > Flashcards

Pigmented Skin Lesions Flashcards

1
Q

Describe the formation and migration of melanocytes

A

Derived from the neural crest and, early in embryogenesis, MELANOBLASTS migrate from here to the skin, uveal tract and leptomeninges (melanomas can occur in the skin and eyes and, rarely, in the meninges)

Once melanoblasts settle in the skin, they form melanocytes

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2
Q

Where are melanocytes in the skin?

A

Solitary cells that are basally situated and surrounded by keratinocytes

Melanocyte : basal keratinocyte = 1 : 5 - 1 : 10

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3
Q

Melanocyte variation amongst different races?

A

Ratio is constant, irrespective of race

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4
Q

Describe the melanocytes in this image

A

Basal melanocytes have a small halo area around them and the keratinocytes adjacent are mostly pigmented

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5
Q

Which gene governs melanin production?

A

Melanocortin 1 receptor gene is central; it encodes MC1R protein (which sits on the cell surface)

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6
Q

Different types of melanin?

A

Eumelanin is responsible for hair colours other than red

Phaeomelanin is responsible for red hair

MC1R turns phaemoelanin into eumelanin

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7
Q

Defective copy/copies of MC1R cause?

A

One defective copy = freckling

Two defective copies = red hair and freckles

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8
Q

What are freckles?

A

AKA epihilides (singular is ephelis); they are patches where there is an increase in melanin pigmentation, due to UV exposure, and they are areas where there is an increase in mealnocytes

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9
Q

What are actinic lentigines (singular is lentigo)?

A

AKA solar lentigines OR age/liver spots; these are related to chronic UV exposure

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10
Q

Common areas with actinic lentigines?

A

Face, forearms, and forsal hands; there is increases melanin and basal melanocytes

Epidermis has elongated rete ridges, that extend between the dermal papillae

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11
Q

Development of melanocytic naevi?

A

AKA mole

May be CONGENITAL (1%) or ACQUIRED (majority in the 1st/2nd decade of life)

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12
Q

Sizes of congenital melanocytic naevi?

A

Small <2 cm

Medium >2 cm but <20 cm diameter

Giant-garment type lesions

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13
Q

Risk of melanoma with congenital melanocytic naevi?

A

Large lesions have a 10-15% increased risk of melanoma

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14
Q

Formation of usual type acquired naevi?

A
  1. During infancy, melanocytes : keratinocyte ratio breaks down at a no. of cutaneous sites
  2. Formation of simple naevi (very common benign lesions with most people having 20-30)
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15
Q

Immune regulation with relation to naevi?

A

Common naevi have low malignant potential; there is a question of whether naevus induction is immune regulated

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16
Q

Well-defined path along which acquired naevi develop?

A

Junctional naevus (CHILDHOOD) - melanocytes proliferate and form clusters/nests of cells at the DEJ , forming a flat mole

Compound naevus (ADOLESCENCE/early adulthood) - nests of naevus cells at the DEJ, as well as within the dermis, forming a central raised area surrounded by a flat patch

Intradermal naevus (ADULTHOOD) - naevus nests are entirely dermal, forming a papule/plaque/nodule with a pedunculated/papillomatous/ smooth surface; all junctional activity has ceased

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17
Q

What type of naevus is this?

A

Junctional naevus - there are nests of melanocytes attached to the epidermis

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18
Q

What type of naevus is this?

A

Intradermal naevus - nests of naevus cells within the dermis

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19
Q

Characteristics of dysplastic naevi?

A

>6 mm diameter

Variegated pigment

Asymmetry of the border

Resemble MM and may be difficult to distinguish from melanoma in-situ

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20
Q

What are the 2 clinical settings in which a dysplastic naevus can present?

A

SPORADIC:

Not inherited

One to several atypical naevi

Risk of MM is slightly increased

FAMILIAL:

Strong FH of melanoma and autosomal inheritance with a high penetrance

Lifetime risk of melanoma is 100%

21
Q

Histological appearance of a dysplastic naevus?

A

Architectural and cellular atypia; the host reaction causes inflammation and fibrosis

However, unlike in melanoma, the epidermis is not effaced (junctional naevus or, more frequently, a compound naevus)

22
Q

Describe halo naevi (rare)

A

Have a peripheral halo of depigmentation around them; these are areas of inflammatory regression that have been invaded by lymphocytes

23
Q

Describe blue naevi (rare)

A

Entirely dermal (deeper than normal moles) and consist of pigment-rich dendritic spindle cells; cellular variant may have mitoses and mimic melanoma

24
Q

Describe Spitz naevi (rare)

A

Benign naevi that may resemble MM (Spitzoid melanoma); they tend to occur on the faces/limbs of children

25
Q

Histology of Spitz naevi?

A

Consist of large spindle and/or epithelioid cells

There is EPIDERMAL HYPERPLASIA

26
Q

Macroscopic appearance of Spitz naevi?

A

Pink colouration, due to prominent vasculature; look like a haemangioma

27
Q

Development of MM?

A

Most arise “de novo” but some arise in dysplastic naevi

28
Q

Occurrence of MM?

A

More common in females (2 : 1) and are rare in childhood; incidence peaks at middle-age

May arise at any site

29
Q

Common MM sites?

A

Sun-exposed sites, e.g: scalp, face, neck, arm, trunk and legs

30
Q

Why do MMs sometimes occur in rare sites, e.g: anus, biliary tract, meninges, oesophagus?

A

Become stuck in these regions during the embryonic migration

31
Q

Red flags of an MM?

A

Change in shape

Irregular pigmentation

Bleeding

Development of satellite nodules (bad prognostic factor)

Ulceration (bad prognostic factor)

New pigmented lesions develop in adulthood

32
Q

Four main types of melanoma?

A

Superficial spreading (most common) - often affecting trunk and limbs and show regressed areas

Acral/mucosal lentiginous - acral, e.g: on the heel or sunungual, and mucosal

Lentigo maligna - affect sun-damaged face/neck/scalp

Nodular - affect various sites but most common on the trunk

33
Q

What is meant by: RGP (radial growth phase) VGP (vertical growth phase) ?

A

RGP - grow as macules when either entirely in-situ or with dermal microinvasion

VGP - eventually, melanoma cells invade the dermis, forming an expansile mass with mitoses

34
Q

Melanomas in which growth phase can metastasise?

A

Only those in VGP

35
Q

What is a melanoma in-situ?

A

Confined to the epidermis, above the basement membrane; when they drop out, this is when they are invasive

36
Q

What is nodular melanoma?

A

MM cells proliferate downwards through the skin – AKA vertical growth (there is no clinical/microscopic RGP and so it may be more aggressive)

Lesion presents as a nodule that has been rapidly enlarging

37
Q

3 types of MM with RGP +/- VGP?

A
  1. Superficial spreading melanoma (SSM)
  2. Acral / mucosal lentiginous melanoma (A/MLM)
  3. Lentigo maligna melanoma (LMM)
38
Q

MM with VGP only?

A

Nodular melanoma

Note: some melanomas cannot be accurately classified

39
Q

What is the Breslow thickness?

A

mm between the deepest tumour cell and the granular layer of the epidermis

40
Q

Stages of melanoma corresponding to different Breslow thicknesses?

A

pTis-melanoma (in-situ) - 100% survival

pT1-tumour 4mm thick - 20% survival

pT2-tumour is 1-2mm - 80% survival

pT3-tumour is 2-4mm - 55% survival

pT4-tumour > 4mm thick - 20% survival

41
Q

Description of ulcerated melanomas?

A

Suffix “b” indicated tumour ulceration, e.g: pT3b is a tumour between 2-4 mm with ulceration but this is equivalent to a non-ulcerated pT4

42
Q

Adverse prognostic factors for MM?

A

High mitotic rate

Lymphovascular invasion

Satellites

Sentinel lymph node involvement

43
Q

Spread of MM?

A
  1. Local dermal lymphatics - satellite deposits of MM
  2. Regional lymph node metastases – common pattern of disease progression; nodes can have a sentinel node biopsy and be excised (radical lymphadenectomy)
  3. Blood spread to various bodily regions
44
Q

MM treatment?

A

Primary excision to give clear margins

Some also receive a sentinel node biopsy and, if +ve, a regional lymphadenectomy (controversial)

Chemo/immunotherapies Genetic therapies

45
Q

Excision of MM based on Breslow thickness?

A

If in-situ then clear by circa 5 mm

If invasive but 1 mm thick - 2cm clearance

SNB if >1 mm thick or thinner with mitoses

46
Q

Mutations in different types of melanoma and how these can be specifically treated?

A

Some acral melanoma have c-kit mutations (treat with imatinib)

On intermittently sun-exposed skin, may have a BRAF mutation

47
Q

Difference between wild Type B-Raf and mutated B-raf?

A

Wild type is a weak proto-oncogene; when mutated, it drives cell proliferation by up-regulating MEK and ERK

48
Q

Drugs that interfere with BRAF, MEK and ERK?

A

Dabrafenib and Vemurafenib

Stop having an effect after 6 month and should be combined with MEK inhibitor

year 2 clinical (119 decks)

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