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2A week 4,7 - skin cancer, hair and nail disorder > Epidermal melanocytic lesions - pathology > Flashcards

Epidermal melanocytic lesions - pathology Flashcards

1
Q

what embryo layer do melanocytes arise from

A

neuroectoderm

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2
Q

do melanocytes proliferate frequently

A

no; they have a low mitotic rate

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3
Q

where do melanocytes migrate to during fetal development

A

migrate from the neural crest to the eye (iris, retina, choroid), medulla oblongata, leptomeninges, schwann cells etc.

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4
Q

where do melanoblasts remain in the body after gestation (3)

A
  1. head and neck;
  2. dorsal aspects of distal extremities;
  3. pre sacral
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5
Q

where are blue naevi and pigmented epitheliod melanocytomas found

A

in areas where melanoblasts remain, especially in dorsal aspects of distal extremities

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6
Q

what cells are melanocytes closely related to

A

keratinocytes

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7
Q

what does a melanocyte-keratinocyte unit comprise of

A

1 melanocyte and 30-40 keratinocytes which recieve melanin granules produced by the melanocyte

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8
Q

what determines the colour of skin

A

the ratio of melanin in membrane bound granules: melanin lying free in cells

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9
Q

% of membrane bound granules in differnet skin types

A

black - 11%
brown - 37%
white - 85%

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10
Q

what are the 2 types of melanin found in skin and what kind of skin are they found in

A
  1. phaeomelanin (yellow-red, oval shape) - found in white skin;
  2. eumelanin (brown-black, round shaped) - found in black skin
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11
Q

how is melanin transferred to keratinocytes

A

via dendritic process

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12
Q

where is melanin located in keratinocytes

A

located above the nucleus (like an umbrella) and shields the nucleus from UV radiation

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13
Q

what 2 hormones affect melanin production

A

proopiomelanocortin (POMC) and alpha-melanocyte stimulating hormone (MSH)

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14
Q

what drives melanin production

A

UV exposure

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15
Q

what enzymes are most implicated in the pathways for melanin production

A

kinases

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16
Q

when do melanocytic lesions generally appear and why (lifespan)

A

start during puberty and end during menopause - the development of these are sensitive to sex hormones

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17
Q

what is an ephelis

A

freckle - increase in melanin within the basal keratinocytes (no increase in melanophages or melanocytes)

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18
Q

what is lentigo

A

linear proliferation of melanocytes in the basal layer, lens shaped

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19
Q

how does lentigo appear clinically

A

well circumscribed lens shaped dark lesion with soft edges

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20
Q

3 types of lentigo

A

acral; actinic; ink spot

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21
Q

what is a junctional naevus

A

a flat mole - progession of a lentiginous lesion - melanocytes arrange themselves in nests at the tip of epidermal rete ridges located at the junction of the epidermis and the dermis

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22
Q

junctional naevi clinical presentation

A

flat pigmented macule, commonly arises during puberty

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23
Q

what is a compound naevus

A

the presence of melanocyte nests at the junction and underlying dermis

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24
Q

how do the cells differ in compound naevi compared to junctional

A

the cells are smaller (size maturation) and not pigmented

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25
Q

what is the most common melanocyte lesion seen

A

compound naevi

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26
Q

where are the cells in compound naevi found

A

majority are in the dermis, some junctional nests present

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27
Q

what is an intradermal naevus

A

benign melanocytic lesion consisting only of nests in dermis

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28
Q

compound naevus presentation

A

A central raised area surrounded by a flat patch

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29
Q

intradermal naevus presentation

A

elevated, dome-shaped bump on the surface of the skin seen in middle ages pts

30
Q

naevus natural progression

A

lentigo -> junctional naeuvus -> compound naevus -> intradermal naevus -> regression (senescence)

31
Q

how do the cells in an intradermal naevus appear

A

nests of small uniform mature cells in the dermis that may be multinucleated; melanin is not usually seen in these cells

32
Q

what is a spitz naevus

A

a benign lesion that shows enlarged melanocytes with a prominent nucleoi; may have kamino bodies at the epidermodermal junction; may show collagen deposition

33
Q

what are kamino bodies

A

pink “blobs” that consist of basement membrane material (collagen type IV/VII, fibronectin etc.)

34
Q

spitz naevus clinical presentation

A

may mimic melanoma - central homogenous black-blue pigmentation surrounded by
streaks, pseudopods, or finger-like projections, which are regularly and symmetrically distributed at the periphery

35
Q

what are blue naevi

A

a type of melanocytic naevus in which spindle-shaped or, less commonly, ovoid naevus cells, are located deep within the dermis

36
Q

how do blue naevi occur

A

cells stop their migration to the epidermis and remain in the dermis, they produce melanin which is picked up by macrophages and histocytes

37
Q

why doe blue naevi appear blue

A

due to the depth of the melanin in the dermis and the Tyndall effect

38
Q

what is the Tyndall effect

A

the preferential absorption
of long light wavelengths by melanin and the scattering of
shorter wavelengths, representing the blue end of the spectrum, by collagen bundles

39
Q

what is a dysplastic naevus

A

a naevus that extends in an irregular manner beyond the border of the intradermal component - shouldering phenomenon

40
Q

junctional naevus vs dysplastic

A

junctional - will
usually end in line with the intradermal component, located at the tips of the rete ridges, no nuclear atypia, no fibrosis;
dysplastic - extends past the jucntional boarder irregularly (shouldering phenomemnon), junctional nests will be present between the rete ridges and will bridge adjacent rete ridges (architectural disorder), enlarged, variable nuclei, characteristic layers of
eosinophilic fibrosis surrounding the elongated epidermal rete ridges, melanophages in the superficial dermis, lymphohistiocytic inflammatory infiltrate

41
Q

how is high grade vs low grade assessed in dysplastic naevus

A

cytological atypia

42
Q

how does lamella fibroplasia occur (pathway)

A

basal keratinocytes/ melanocytes die -> melanin released -> picked up by macrophages forming melanophages -> invoked healing sequence ->chronic inflammation followed by fibrosis

43
Q

what is regression

A

the process of lymphocitic inflammation -> melanophase accumulation -> vascular proliferation -> fibrosis in a melanocytic lesion

44
Q

what does regression look like clinically

A

melanocytic pattern but with a clearing (white/pale area) in the middle of the lesion where melanin is being taken up by melanophages

45
Q

what other lesions are characterised by lymphocytic reaction and regression

A

kertatoacanthoma and melanoma

46
Q

what is the critera used for melanoma diagosis

A

A - asymmetry
B - boarder irregularity
C - conspicuous junctional activity
D - dermal mitotic activity

47
Q

what are the 4 main types of malignant melanoma

A
  1. lentigo maligna/LMM
  2. superficial spreading
  3. nodular
  4. acral-lentiginous
48
Q

which melanoma is not related to sun exposure

A

acral lentiginous melanoma

49
Q

lentigo maligna melanoma -pathology

A
  1. lentiginous proliferation of single cells at the epidermodermal
    junction, which can also colonise hair follicles;
  2. The dermis usually shows a lot of sun damage and the epidermis is often quite atrophic with flattening of the rete ridges;
  3. When lentigo maligna invades, the malignant cells will be present in the
    dermis where they can have an epithelioid or spindle cell
    appearance
50
Q

superficial spreading pathology

A

lots of chaotic cells arranged in nests and single cells at the junction with prominent pagetoid extension of malignant melanocytes into
the upper layers of the epidermis

51
Q

nodular melanoma pathology

A
  1. a nodule of pleomorphic, mitotically active melanocytes in the dermis;
  2. no junctional activity beyond the border of the main lesion;
  3. often arises
    on intermittently sun exposed skin
52
Q

acral melanoma pathology

A

lentiginous proliferation of
single cells along the epidermodermal junction and when it invades comprises nests of pleomorphic melanocytes within the dermis

53
Q

what are the 2 growth phases in melanoma

A

radial and verticle

54
Q

what is the radial growth phase

A

growth horizontally - don’t have capacity to get into lymphatics and metastasise

55
Q

what is the vertical growth phases

A

grow vertically/downwards into the dermis - can metastesise

56
Q

clinical appearance of a tumour in the radial growth phase

A

flat, pigmented lesions

57
Q

clinical appearance on transformation from radial to vertical growth phase

A

nodule forms on an otherwise flat pigmented lesion

58
Q

why can tumours not metastasise in the radial phase

A

the majority of the malignant melanocytes are present within the epidermis and at the epidermodermal junction in a radial growth phase

59
Q

what does pleomorphic mean

A

nuclei vary in shape and size

60
Q

what would a melanoma biopsy show (3)

A
  1. pleomorphic cells - some show prominent eosinophilic
    nucleoli, reflecting their increased metabolic activity;
  2. nests
  3. mitotic activity
61
Q

what does a biopsy of lentigo maligna show

A

irregular proliferation of single dark atypical
melanocytes distributed along the base of the
epidermis -> when it invades it forms nests of malignant cells, characteristic of invasive lentigo maligna melanoma

62
Q

what does a superficial spreading melanoma biopsy show

A
  1. chaotic proliferation of very atypical melanocytes distributed at all levels of the
    epidermis in a buckshot pattern (pagetoid spread);
  2. When this tumour invades the dermis it forms nests of mitotically active pleomorphic cells
63
Q

acral melaonoma biopsy

A
  1. crowded proliferation of single atypical melanocytes distributed along the base of the thick epidermis;
  2. these single cells also extend upwards into all layers of the epidermis
64
Q

what is Breslow’s thickness

A

a measure of the granular layer of the epidermis to the deepest melaoncyte in the dermis -> the thicker the layer the more likely it will metastesise

65
Q

what is used to determine the T staging on the melanoma

A

the breslow thickness

66
Q

what else impacts the T staging of melanoma (2)

A
  1. ulceration;
  2. mitotic activity;
  3. perinerual invasion - increases risk of vascular invasion and metastasis
67
Q

what marker can be used for identifying lymphatic channels in tissue sections

A

D240 - an immunohistochemical marker

68
Q

what is a good prognostic sign in melanoma

A

tumour infiltrating lymphocytes - indicate that the host’s immune system is responding to the tumour

69
Q

what contributes to the N classification of staging melanoma

A

microstellites - small deposits of tumour away from the main tumour mass (within 2cm, if further then they are ‘in-transit’ metastesies)

70
Q

mutation in what gene is highly involved in melanoma

A

p53

71
Q

what other pathway is implicated in melanoma

A

MAP-kinase

2A week 4,7 - skin cancer, hair and nail disorder (5 decks)

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