Pathology of Pigmented Lesions Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

where do melanoblasts migrate to from the neural crest to become melanocytes?

A

skin
uveal tract
leptomeninges

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is the melanocyte:basal cell ratio affected by race?

A

its the same

just produce more melanin in darker skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do melanocytes look like?

A

have a slight halo around them
don’t have pigment around them
the ones with pigment are squamous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what does the MC1R gene do?

A

encodes MC1R protein that sits on cell surface
determines the balance of pigment in skin/hair
2 mutated gene = red hair and freckles
1 mutated gene = one or the other
turns phaelomelanin into eumelanin (brown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are freckles?

A

ephilides

patchy increase in melanin production due to mutated MC1R gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are actinic lentigines?

A

“liver spots” or “age spots” related to sun exposure

causing increase in basal melanocytes and therefore melanin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are melanocytic naevi?

A

Moles
can be congenital or acquired
rare to be born with them but can develop in 1st and 2nd decade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 3 types of melanocytic naeivi?

A

dysplastic
spitz
blue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the 3 types of congenital melanocytic naevi?

A

small (<2cm)
medium (>2cm <20cm)
giant garment type lesions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

do congenital melanocytic naevi carry a melanoma risk?

A

if large

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are usual type acquired naevi?

A

melanocyte:keratinocyte ratio breaks down at some cutaneous sites
causes formation of simple naevi
- very common
- very low malignant potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

are naevi immune related?

A

possibly

immunosuppressed have more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the 3 stages of naevi development?

A

junctional naevus - melanocytes proliferate causing nests of cells at junction
compound naevus - nests of cells at junction and some in dermis
intradermal naevus - all nests of melanocytes in dermis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do naevi look like on histology?

A

melanocytes form a nest

can be near the junction if younger or dropped into dermis if older

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what are dysplastic naevi?

A

> 6mm
asymmetric border
variegated pigment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the 2 clinical settings of dysplastic naevi?

A
sporadic
- a couple of atypical naevi
- low malignant risk
- not inherited
familial
- inherited (autosomal)
- hundreds of atypical naevi
- almost 100% melanoma lifetime risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

name 2 rarer types of naevi?

A

halo - peripheral halo of depigmentation (benign)

blue - only dermal (never been junctional) with pigment rich dendritic cells, can mimic melanoma

18
Q

which naevi is common in young children?

A

spitz naevi

19
Q

describe spitz naevi

A

large spindle and/or epitheloid cells
can closely mimic melanoma but are usually benign
difficult diagnosis as there is a malignant variant

20
Q

what do spitz naevi look like on histology?

A

clefting around the nests of melanocytes

21
Q

how do most melanoma arise?

A

most are de novo
but some can arise in dysplastic naevi
multifactorial - sun, genetics (skin type, dysplastic naevi)

22
Q

who/where is melanoma more common in?

A

females
incidence peaks in middle aged
in sun exposed sites

23
Q

what are some characteristics of a melanoma?

A
change in shape
irregular colour
bleeding
ulceration
new pigmented lesion in adulthood
development of small nodules around the mole
or ABCDE
24
Q

what are the 4 main types of melanoma?

A

superficial spreading - trunk and limbs
acral/mucosal lentiginous - acral and mucosal
lentigo maligna - sun exposed face, neck, scalp
nodular - trunk

25
Q

what are regressed areas and what do they suggest?

A

depigmented areas of a lesion

indicate a melanoma whch has began to invade? as immune response is attacking parts

26
Q

what is subungual acral melanoma?

A

black fingernail

melanoma at fingernail

27
Q

how do SSM, A/MLM and LMM all begin?

A

flat macules which radiate outwards (RGP)

melanoma cells then invade downwards into dermis forming a mass (VGP)

28
Q

which phase of melanomas can metastasise?

A

melanomas in VGP

29
Q

what is pagetoid/in situ invasion?

A

hasn’t crossed basement membrane so is basically harmless

shot gun groups of melanoma cells

30
Q

how do nodular melanomas develop?

A

don’t have a RGP/flat phase so just suddenly appear as a lump/nodule
very aggressive/invasive

31
Q

what is Breslow thickness?

A

depth from granular layer

32
Q

what are the categories of Breslow thickness and survival rate?

A
pTis = in situ = 100% survival
pT1 = <1mm = 90%
pT2 = 1-2mm = 80%
pT3 = 2-4 = 55%
pT4 = >4mm = 20%
33
Q

what other factor of melanoma determines prognosis?

A

ulceration

indicated by suffix b

34
Q

through what 3 methods can melanoma spread?

A

local dermal lymphatics (satellite deposits in skin)
regional lymph node metastases
blood spread (soft tissue, GI etc)

35
Q

what is sentinel node?

A

the lymph node draining the melanoma

often removed

36
Q

how is melanoma treated?

A

primary excision to remove lesion
some have a sentinel node biopsy and if +ve have a regional lyphadenectomy
chemo/immunotherapy, genetic therapy

37
Q

how can melanomas be treated genetically?

A

some have c-kit or b-raf mutations which can be targetted

38
Q

how are B-RAF inhibitors used?

A

often in conjunction with MEK inhibitor

39
Q

what is seen in actinic lentigines on histology?

A

elongated rete ridges

40
Q

what are the features of dysplasia?

A

architectural and cellular atypia
fibrosis and inflammation
epidermis unaffected

41
Q

what is BRAF?

A

cytosolic proto-oncogene which when mutated drives cell proliferation by up-regulating MEK and ERK