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Dermatology > Pigmented Skin lesions - PATHOLOGY > Flashcards

Pigmented Skin lesions - PATHOLOGY Flashcards

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1
Q

Where do melanocytes derive from?

A

The Neural crest

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2
Q

Melanocyte - embryonic origins

A

Early in embryogenesis MELANOBLASTS migrate from neural crest to…

  • the skin
  • uveal tract
  • leptomeninges
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3
Q

What happens once melanoblasts settle in the skin?

A

Form melanocytes

Basally situated

Melanocyte ratio: basal keratinocyte is constant irrespective of race

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4
Q

Under a microscope, what do melanocytes look like?

A

Dark cells with pale “halos”

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5
Q

MC1R genetics

A

Melanocortin 1 receptor gene is central

Encodes MC1R protein - sits on cell surface

Determines balance of pigment in skin and hair

Eumelanin hair colour other than red

Phaeomelanin causes red hair

MC1R turns phaeomelanin into eumelanin

One defective copy of MC1R causes freckling

Two defective copies - red hair and freckles

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6
Q

Ephilides

A

Freckles. (ephilis)

Patchy increase in melanin pigmentation

Occurs after UV exposure

Most common in fair skinned and red heads

Reflects clumpy distribution of melanocytes

Islands with most melanocytes tan

Pale intervening skin has fewer melanocytes

Have one defective copy of MC1R gene

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7
Q

Actinic lentigines

A

Actinic/solar lentigines (lentigo sg)

Age/liver spots

Related to UV exposure

Epidermis has elongated rete ridges.

Increase melanin and basal melanocytes

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8
Q

Melanocytic naevi

A

> Broad range of lesions

> May be congenital or acquired

> most naevi acquired in 1st 2 decades

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9
Q

Congenital melanocytic naevi

A

Small < 2cm diameter

Medium >2cm but < 20cm

LARGE > 20cm

Giant - garment type lesions

Large lesions have a 10-15% risk of melanoma

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10
Q

Acquired naevi

A

During infancy the melanocytes: keratinocyte ratio breaks down at a number of cutaneous sites

–>

Formation of SIMPLE NAEVI

  • common benign lesions
  • average person has 20-30 naevi
  • low malignant potential
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11
Q

Type of naevus present in childhood?

A

Junctional naevus.

Melanocytes proliferate –> clusters of cells at DEJ

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12
Q

Type of naevus present in adolescence?

A

Compound naevus.

Junctional clusters/nests + groups of cells in dermis

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13
Q

Type of naevus present in Adulthood

A

Intradermal naevus

  • all junctional activity has ceased; entirely dermal

Become flattened, become like nerves

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14
Q

Dysplastic naevi

> size
colour
symmetry

A

over 6mm diameter

Variegated pigment

Asymmetry of border

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15
Q

Dysplastic naevi - 2 clinical settings

A

Sporadic

  • not inherited
  • one to several atypical naevi
  • risk of malignant melanoma slightly raised.

Familial

  • strong FH of melanoma
  • autosomal inheritance
  • high penetrance
  • atypical naevi
  • lifetime risk of melanoma 100%
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16
Q

Dysplastic naevi vs melanoma

A

Architectural atypic and cellular atypic

Host reaction - fibrosis and inflammation

Unlike melanoma epidermis is not effaced

Severe dysplasia may be difficult to distinguish from melanoma in situ

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17
Q

Halo naevi

A

Rarer

Peripheral halo of depigmentation.

Overrun by lymphocytes

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18
Q

Blue naevi

A

Entirely dermal

Pigment rich dendritic spindle cells

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19
Q

Spitz naevus

A

Consist of large spindle &/or epithelioid cells

May mimic melanoma

Mostly benign

Can be malignant

Often pink/red because they are well vascularised

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20
Q

When to suspect melanoma

A 
> Change in shape
> Irregular pigmentation
> Bleeding
> Development of satellite nodules
> ulceration
> New pigmented lesion develops in adulthood
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21
Q

Types of malignant melanoma

A

Four types

> Superficial spreading - trunks and limbs

> Acral/mucosal lentiginous - acral and mucosal

> Lentigo maligna - sun damaged face/neck/scalp

> Nodular - often trunk

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22
Q

Acral/mucosal lentiginous

A

Type of malignant melanoma

Acral (toes and fingers) and mucosal

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23
Q

Lentigo maligna

A

Sun damaged face/neck/scalp

Type of melanoma

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24
Q

Superficial spreading melanoma; acral/mucosal lentiginous melanoma; lentigo maligna

Growing pattern

A

Grow as macule when either entirely in-situ or with dermal microinvasion - radial growth phase

Eventually melanoma cels invade the dermis
–> expansile mass with mitoses (VERTICAL GROWTH PHASE)

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25
Which melanomas can metastasise?
Only Vertical growth phase melanomas
26
Nodular melanoma
> No clinical or microscopic evidence of RGP > Simply a nodule of VERTICAL GROWTH PHASE tumour (no macule present) > Considered more aggressive
27
Melanoma prognosis
Relates to Breslow depth and ulceration pTis - in situ (100%) pT1-tumour <1mm pT2 tumour 1-2mm pT3 is 2-4mm pT4 >4mm thick (20%) ULCERATION is a strong adverse indicator Suffic "b" indicates tumour ulceration High mitotic rate, lymphovascular invasion, satellites, sentinel lymph node involvement
28
Definition of Breslow thickness?
Deepest tumour from granular layer mm
29
Malignant melanoma - spread
1. Local dermal lymphatics --> satellite deposits of MM ``` 2. Regional lymph node metastases - common pattern Nodes excised (radical lymphadenectomy) ``` 3. Blood spread - -> Skin/soft tissue - -> heart - -> lungs - -> GI tract - -> Liver - -> Brain
30
Melanoma treatment
> Primary excision to give clear margins > Sentinel node biopsy - if positive then regional lymphadenectomy > Treatment of advanced disease is difficult
31
If cancer is in situ, how much is cleared?
5mm ish
32
If cancer is invasive by <1mm thick - how much clearance?
1cm
33
If invasive and >1mm thick -clearance?
2cm
34
Sentinel node biopsy if...
>1mm thick or thinner with mitoses
35
Ckit mutations treated with
Imatinib
36
BRAF
Weak cytosolic proto-oncogene Mutated: drives cell proliferation by up-regulating MEK and ERK Dabrafenib Vemurafenib + MEK inhibitor
37
Benign seborrhoeic keratosis
Epidermal tumour Look stuck on - rice crispy on the skin. Greasy hyperkeratotic surface Benign proliferation of epidermal keratinocytes Face & trunk Epidermal acanthosis, hyperkeratosis, horn cysts
38
Precancerous dysplasias
Bowen's disease Actinic keratosis Viral lesions
39
Invasive malignancies
Basal and squamous cell carcinoma
40
Epidermal acanthosis
Thickening
41
Eruptive appearance may indicate...
Internal malignancy Leser-Trelat sign
42
Leser-Trelat sign
the explosive onset of multiple seborrheic keratoses (many pigmented skin lesions) often with an inflammatory base.
43
BCC subtypes
1. Nodular 2. Superficial 3. Infiltrative (morphoeic)
44
Where do BCCs sprout from?
From epidermis. Groups of cells invade the dermis. Peripheral palisading. Mitoses and apoptosis very numerous
45
Are BCCs slow or fast growing?
Slow growing Locally destructive Almost never metastasises Could invade eye --> brain
46
Most important type of BCC?
Infiltrative. May infiltrate tissues widely. Prominent desmoplastic fibrous stroma Margins are poorly defined May spread along nerves Resection may be challenging.
47
Precursors of SCC
Range of precursors for SCC Bowen's disease - especially on legs Actinic keratosis - esp head and neck Viral lesions - especially on anogenital skin Precursors show squamous DYSPLASIA
48
Precursors of SCC show?
Dysplasia
49
BOWEN'S DISEASE
SCC in situ Mostly on lower leg Scaly patch/plaque Irregular border No dermal invasion.
50
Actinic keratosis
Common Sun exposed skin Variable epidermal dysplasia Common precursor of invasive SCC
51
Viral precursors
> Viral genital lesions often dysplastic > Erythroplasia of Queryat- Bowen's of glans > Associated with HPV
52
HPV Type 16 associated with...
Dysplasia
53
HPV in 100% of
Penile dysplasia
54
HPV found in 50% of
Invasive penile SCC
55
Most common clinical setting for SCC
Elderly, sun exposed sites UV implicated
56
Occasional setting for SCC Rare
> Chronic leg ulcers > Sites of burns > Chronic lupus vulgaris Rare - xeroderma pigmentosum (dystrophic varian of epidermolysis bullosa)
57
Xeroderma pigmentosum
Cant repair the DNA Accumulate mutations very quickly and develop numerous skin tumours.
58
SCC > Behaviour >Adverse Prognostic features
BEHAVIOUR: > generally good prognosis > locally invasive > low but definite risk of metastasis ADVERSE PROGNOSTIC FEATURES - Thickness > 4mm and poor differentiation - lymphatic / vascular space invasion - perineural spread - specific sites poorer prognosis - scalp, ear, nose
59
Columella
columella is the bridge of tissue that separates the nostrils at the nasal base
60
1.Dermatofibroma Dermatofibrosarcoma protuberans
1. overgrowth of the fibrous tissue situated in the dermis | 2. very rare tumor. It is a rare neoplasm of the dermis layer of the skin,[2] and is classified as a sarcoma.
61
Angiosarcoma
diffuse Bruise-like lesion Highly malignant
62
Merkel cell carcinoma
HIGHLY AGGRESSIVE SKIN CANCER Pressure receptor cells beneath the basement membrane Cutaneous equivalent of small cell carcinoma of lung Merkel cell polyomavirus (Primary small cell neuroendocrine)
63
Mycosis fungoides
Cutaneous T cell lymphoma T cells move towards epidermis Neoplastic T cells Epidermotropic
64
Cutaneous B cell lymphoma
Tumours of the lymph nodes and lymphatic system | Malignant proliferation of B cell lymphocytes

Dermatology (8 decks)

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