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Dermatology > Pigmented Skin lesions - PATHOLOGY > Flashcards

Pigmented Skin lesions - PATHOLOGY Flashcards

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Dermatology Board Prep flashcards
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
Q

Which melanomas can metastasise?

A

Only Vertical growth phase melanomas

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26
Q

Nodular melanoma

A

> No clinical or microscopic evidence of RGP

> Simply a nodule of VERTICAL GROWTH PHASE tumour (no macule present)

> Considered more aggressive

27
Q

Melanoma prognosis

A

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
Q

Definition of Breslow thickness?

A

Deepest tumour from granular layer mm

29
Q

Malignant melanoma - spread

A
  1. Local dermal lymphatics –> satellite deposits of MM
2. Regional lymph node metastases - common pattern
Nodes excised (radical lymphadenectomy)
  1. Blood spread
    - -> Skin/soft tissue
    - -> heart
    - -> lungs
    - -> GI tract
    - -> Liver
    - -> Brain
30
Q

Melanoma treatment

A

> Primary excision to give clear margins

> Sentinel node biopsy
- if positive then regional lymphadenectomy

> Treatment of advanced disease is difficult

31
Q

If cancer is in situ, how much is cleared?

A

5mm ish

32
Q

If cancer is invasive by <1mm thick - how much clearance?

A

1cm

33
Q

If invasive and >1mm thick -clearance?

A

2cm

34
Q

Sentinel node biopsy if…

A

> 1mm thick or thinner with mitoses

35
Q

Ckit mutations treated with

A

Imatinib

36
Q

BRAF

A

Weak cytosolic proto-oncogene

Mutated: drives cell proliferation by up-regulating MEK and ERK

Dabrafenib
Vemurafenib
+ MEK inhibitor

37
Q

Benign seborrhoeic keratosis

A

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
Q

Precancerous dysplasias

A

Bowen’s disease

Actinic keratosis

Viral lesions

39
Q

Invasive malignancies

A

Basal and squamous cell carcinoma

40
Q

Epidermal acanthosis

A

Thickening

41
Q

Eruptive appearance may indicate…

A

Internal malignancy

Leser-Trelat sign

42
Q

Leser-Trelat sign

A

the explosive onset of multiple seborrheic keratoses (many pigmented skin lesions) often with an inflammatory base.

43
Q

BCC subtypes

A
  1. Nodular
  2. Superficial
  3. Infiltrative (morphoeic)
44
Q

Where do BCCs sprout from?

A

From epidermis.

Groups of cells invade the dermis.

Peripheral palisading.

Mitoses and apoptosis very numerous

45
Q

Are BCCs slow or fast growing?

A

Slow growing
Locally destructive

Almost never metastasises

Could invade eye –> brain

46
Q

Most important type of BCC?

A

Infiltrative.

May infiltrate tissues widely.

Prominent desmoplastic fibrous stroma

Margins are poorly defined

May spread along nerves

Resection may be challenging.

47
Q

Precursors of SCC

A

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
Q

Precursors of SCC show?

A

Dysplasia

49
Q

BOWEN’S DISEASE

A

SCC in situ

Mostly on lower leg

Scaly patch/plaque

Irregular border

No dermal invasion.

50
Q

Actinic keratosis

A

Common

Sun exposed skin

Variable epidermal dysplasia

Common precursor of invasive SCC

51
Q

Viral precursors

A

> Viral genital lesions often dysplastic

> Erythroplasia of Queryat- Bowen’s of glans

> Associated with HPV

52
Q

HPV Type 16 associated with…

A

Dysplasia

53
Q

HPV in 100% of

A

Penile dysplasia

54
Q

HPV found in 50% of

A

Invasive penile SCC

55
Q

Most common clinical setting for SCC

A

Elderly, sun exposed sites

UV implicated

56
Q

Occasional setting for SCC

Rare

A

> Chronic leg ulcers
Sites of burns
Chronic lupus vulgaris

Rare - xeroderma pigmentosum (dystrophic varian of epidermolysis bullosa)

57
Q

Xeroderma pigmentosum

A

Cant repair the DNA

Accumulate mutations very quickly and develop numerous skin tumours.

58
Q

SCC

> Behaviour
Adverse Prognostic features

A

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
Q

Columella

A

columella is the bridge of tissue that separates the nostrils at the nasal base

60
Q

1.Dermatofibroma

Dermatofibrosarcoma protuberans

A
  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
Q

Angiosarcoma

A

diffuse

Bruise-like lesion

Highly malignant

62
Q

Merkel cell carcinoma

A

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
Q

Mycosis fungoides

A

Cutaneous T cell lymphoma

T cells move towards epidermis

Neoplastic T cells

Epidermotropic

64
Q

Cutaneous B cell lymphoma

A

Tumours of the lymph nodes and lymphatic system

Malignant proliferation of B cell lymphocytes

Dermatology (8 decks)

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