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Dermatology > Pathology of Pigmented Lesions > Flashcards

Pathology of Pigmented Lesions Flashcards

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Dermatology Board Prep flashcards
1
Q

What components of the skin can give rise to tumours?

A

All of them = epidermis, dermis, melanocytes, appendages, lymphoid elements

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2
Q

Where are melanocytes derived from?

A

The neural crest

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3
Q

How are melanocytes formed?

A

Early in embryogenesis melanoblasts migrate from the neural crest to the skin, uveal tract and leptomeninges, once melanoblasts settle in the skin they from melanocytes

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4
Q

Where are the melanocytes located in the skin?

A

Basally located

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5
Q

What is the melanocytes to basal keratinocytes ratio?

A

From 1:5 to 1:10 (constant irrespective of race)

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6
Q

What does the melanocortin 1 gene do?

A

Encodes MC1R protein (sits on cell surface), determines balance of pigment in skin and hair

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7
Q

What gives hair a red colour?

A

Phaeomelanin

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8
Q

What causes hair to be any colour except red?

A

Eumelanin

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9
Q

How can MC1R impact hair colour?

A

Changes phaeomelanin to eumelanin

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10
Q

What does one defective copy of MC1R cause?

A

Freckling

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11
Q

What does two defective copies of MC1R cause?

A

Red hair and freckling

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12
Q

What are freckles (ephilides)?

A

Patchy increases in melanin production that occur after sun exposure

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13
Q

Who are freckles most common in?

A

Fair skinned people and red heads

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14
Q

What do freckles reflect?

A

The clumpy distribution of melanocytes, islands with most melanocytes tan

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15
Q

What is the other name for actinic/solar lentigines?

A

Age/liver spots

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16
Q

What are some features of actinic lentigines?

A

Reflect UV exposure, found on face, forearms and dorsal hands, epidermis elongated rete edges, increases melanin and basal melanocytes

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17
Q

When do most melanocytic naevi occur?

A

Most naevi acquired in first two decades, 1% of babies born with congenital nauvus

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18
Q

What are the different size categories of naevi?

A 
Small = <2cm diameter
Medium = >2cm but <20cm diameter (giant garment-type lesions)
Large = >20cm diameter (10-15% of melanoma, may need staged surgical excision)
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19
Q

How do usual type acquired naevi develop?

A

During infancy the melanocyte to keratinocyte ratio breaks down at a number of cutaneous sites (immune related), allows for formation of simple naevi

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20
Q

How many naevi does the average person have?

A

20-30 (normal naevi have low malignant potential)

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21
Q

How do acquired naevi develop over time?

A

Junctional naevus = melanocytes proliferate causing cluster of cells at DEJ (childhood)
Compound naevus = junctional clusters plus groups of cells (adolescence/early adulthood)
Intradermal naevus = all junctional activity has stopped so is now entirely dermal (adulthood)

22
Q

What are some features of dysplastic naevi?

A

Generally >6cm, variegated pigment, border asymmetry, architectural and cellular atypia, epidermis not effaced, host reaction (fibrosis and inflammation)

23
Q

What are the two kinds of dysplastic naevi?

A 
Sporadic = not inherited, one to several atypical naevi, risk of malignant melanoma slightly raised
Familial = strong family history of melanoma, autosomal inheritance, high penetrance, atypical naevi, lifetime risk of melanoma up to 100%
24
Q

What are some examples of rarer naevi?

A

Halo naevi, Blue naevi, Spitz naevi

25
Q

What are some features of halo naevi?

A

Have peripheral halo of depigmentation, show inflammatory regression and are overrun by lymphocytes

26
Q

What are some features of blue naevi?

A

Entirely dermal and consist of pigment rich dendritic spindle cells, cellular variant may have mitoses and mimic melanoma

27
Q

What are some features of Spitz naevi?

A

Described in 1948, used to be called benign juvenile melanoma, usually occur in < 20 year olds, consist of large spindle and/or epithelioid cells, may closely mimic melanoma, most are entirely benign but there is a malignant variant

28
Q

Why can dysplastic naevi be difficult to distinguish from melanomas?

A

They have severe dysplasia

29
Q

How do most malignant melanomas arise?

A

Arise de-novo, some come from dysplastic naevi

30
Q

What is the female to male incidence of malignant melanoma?

A

2:1 (more common in females)

31
Q

What age group are most likely to get malignant melanomas?

A

Incidence peaks in middle age, rare in childhood

32
Q

Where is melanoma most common on the skin?

A

Sun exposed areas = scalp, neck, face, arms, trunk, legs (can occur anywhere, sun and UV exposure plays major role)

33
Q

Where are some rare sites for melanomas to form?

A

Eyes, meninges, oesophagus, biliary tract and anus

34
Q

When should you suspect a melanoma?

A

Change in shape, irregular pigmentation, bleeding, ulceration, development of satellite nodules, new pigmented lesion develops in adulthood

35
Q

What are the four main types of melanoma?

A 
Superficial spreading (SS) = most common, trunk and limbs
Acral/mucosal lentiginous  (A/ML) = acral and mucosal sites 
Lentigo maligna (LM) = sun damaged face, neck or scalp
Nodular = varied sites but often trunk
36
Q

How do all the types of melanoma except nodular develop?

A

Grow as macules when either entirely in-situ or with dermal microinvasion (RGP), eventually the melanoma cells invade the dermis forming an expansive mass with moles (VGP)

37
Q

What are the only category of melanoma that can metastasise?

A

VGP melanomas

38
Q

How do nodular melanomas develop?

A

No clinical or microscopic evidence of RGP, simply a nodule of VGP tumour (some say this is more aggressive)

39
Q

What measures are used to decide melanoma prognosis?

A

Ulceration (strong adverse indicator) and Breslow depth (deepest tumour from granular layer in mm)

40
Q

What are the different grades of Breslow depth?

A 
pTis = melanoma in-situ (100% survival)
pT1 = tumour is < 1mm (90% survival)
pT2 = tumour is 1-2 mm (80% survival)
pT3 = tumour is 2-4 mm (55% survival)
pT4 = tumour > 4mm thick (20% survival)
41
Q

What are some tumour features that can influence prognosis?

A

High mitotic rate, lymphovascular invasion, satellites, sentinel lymph node involvement

42
Q

What occurs if there is spread of the melanoma to local dermal lymphatics?

A

Satellite deposits of malignant melanoma

43
Q

Where can melanomas spread to after local dermal lymphatics?

A

Regional lymph node metastases = common pattern of disease progression, nodes excised (regional lymphadenectomy)

44
Q

Where can a melanoma spread to once its in the blood?

A

Skin/soft tissue, heart, lungs, GI tract, liver, brain

45
Q

What are some treatment options for melanomas?

A

Primary excision to give clear margins
Some also receive sentinel node biopsy (SNB)
If SNB positive then regional lymphadenectomy

46
Q

What are the treatment options for advanced melanomas?

A

Chemotherapy, immunotherapy, genetic therapies (treatment of advanced disease difficult)

47
Q

How much should the melanoma be cleared by when carrying out a narrow complete excision?

A 
Depends on size
In-situ = clear by circa 5mm
Invasive but <1 cm thick = 1cm clearance
Invasive and >1 cm thick = 2cm clearance
Do an SNB if thicker than > 1cm or thinner with mitoses
48
Q

What are some genetic treatments for melanomas?

A

Some acral melanomas have c-kit mutations and may be treated with imatinib
Melanomas on intermittently sun-exposed skin may have a BRAF mutation which is a potential target
Can test for mutations on paraffin fixed tissue

49
Q

What is the BRAF gene?

A

Weak cytosolic proto-oncogene

50
Q

What happens when the BRAF gene is mutated?

A

Drives cell proliferation by up-regulating MEK and ERK

51
Q

What are some drugs developed to interfere with the BRAF pathway?

A

Dabrafenib, vemurafenib

52
Q

What are some limitations of BRAF drugs?

A

Response times are limited, may be better in combination with MEK inhibitor, may be better in adjuvant setting for high risk lesions before metastases develop

Dermatology (31 decks)

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