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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

How can melanomas of odd body sites (e.g the liver) be explained?

A

Melanocytes become lost during migration from the neural crest and later become cancerous

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2
Q

What is the function of the melanocortin 1 receptor (MC1R) gene?

A

Production of the melanocortin 1 protein which is involved in the conversion of phaeomelanin into eumelanin (controls pigmentation of hair & skin)

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3
Q

What happens when there are mutations in the MC1R gene?

A

Freckling (one defective copy) and red-hair (two defective copies)

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4
Q

What is another name for freckles? What are freckles?

A

Ephilides. Patchy increases in melanin pigment

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5
Q

What are actinic/solar lentingines? How do they occur?

A

Age/liver spots. UV exposure causes changes within the epidermis (elongated rete ridges, increased melanocytes & pigment)

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6
Q

Where are actinic lentingines typically found?

A

Dorsal hands, face & forearms

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7
Q

What are melanocytic naevi? How are they acquired?

A

A broad catagory of moles/raised skin lesions. Congenital or developing over time (often within the first two decades of life)

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8
Q

How are congenital melanocytic naevi classified?

A

Small - 2cm but 20cm

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9
Q

What is the risk of progression to cancer with congenital melanocytic naevi?

A

Giant melanocytic naevi has a 10-20% risk of progression to melanoma

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10
Q

How are congenital melanocytic naevi treated?

A

Small lesions are generally left along while larger lesions may be surgically excised (may need to be a staged excision)

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11
Q

How are simple naevi acquired?

A

Melanocyte : keratinocyte ratio breaks down at specific cutaneous sites during childhood > simple naevus forms

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12
Q

What is the risk of progression to cancer with simple naevi?

A

Minimal

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13
Q

What is the relation to simple naevi and the immune system?

A

Immunosuppressed children develop more naevi

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14
Q

How do simple naevi develop?

A

Melanocytes proliferate creating a junctional naevi > compound naevi form as clusters of melanocytes form in the DEJ and dermis > intradermal naevi form when DEJ melanocyte clusters disappear and the naevi is entirely dermal

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15
Q

What is the presentation of dysplastic naevi?

A

Asymmetrical border, variegated pigment & generally >6mm diameter

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16
Q

What are the features of sporadic dysplastic naevi?

A

Not inherited, generally only a few naevi, slightly increased risk of progression to melanoma

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17
Q

What are the features of inherited dysplastic naevi?

A

Family history of melanoma (autosomal inheritance), high penetrance, many atypical naevi, high risk of progression to melanoma

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18
Q

What differentiates dysplastic naevi from typical naevi in terms of architecture and histology?

A

Dysplastic naevi is architecturally AND histologically abnormal (with evidence of inflammation and fibrosis)

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19
Q

What is the main distinguishing feature between melanoma and dysplastic naevi?

A

The epidermis is not effaced in cases of dysplastic naevi

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20
Q

What are halo naevi? Why does this occur?

A

A naevi surrounded by a ring of depigmentation. The body is attacking the melanocytes of the naevi and surrounding skin to cause regression

21
Q

What are blue naevi?

A

Dermal proliferations of pigment rich dendritic spindle cells (may mimic melanoma)

22
Q

At what age is halo naevi most common?

A

Late teens/early twenties

23
Q

What is a spitz naevi?

A

A (commonly) benign skin tumour composed of large spindle and/or epithelioid cells which may resembled melanoma

24
Q

Which age group most commonly develops spitz naevi?

A
25
Q

Spitz naevi with prominent vasculature are commonly red in colour. T/F

A

True

26
Q

How are malignant melanomas acquired?

A

De novo or transformation from a dysplastic naevi

27
Q

What is the sex distribution of malignant melanoma?

A

More common in females

28
Q

Which age groups most commonly develop malignant melanoma?

A

Middle aged (rare in children)

29
Q

What is the aetiology of malignant melanoma?

A

Childhood sunburn, UV exposure, genetic risk, dysplastic naevi, skin type

30
Q

When should malignant melanoma be suspected?

A

Change in shape of existing naevi, irregularly pigmented lesion, bleeding lesion, development of satellite nodules, ulceration, new pigmented lesion developing in adulthood

31
Q

What are the four main types of malignant melanoma?

A

Superficial spreading, acral/mucosal lentiginous, lentigo maligna, nodular

32
Q

What the the most common type of melanoma and where is it most commonly found?

A

Superficial spreading & on the arms and trunk

33
Q

What is the second most common type of melanoma and where is it most commonly found?

A

Lentigo maligna & on sun-damaged skin of the face, scalp and neck

34
Q

Where is nodular melanoma most commonly found?

A

Trunk

35
Q

A mole which shows some patchy regression is typical of what?

A

Malignant melanoma

36
Q

What are acral melanomas commonly misdiagnosed as?

A

Trauma related

37
Q

What is the pathogenesis of non-nodular malignant melanomas?

A

Grow as macules in situ or with microinvasion (radio growth phase) > melanoma invades dermis forming expansile mass with mitoses (vertical growth phase) > metastases

38
Q

RGP and VGP melanomas can both metastasise. T/F

A

False - only VGP melanomas can metastasise

39
Q

Nodular melanomas have both a RGP and VGP. T/F

A

False - they do not have a RGP and instead present as nodules of VGP tumour

40
Q

Which is the most aggressive form of melanoma?

A

Nodular

41
Q

Describe Breslow classification of melanoma

A 
pTis = melanoma in situ
pT1 = tumour 4mm
42
Q

What are the adverse prognostic factors of melanoma?

A

Increasing breslow classification, ulceration (suffix b), high mitotic rate, lymphovascular invasion, satellite lesions, sentinel lymph node involvement

43
Q

How does melanoma spread?

A
  • local dermal lymphatics (satellite deposits)
  • regional lymph node metastases
  • blood spread
44
Q

How is melanoma treated?

A

Primary excision with clear markings, sentinal node biopsy, regional lymphadenectomy (questionable), chemotherapy, immunotherapy, genetic therapies

45
Q

What is the process for excision of suspected melanoma?

A

Narrow excision (confirms diagnosis & breslow thickness) > re-excision margins based on breslow thickness

pTis = 5mm clearance 
pT1 = 1cm clearance 
pT2,3,4 = 2cm clearance & SNB
46
Q

How may acral melanomas with c-kit mutations be treated?

A

Imatinib

47
Q

When might BRAF-inhibitors be particularly useful in melanoma treatment?

A

Melanomas on intermittently sun exposed skin

48
Q

What is BRAF? What happens when it mutates?

A

Weak cytosolic proto-oncogene. Drives cell proliferation via MEK and ERK

49
Q

Name 2 BRAF inhibitors

A

Dabrafenib & vemurafenib

Dermatology (26 decks)

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