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Dermatology > Pathology > Flashcards

Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

Seborrhoeic keratosis

  • What is it?
  • Who is it common in and where on the body?
  • How do the lesions appear?
  • Pathological features?
A
  • Benign proliferation of epidermal keratinocytes
  • Very common in ageing/elderly skin
  • Common on face, chest and back
  • Stuck on appearance - greasy hyperkeratotic surface
  • Epidermal acanthosis, hyperkeratosis, horn cysts
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2
Q

Eruptive appearance of many seborrhoeic lesions lesions in a short time period may indicate internal malignancy.
What sign is this?

A

Leser-Trelat sign

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3
Q

Very hyperplastic keratin layer and horn cysts.

This is the histology of which condition?

A

Seborrhoeic keratosis

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4
Q

How should you investigate seborrhoeic keratosis?

A

Curette and send for histology

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5
Q

Who is basal cell carcinoma common among?

A
  • Sun exposed sites
  • UK - middle aged and elderly
  • Australia - younger age groups
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6
Q

What are the three main subtypes of basal cell carcinoma?

A
  1. Nodular
  2. Superficial
  3. Infiltrative (morphoeic)
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7
Q

How does a basal cell carcinoma develop?
Does it metastasize?
Can it kill?

A
  • Basal cells sprout from epidermis
  • Groups of cells invade dermis
  • Peripheral palisading
  • Mitoses and apoptoses very numerous
  • Slow growing, locally destructive

Almost never metastasises
May kill by invading eye -> brain

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8
Q

What is the most severe type of basal cell carcinoma and why?

A

Infiltrative type

  • Margins are poorly defined
  • May spread along nerves
  • Resection may be challenging
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9
Q

How does nodular basal cell carcinoma appear on histology?

A

Very well defined; nodules of basal cells which spread down into the dermis

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10
Q

What can superficial BCC mimic?

A

Eczema

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11
Q

How does infiltrative BCC show on histology?

A

Desmoplastic stroma

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12
Q

Give three common precursors of squamous cell carcinoma.

What do they have in common?

A
  1. Bowen’s disease – occurs especially on legs
  2. Actinic keratosis – little scaly things especially on head/neck
  3. Viral lesions - especially on anogenital skin
    All show squamous dysplasia
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13
Q

Bowen’s disease

  • What is it?
  • Who gets it and where on the body?
  • How does it appear?
  • is it invasive?
  • What can it mimic?
A
  • This is squamous cell carcinoma in –situ
  • Female excess – mostly presents on lower leg
  • A well-defined, slowly enlarging, red scaly plaque with irregular border
  • No dermal invasion
  • Can be erythematous and hence mimic inflammatory conditions in some cases
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14
Q

Actinic keratosis

  • Where on the body?
  • Precursor of?
  • What does histology show?
A
  • Sun-exposed skin esp. scalp, face, hands
  • Common precursor of invasive SCC
  • Histology shows parakeratosis with moderate squamous dysplasia
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15
Q

What is Erythroplasia of Queryat

Which pathogen is it associated with?

A

Penile Bowen’s disease

Associated with HPV

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16
Q

What are the most common sites for SCC?

What are some less common sites?

A

Elderly, sun exposed sites (face, ears, dorsal hands)
Occasionally arises
- Chronic leg ulcers e.g. stasis ulcers
- Sites of burns; sinuses e.g. chronic osteomyelitis
- Chronic lupus vulgaris

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17
Q

How does SCC tend to behave?

A
  • Generally good prognosis
  • Locally invasive
  • Low but definite risk of metastasis
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18
Q

What are some adverse prognostic features of SCC?

A
  • Thickness > 4mm and poor differentiation
  • Lymphatic / vascular space invasion
  • Perineural spread
  • Specific sites poorer prognosis - scalp, ear, nose
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19
Q

Where does SCC tend to metastasize to?

A

Lymph nodes

20
Q

Which type of tumour can develop after an insect bite?

A

Dermatofibroma

21
Q

What is Merkel cell cancer?

A

Neuroendocrine cancer of cells which detect pressure

22
Q

Where are melanocytes derived from?

A

Neural crest

23
Q

Aside from the skin where else can you get melanomas?

A

Eye

Meninges

24
Q

Where in the skin do melanocytes reside?

A

Basal layer

25
Q

How does melanocyte ratio vary with race?

A

Ratio is constant irrespective of race

26
Q

Which gene governs production of melanin?
Which type of melanin determines hair colour?
Which type for red hair?

A

Eumelanin (other than red)

Phaeomelanin for red hair

27
Q

What is the tole of MC1R in red hair?

A

MC1R turns phaeomelanin into eumelanin
One defective copy of MC1R causes freckling
Two defective copies-red hair and freckles!

28
Q

What is the proper name for freckle?

What is a freckle?

A

Ephilide

Patchy increase in melanin pigmentation – where the distribution of melanocytes is increased in a particular area

29
Q

What is actinic lentigines?

A

Aka sun spot - related to UV exposure

Basically increased melanin and basal melanocytes

30
Q

What are most melanocytic naevi acquired?

A

1st and 2nd decades

31
Q

What is the risk with giant congenital melanocytic naevus?

A

Melanoma

32
Q

Describe the steps of melanocytis naevus development

A
  1. Childhood - junctional naevus - melanocytes proliferate, clusters of cells at DEJ
  2. Adolescense - compound naevus - junctional clusters + groups of cells in dermis
  3. Adulthood - intradermal naevus - all junctional activity has ceased, entirely dermal
33
Q

What is a dysplastic naevi?

Clinical features?

A

These are an intermediate between melanocytic naevi and melanoma

  • Generally >6mm diameter
  • Variegated pigment
  • Border asymmetry
34
Q

What are the two typical clinical settings for dysplastic naevus?
Give some features of each.

A

Sporadic

  • Not inherited
  • One to several atypical naevi
  • Risk of MM slightly raised

Familial

  • Strong FH of melanoma
  • Autosomal inheritance
  • High penetrance
  • Atypical naevi+++
  • Lifetime risk melanoma up to 100%
35
Q

Halo naevi

  • How does it appear?
  • Associated with which cell type?
  • Pathology?
A
  • Have a peripheral halo of depigmentation. - Show inflammatory regression and are overrun by lymphocytes
  • Body decides to attack the naevus and the skin surrounding it loses its pigment
36
Q

Blue naevi

  • Which layer of skin?
  • Consist of which type of cell?
  • How do they appear?
A
  • Entirely dermal
  • Consist of pigment rich dendritic spindle cell
  • Looks blue because of light scattering effect of the epidermis
37
Q

Spitz naevus

  • Age group?
  • Consist of which type of cell?
  • What do they mimic?
  • What do they often look like?
A
  • Usually occur <20 years
  • Consist of large spindle and/or epithelioid cells
  • May closely mimic melanoma, although most are entirely benign - difficult area as there is a malignant variant!
  • Often look like haemangioma – note pink colouration opposite due to prominent vasculature
38
Q

What does a Spitz naevus closely resemble on histology?

A

Melanoma

39
Q

Melanoma

  • Which sites on the body?
  • Where else do they rarely occur?
A

Melanoma most common on sun-exposed sites scalp, face, neck, arm, trunk, leg.
Rarely occur in eye, meninges, oesophagus, biliary tract, anus.

40
Q

What clinical features should make you suspect melanoma?

A
  • Change in shape
  • Irregular pigmentation
  • Bleeding
  • Development of satellite nodules
  • Ulceration
  • New pigmented lesion develops in adulthood
41
Q

What are the four main types of MM?

A
  1. Superficial spreading – most common in trunk and limbs
  2. Acral/mucosal lentiginous - acral and mucosal
  3. Lentigo maligna - sun-damaged face/neck/scalp
  4. Nodular - varied sites but often trunk
42
Q

Which types of malignant melanoma grow similarly?

How do they tend to grow?

A
  1. Superficial spreading melanoma
  2. Acral/mucosal melanoma
  3. Lentigo maligna
    Grow as macules when either entirely in-situ or with dermal microinvasion - this is RGP
    Eventually the melanoma cells invade the dermis forming an expansile mass with mitoses - this is VGP
    Only VGP melanomas can metastasise
43
Q

How is the growth of nodular melanoma different to that of the others?

A

Nodular melanoma – seems to bypass radial growth, instead just looks like a nodule from the outset

44
Q

How can you measure prognosis of melanoma?

A

Breslow depth = deepest tumour from granular layer

45
Q

Name and describe three ways in which melanomas can spread

A
  1. Local dermal lymphatics -> satellite deposits of MM
  2. Regional lymph node metastases – common pattern of disease progression
    Nodes excised (radical lymphadenectomy)
  3. Blood spread
    - Skin / soft tissue
    - Heart, lungs
    - GI tract, liver
    - Brain
46
Q

Describe the treatment of melanoma

A
  • Primary excision to give clear margins
  • Some also receive a sentinel node biopsy
  • If SN positive - regional lymphadenectomy
  • Treatment of advanced disease difficult
  • Chemo, immunotherapy, genetic therapies

Dermatology (17 decks)

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