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Dermatology > Skin Pathology > Flashcards

Skin Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

What are prickle cells?

A

Prominent desmosomes

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2
Q

What is the granular layer rich in?

A

Keratohyalin granules

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3
Q

What is present in the corneal layer?

A

Differentiated keratinised cells

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4
Q

Where is the papillary dermis found?

A

Lies just beneath epidermis, thin

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5
Q

What is present in the reticular dermis?

A

Thick bundles of type 1 collagen, also appendage structures: sweat glands, pilosebaceous units

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6
Q

What is the epidermal basement membrane made of?

A

Laminin and collagen IV

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7
Q

What are the 4 main reaction patterns in classification of inflammatory skin diseases?

A

Spongiotic, Psoriasiform, Lichenoid, Vesiculobullous

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8
Q

What does Psoriasiform mean?

A

Elongation of the rete ridges e.g. psoriasis

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9
Q

What does Lichenoid mean?

A

Basal layer damage e.g. lichen planus and lupus

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10
Q

What does Vesiculobullous mean?

A

Blistering e.g. pemphigoid, pemphigus and dermatitis herpetiformis

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11
Q

What is the Koebner phenomenon?

A

New psoriasis lesions arising at the sites of trauma

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12
Q

What possible pathogenesis occurs to form psoriasis?

A

Epidermal hyperplasia resulting in increased epidermal turnover. Complement mediated attack on keratin layer- complement attracts neutrophils to layer

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13
Q

What are the causes of acne?

A

Increased androgens at puberty, increased androgen sensitivity of sebaceous glands, increased keratin plugging of pilosebaceous units, infection with anaerobic bacterium corynebacterium acnes

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14
Q

What is the term for thickening of the skin in rosacea?

A

Rhinophyma

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15
Q

What are some factors involved in rosacea pathology?

A 
Vascular ectasia
Patchy inflammation with plasma cells
Pustules
Perifollicular granulomas
Follicular Demodex mites often noted
Allergic reaction to mites? 
Or reaction to bacteria on mite
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16
Q

What is the primary features of immunobullous diseases?

A

Blisters

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17
Q

What occurs in the epidermis in pemphigus?

A

Loss of integrity of epidermal cell adhesion

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18
Q

What is Pemphigus vulgaris?

A

AI condition, IgG auto-antibodies made against desmoglein 3.

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19
Q

What is the pathophysiology of pemphigus vulgaris?

A

Desmoglein 3 maintains desmosomal attachments, immune complexes form on cell surface. Complement activation and protease release. Disruption of desmosomes. End result is Acantholysis

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20
Q

What kind of blister is found in Bullous pemphigoid?

A

Subepidermal

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21
Q

What is the pathophysiology of Bullous pemphigoid?

A

Circulating antibodies (IgG) react with a major and/or minor antigen of the hemidesmosomes anchoring basal cells to basement membrane. The result is local complement activation and tissue damage

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22
Q

What haplotype is dermatitis herpetiformis associated with?

A

HLA-DQ2

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23
Q

What disease is strongly associated with Dermatitis herpetiformis?

A

Coeliac disease

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24
Q

What is the hallmark of Dermatitis herpetiformis?

A

Papillary dermal microabscesses

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25
Q

What is the pathophysiology surrounding IgA in dermatitis herpetiformis?

A

DIF shows deposits of IgA in dermal papillae

IgA antibodies target gliadin component of gluten but cross react with connective tissue matrix proteins

Immune complexes form in dermal papillae and activate complement and generate neutrophil chemotaxins.

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26
Q

Where are melanocytes derived from?

A

Neural crest

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27
Q

Early in embryogenesis melanoblasts migrate from the neural crest to where to form melanocytes?

A

Skin, uveal tract, leptomeninges

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28
Q

What gene encodes MC1R protein?

A

Melanocortin 1 receptor gene

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29
Q

What does MC1R protein and gene determine?

A

Balance of pigment in skin and hair

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30
Q

What melanin colours hair apart from red, and which one colours red?

A

Eumelanin all apart from red, phaeomelanin causes red

31
Q

What does MC1R to do phaeomelanin?

A

Turns it into eumelanin

32
Q

What does 1 defective copy of MC1R cause?

A

Freckles

33
Q

What do 2 defective copies of MC1R cause?

A

Freckles and red hair

34
Q

What is the medical term for freckles?

A

Ephilides (single ephelis)

35
Q

What do ephilidies reflect?

A

Clumpy distribution of melanocytes

36
Q

What are age/liver spots called?

A

Actinic or solar lentigines

37
Q

Where can actinic lentigines be found on the surface and histologically?

A

Face, forearms and dorsal hands. Found in epidermis elongated rete ridges.

38
Q

What do actinic lentigines represent?

A

Increased melanin and basal melanocytes

39
Q

How are congenital melanocytic naevi sized?

A

Small 2cm but

40
Q

What causes the formation of simple naevi?

A

During infancy the melanocytes : keratinocyte ratio breaks down at several cutaneous sites

41
Q

Describe acquired naevi development

A

Junctional naevus- melanocytes proliferate > clusters of cells at DEJ. Compound naevus- junctional clusters + groups of cells in dermis. Intradermal naevus- all junctional activity has ceased; entirely dermal

42
Q

What are common features of dysplastic naevi?

A

Generally >6mm diameter, variegated pigment, border asymmetry

43
Q

Describe sporadic dysplastic naevi

A

Not inherited, one to several atypical naevi, risk of MM slightly raised

44
Q

Describe familial dysplastic naevi

A

Strong FHx of melanoma, autosomal inheritance, high penetrance e.g.CDKN2A, atypical naevi++, lifetime risk of melanoma up to 100%

45
Q

What atypia occurs in dysplastic naevi?

A

Architectural and cellular

46
Q

What is the host reaction in dysplastic naevi?

A

Fibrosis and inflammation.

47
Q

What occurs to the epidermis in dysplastic naevi?

A

Epidermis is not effaced (unlike melanoma)

48
Q

What are halo naevi?

A

Rare naevi that have a peripheral halo of depigmentation. Show inflammatory regression and are overrun by lymphocytes

49
Q

What are blue naevi?

A

Rare naevi, entirely dermal and consist of pigment rich dendritic spindle cells. Cellular variant may have mitoses and mimic melanoma

50
Q

What are Spitz naevi?

A

Rare naevi, used to be known as benign juvenile melanoma. Usually occur

51
Q

Where are malignant melanoma commonly found?

A

Any site in skin, for females leg is most common, trunk for men. Females 2:1 Males. Rare in childhood, incidence peaks middle age. Sun exposed sites most common

52
Q

What is the aetiology of malignant melanoma?

A

Sun exposure (esp childhood). UV exposure important in skin/eye melanomas. Multifactorial, genetic risk)- skin colour and/or dysplastic naevi.

53
Q

Where does malignant melanoma rarely occur?

A

Eye, meninges, oesophagus, biliary tract, anus

54
Q

What factors would you look out for to make you suspect melanoma?

A

New pigmented lesion develops in adulthood, change in shape, irregular pigmentation, bleeding, development of satellite nodules, ulceration

55
Q

What are the 4 main types of melanoma?

A

Superficial spreading-commonest-trunk and limbs

Acral/mucosal lentiginous-acral and mucosal

Lentigo maligna-sun-damaged face/neck/scalp

Nodular-varied sites but often trunk

56
Q

What does acral mean?

A

On palms, soles or under nails

57
Q

Describe the growth of SSM, A/MLM, LMM

A

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

58
Q

Describe growth of nodular melanoma

A

No clinical/microscopic evidence of RGP. Simply nodule of VGP tumour, possibly more aggressive

59
Q

What melanoma lesions have RGP +/- VGP?

A

SSM, A/MLM, LMM

60
Q

What melanoma lesions have VGP only?

A

Nodular melanoma

61
Q

What does Breslow mean?

A

Deepest tumour from granular layer in mm

62
Q

Describe the classification of melanoma prognosis

A

pTis-melanoma is in-situ-100% survival

pT1-tumour 4mm thick-20% survival. Suffix b (pT4b) indicates tumour with ulceration

63
Q

What is a strong prognostic indicator in melanoma?

A

Ulceration

64
Q

What are other strong prognostic indicators other than ulceration in melanomas?

A

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

65
Q

What is the order of spread of malignant melanoma?

A
  1. Local dermal lymphatics > satellite deposits of MM
  2. Regional lymph node metastases-common pattern. Nodes will be excised (radical lymphadenectomy).
  3. Blood spread > skin/soft tissue, heart, lungs, GI tract, liver, brain
66
Q

Describe melanoma treatment

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

67
Q

Describe melanoma excision treatment

A

Narrow complete excision needed. If in-situ then clear by circa 5mm, if invasive but 1mm thick: 2cm clearance. SNB if >1mm thick or thinner with mitoses

68
Q

What genetic angles have been discovered in melanoma?

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

Can test for mutations on paraffin fixed tissue

69
Q

What is wild type BRAF?

A

Weak cytosolic proto-oncogene

70
Q

What happens if BRAF is mutated, and what drugs have been developed to interfere with this pathway?

A

Drives cell proliferation by up regulating MEK/ERK. Dabrafenib and vemurafenib used to block action of BRAF

71
Q

Name some epidermal tumours

A

Benign-seborrhoeic keratosis

Precancerous dysplasias-Bowen’s disease, actinic keratosis and viral lesions

Invasive malignancies-basal and squamous cell carcinoma

72
Q

Descrive seborrhoeic keratosis’

A

Benign proliferation of epidermal keratinocytes. Common face/trunk. Stuck on appearance- greasy hyperkeratotic surface.

73
Q

Describe the pathophysiology of BCC

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

Dermatology (14 decks)

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