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Skin Pathology 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
What is the pathophysiology surrounding IgA in dermatitis herpetiformis?
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.
26
Where are melanocytes derived from?
Neural crest
27
Early in embryogenesis melanoblasts migrate from the neural crest to where to form melanocytes?
Skin, uveal tract, leptomeninges
28
What gene encodes MC1R protein?
Melanocortin 1 receptor gene
29
What does MC1R protein and gene determine?
Balance of pigment in skin and hair
30
What melanin colours hair apart from red, and which one colours red?
Eumelanin all apart from red, phaeomelanin causes red
31
What does MC1R to do phaeomelanin?
Turns it into eumelanin
32
What does 1 defective copy of MC1R cause?
Freckles
33
What do 2 defective copies of MC1R cause?
Freckles and red hair
34
What is the medical term for freckles?
Ephilides (single ephelis)
35
What do ephilidies reflect?
Clumpy distribution of melanocytes
36
What are age/liver spots called?
Actinic or solar lentigines
37
Where can actinic lentigines be found on the surface and histologically?
Face, forearms and dorsal hands. Found in epidermis elongated rete ridges.
38
What do actinic lentigines represent?
Increased melanin and basal melanocytes
39
How are congenital melanocytic naevi sized?
Small 2cm but
40
What causes the formation of simple naevi?
During infancy the melanocytes : keratinocyte ratio breaks down at several cutaneous sites
41
Describe acquired naevi development
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
What are common features of dysplastic naevi?
Generally >6mm diameter, variegated pigment, border asymmetry
43
Describe sporadic dysplastic naevi
Not inherited, one to several atypical naevi, risk of MM slightly raised
44
Describe familial dysplastic naevi
Strong FHx of melanoma, autosomal inheritance, high penetrance e.g.CDKN2A, atypical naevi++, lifetime risk of melanoma up to 100%
45
What atypia occurs in dysplastic naevi?
Architectural and cellular
46
What is the host reaction in dysplastic naevi?
Fibrosis and inflammation.
47
What occurs to the epidermis in dysplastic naevi?
Epidermis is not effaced (unlike melanoma)
48
What are halo naevi?
Rare naevi that have a peripheral halo of depigmentation. Show inflammatory regression and are overrun by lymphocytes
49
What are blue naevi?
Rare naevi, entirely dermal and consist of pigment rich dendritic spindle cells. Cellular variant may have mitoses and mimic melanoma
50
What are Spitz naevi?
Rare naevi, used to be known as benign juvenile melanoma. Usually occur
51
Where are malignant melanoma commonly found?
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
What is the aetiology of malignant melanoma?
Sun exposure (esp childhood). UV exposure important in skin/eye melanomas. Multifactorial, genetic risk)- skin colour and/or dysplastic naevi.
53
Where does malignant melanoma rarely occur?
Eye, meninges, oesophagus, biliary tract, anus
54
What factors would you look out for to make you suspect melanoma?
New pigmented lesion develops in adulthood, change in shape, irregular pigmentation, bleeding, development of satellite nodules, ulceration
55
What are the 4 main types of melanoma?
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
What does acral mean?
On palms, soles or under nails
57
Describe the growth of SSM, A/MLM, LMM
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
Describe growth of nodular melanoma
No clinical/microscopic evidence of RGP. Simply nodule of VGP tumour, possibly more aggressive
59
What melanoma lesions have RGP +/- VGP?
SSM, A/MLM, LMM
60
What melanoma lesions have VGP only?
Nodular melanoma
61
What does Breslow mean?
Deepest tumour from granular layer in mm
62
Describe the classification of melanoma prognosis
pTis-melanoma is in-situ-100% survival | pT1-tumour 4mm thick-20% survival. Suffix b (pT4b) indicates tumour with ulceration
63
What is a strong prognostic indicator in melanoma?
Ulceration
64
What are other strong prognostic indicators other than ulceration in melanomas?
High mitotic rate, lymphovascular invasion, satellites, sentinel lymph node involvement
65
What is the order of spread of malignant melanoma?
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
Describe melanoma treatment
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
Describe melanoma excision treatment
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
What genetic angles have been discovered in melanoma?
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
What is wild type BRAF?
Weak cytosolic proto-oncogene
70
What happens if BRAF is mutated, and what drugs have been developed to interfere with this pathway?
Drives cell proliferation by up regulating MEK/ERK. Dabrafenib and vemurafenib used to block action of BRAF
71
Name some epidermal tumours
Benign-seborrhoeic keratosis Precancerous dysplasias-Bowen’s disease, actinic keratosis and viral lesions Invasive malignancies-basal and squamous cell carcinoma
72
Descrive seborrhoeic keratosis'
Benign proliferation of epidermal keratinocytes. Common face/trunk. Stuck on appearance- greasy hyperkeratotic surface.
73
Describe the pathophysiology of BCC
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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