Pathology of Rashes Flashcards

(68 cards)

1
Q

What are the functions of the skin?

A

Strong barrier to antigens and organisms, thermoregulation, fluid and electrolyte balance, endocrine function, protection from UV rays, immune function, sensory function

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2
Q

What makes up the epidermis in normal skin?

A

Mainly maturing squamous cells

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3
Q

Where is the mitotic pool of the skin?

A

Basal layer

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4
Q

Where are melanocytes found?

A

At the Dermo-epidermal junction

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5
Q

What is the ration of melanocytes to basal cells?

A

1:10

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6
Q

What cell type makes up the epidermis?

A

Stratified keratinising squamous cells

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7
Q

What is found in the prickle layer?

A

Prominent desmosomes

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8
Q

What is the granular layer rich in?

A

Keratohyalin granules

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9
Q

What cells make up the corneal layer?

A

Differentiated keratinised cells

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10
Q

What is house dust?

A

Corneocytes shed from the skin surface

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11
Q

What do melanocytes do and where are they found?

A

Synthesise melanin and transfer pigment to keratinocytes via dendritic processes; found in basal layer

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12
Q

What is the function of Langerhans cells and where are they found?

A

Dendritic cells that act as sentinels monitoring the environment for antigens, important in initiating inflammation; located in upper and mid-epidermis

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13
Q

What makes up the matrix of the dermis?

A

Type I and type III collagen

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14
Q

What are some structures that can be found in the dermis?

A

Elastic fibres and ground substances (hyaluronic acid and chondroitin sulphate)

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15
Q

What is the papillary dermis like and where is it found?

A

Thin; lies just beneath the epidermis

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16
Q

What are some features of the reticular dermis?

A

Thicker bundles of type I collagen, contains appendages (e.g sweat glands, pilosebaceous units)

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17
Q

What makes up the basement membrane of the epidermis?

A

Laminin and collagen IV

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18
Q

What does Hyperkeratosis mean?

A

Increased thickness of keratin layer

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19
Q

What does Parakeratosis mean?

A

Persistence of nuclei in the keratin layer

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20
Q

What does Acanthosis mean?

A

Increased thickness of the epithelium

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21
Q

What is the definition of Papillomatosis?

A

Irregular epithelial thickening

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22
Q

What is Spongiosis?

A

Oedema fluid between squames which causes an increase in the prominence of intercellular prickles

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23
Q

What happens if Spongiosis is severe?

A

Vesicles become filled by oedema fluid

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24
Q

What are the classes of inflammatory skin diseases?

A

Spongiotic-intraepidermal oedema (e.g eczema), Psoriasiform-elongation of the rete ridges (e.g psoriasis), Lichenoid-basal layer damage (e.g lichen planus), Vesiculobullous-blistering (e.g pemphigoid)

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25
What genes are associated with psoriasis?
Specific special HLA types
26
What is the Koebner phenomenon?
New lesions of psoriasis arise at sites of trauma
27
How it epidermal hyperplasia linked to psoriasis?
It increases epidermal turnover
28
How is the complement system linked to psoriasis?
Proposed pathogenesis mechanism-complement mediated attack on keratin layer, complement attracts neutrophils to keratin layers causing Munro micro-abscesses
29
What characterises Lichenoid disorders?
Damage to the basal epidermis
30
What is the prototypic condition of Lichenoid disorders?
Lichen planus
31
What is the common appearance of Lichenoid disorders?
Itchy flat-topped violaceous papules
32
What is the histology of Lichen planus?
Irregular sawtooth acanthosis, hypergranulosis and orthohyperkeratosis, band-like upper dermal infiltrate of lymphocytes, basal damage with formation of cytoid bodies
33
What other Lichenoid disorders resemble lichen planus?
Discoid lupus, some drug rashes
34
What are two life threatening Lichenoid disorders, and how do they differ from lichen planus?
Erythema multiforme and Toxic epidermal necrolysis; have more marked vacuolar interface change than lichen planus
35
What are the primary feature of Immunobullous disorders?
Blisters
36
What can sometimes occur as a secondary phenomenon in many skin diseases (e.g eczema, herpes, burns)?
Vesicles and bullae
37
What are some examples of Immunobullous disorders?
Pemphigus, Bullous pemphigoid, Dermatitis herpetiformis
38
What is Pemphigus?
Rare autoimmune bullous disease, loss of integrity of epidermal cell adhesion
39
Who normally gets Pemphigus?
Has equal sex incidence, usually middle-aged people
40
What is a feature of all forms of Pemphigus?
Acantholysis
41
Can Pemphigus be fatal?
Yes-has variable severity and responds to steroids
42
How many subtypes of Pemphigus are there?
4-all separable clinically and histologically
43
What type of Pemphigus is responsible for 80% of cases?
Pemphigus vulgaris
44
What happens in Pemphigus vulgaris?
IgG auto-antibodies are made against desmoglein 3, immune complexes form on cell surface causing compliment activation and protease release disrupting the desmosomes, end result is acantholysis
45
What does desmoglein 3 do in the skin?
Maintains desmosomal attachments
46
What is acantholysis?
Lysis of intercellular adhesion sites
47
What areas are involved in Pemphigus vulgaris?
Scalp, face, axillae, groin and trunk
48
Can the mucosa become affected in Pemphigus vulgaris?
Yes- extensive mucosal involvement may be fatal
49
What does Pemphigus vulgaris produce on the skin?
Produces fluid filled blisters which rupture to form shallow erosions
50
How does Bullous pemphigoid differ from Pemphigus vulgaris?
There is no evidence of acantholysis (only formation of sub-epidermal blisters)
51
What occurs in Bullous pemphigoid?
Circulating IgG react with major and/or minor antigen of the hemidesmosomes anchoring basal cells to the basement membrane, causing local complement activation and tissue damage
52
What does immunofluorescence of Pemphigus vulgaris show?
Linear IgG+ complement deposited around the basement membrane
53
What do old lesions of Pemphigus show?
Re-epithelialisation of their floor, mimicking Pemphigus vulgaris
54
What is Dermatitis herpetiformis?
Relatively rare autoimmune bullous disease, intensely itchy symmetrical lesions
55
What is Dermatitis herpetiformis associated with?
Coeliac disease, HLA-DQ2 haplotype
56
Where do lesions tend to appear in Dermatitis herpetiformis?
Elbows, knees and buttocks (often excoriated)
57
What is the hallmark of Dermatitis herpetiformis?
Papillary dermal micro-abscesses
58
What do 90% of people with Dermatitis herpetiformis also have?
Gluten sensitive enteropathy (may be asymptomatic)
59
What does DIF show in Dermatitis herpetiformis?
IgA in dermal papillae
60
What occurs in Dermatitis herpetiformis?
IgA antibodies target gliadin components of gluten but cross react with connective tissue matrix proteins, immune complexes form in dermal papillae and activate complement and generate neutrophil chemotaxis
61
What does the distribution of acne reflect?
Sebaceous gland sites (face, upper back, anterior chest)
62
What is the suspected aetiology of acne?
Increased androgens at puberty, possible increased androgen sensitivity of sebaceous glands, keratin plugging of pilosebaceous units, infection with anaerobic bacterium bacterium Corynebacterium acnes
63
How does acne develop?
Sebum produced by sebaceous glands plugs pilosebaceous unit, keratin and sebum build up produce comedones, rupture causes acute inflammation plus foreign body granulomas
64
What are comedones?
Black/whitehead spots
65
What gender is Rosacea more common in?
Females
66
What occurs in Rosacea?
Recurrent facial flushing, visible blood vessels, pustules, thickening of skin (rhinophyma)
67
What are some triggers of Rosacea?
Sunlight, alcohol, spicy foods, stress, some respond to tetracyclines
68
What is the pathology of Rosacea?
Vascular ectasia, patchy inflammation with plasma cells, pustules, perifollicular granulomas, follicular demodex mites often noted