Pathology of Rashes Flashcards

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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
Q

What genes are associated with psoriasis?

A

Specific special HLA types

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26
Q

What is the Koebner phenomenon?

A

New lesions of psoriasis arise at sites of trauma

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27
Q

How it epidermal hyperplasia linked to psoriasis?

A

It increases epidermal turnover

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28
Q

How is the complement system linked to psoriasis?

A

Proposed pathogenesis mechanism-complement mediated attack on keratin layer, complement attracts neutrophils to keratin layers causing Munro micro-abscesses

29
Q

What characterises Lichenoid disorders?

A

Damage to the basal epidermis

30
Q

What is the prototypic condition of Lichenoid disorders?

A

Lichen planus

31
Q

What is the common appearance of Lichenoid disorders?

A

Itchy flat-topped violaceous papules

32
Q

What is the histology of Lichen planus?

A

Irregular sawtooth acanthosis, hypergranulosis and orthohyperkeratosis, band-like upper dermal infiltrate of lymphocytes, basal damage with formation of cytoid bodies

33
Q

What other Lichenoid disorders resemble lichen planus?

A

Discoid lupus, some drug rashes

34
Q

What are two life threatening Lichenoid disorders, and how do they differ from lichen planus?

A

Erythema multiforme and Toxic epidermal necrolysis; have more marked vacuolar interface change than lichen planus

35
Q

What are the primary feature of Immunobullous disorders?

A

Blisters

36
Q

What can sometimes occur as a secondary phenomenon in many skin diseases (e.g eczema, herpes, burns)?

A

Vesicles and bullae

37
Q

What are some examples of Immunobullous disorders?

A

Pemphigus, Bullous pemphigoid, Dermatitis herpetiformis

38
Q

What is Pemphigus?

A

Rare autoimmune bullous disease, loss of integrity of epidermal cell adhesion

39
Q

Who normally gets Pemphigus?

A

Has equal sex incidence, usually middle-aged people

40
Q

What is a feature of all forms of Pemphigus?

A

Acantholysis

41
Q

Can Pemphigus be fatal?

A

Yes-has variable severity and responds to steroids

42
Q

How many subtypes of Pemphigus are there?

A

4-all separable clinically and histologically

43
Q

What type of Pemphigus is responsible for 80% of cases?

A

Pemphigus vulgaris

44
Q

What happens in Pemphigus vulgaris?

A

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
Q

What does desmoglein 3 do in the skin?

A

Maintains desmosomal attachments

46
Q

What is acantholysis?

A

Lysis of intercellular adhesion sites

47
Q

What areas are involved in Pemphigus vulgaris?

A

Scalp, face, axillae, groin and trunk

48
Q

Can the mucosa become affected in Pemphigus vulgaris?

A

Yes- extensive mucosal involvement may be fatal

49
Q

What does Pemphigus vulgaris produce on the skin?

A

Produces fluid filled blisters which rupture to form shallow erosions

50
Q

How does Bullous pemphigoid differ from Pemphigus vulgaris?

A

There is no evidence of acantholysis (only formation of sub-epidermal blisters)

51
Q

What occurs in Bullous pemphigoid?

A

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
Q

What does immunofluorescence of Pemphigus vulgaris show?

A

Linear IgG+ complement deposited around the basement membrane

53
Q

What do old lesions of Pemphigus show?

A

Re-epithelialisation of their floor, mimicking Pemphigus vulgaris

54
Q

What is Dermatitis herpetiformis?

A

Relatively rare autoimmune bullous disease, intensely itchy symmetrical lesions

55
Q

What is Dermatitis herpetiformis associated with?

A

Coeliac disease, HLA-DQ2 haplotype

56
Q

Where do lesions tend to appear in Dermatitis herpetiformis?

A

Elbows, knees and buttocks (often excoriated)

57
Q

What is the hallmark of Dermatitis herpetiformis?

A

Papillary dermal micro-abscesses

58
Q

What do 90% of people with Dermatitis herpetiformis also have?

A

Gluten sensitive enteropathy (may be asymptomatic)

59
Q

What does DIF show in Dermatitis herpetiformis?

A

IgA in dermal papillae

60
Q

What occurs in Dermatitis herpetiformis?

A

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
Q

What does the distribution of acne reflect?

A

Sebaceous gland sites (face, upper back, anterior chest)

62
Q

What is the suspected aetiology of acne?

A

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

63
Q

How does acne develop?

A

Sebum produced by sebaceous glands plugs pilosebaceous unit, keratin and sebum build up produce comedones, rupture causes acute inflammation plus foreign body granulomas

64
Q

What are comedones?

A

Black/whitehead spots

65
Q

What gender is Rosacea more common in?

A

Females

66
Q

What occurs in Rosacea?

A

Recurrent facial flushing, visible blood vessels, pustules, thickening of skin (rhinophyma)

67
Q

What are some triggers of Rosacea?

A

Sunlight, alcohol, spicy foods, stress, some respond to tetracyclines

68
Q

What is the pathology of Rosacea?

A

Vascular ectasia, patchy inflammation with plasma cells, pustules, perifollicular granulomas, follicular demodex mites often noted