Pathology of rashes Flashcards

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1
Q

What are the functions of the skin?

A
  • barrier to antigens/organisms
  • thermoregulation
  • fluid & electrolyte balance
  • endocrine function
  • protection from UV
  • immune function
  • sensory
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2
Q

Which types of collagen are found in the dermis?

A

Type 1 or type 3

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3
Q

What is the ground substance of the dermis composed of?

A

Hyaluronic acid & chondroitin

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4
Q

The reticular/papillary contains sweat glands ad pilosebaceous units

A

Reticular

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5
Q

Which part of the dermis (papillary or reticular) is thickest?

A

Reticular

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6
Q

What is typical histological feature of a melanocyte?

A

A clear halo (surrounding a dense purple nuclei)

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7
Q

What is the epidermal basement membrane composed of?

A

Laminin and collagen IV

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8
Q

Spongiotic oedema causes the prickle cell desmosomes to be stretched. T/F

A

True

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9
Q

What are the four classifications of inflammatory skin disease?

A
  • spongiotic (intra-epidermal oedema)
  • psoriasiform (elongation of rete ridges)
  • lichenoid (basal layer damage)
  • vesiculobullous (blistering)
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10
Q

Give an example of each of the four classifications of inflammatory skin disease

A
  • eczema
  • psoriasis
  • lichen planus
  • eczema herpetiformis
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11
Q

Describe the pathogenesis of psoriasis.

A

I would if anyone knew it

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12
Q

Which factors can contribute/exaggerate/trigger psoriasis?

A

Hereditary HLA type, koebner phenomenon, strep. throat (guttate variety)

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13
Q

What are the histological features of psoriasis?

A

Parakeratosis and munro microabsesses

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14
Q

What causes munro microabsesses?

A

Complement proteins attracting neutrophils to the keratin layer

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15
Q

What is the auspitz sign? Which condition is it typical of?

A

Pinpoint bleeding where the scale of a plaque is rubbed off. Psoriasis

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16
Q

What factors of erythrodermic psoriasis makes it life threatening?

A

Fluid and electrolyte loss. Risk of infection

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17
Q

How do psoriasis affected nails appear?

A

Crumbly (but no fungal infection)

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18
Q

Why do nails become more crumbly when affected with psoriasis?

A

Increased epithelial turnover

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19
Q

Where is acne vulgaris distributed? Which pattern does this follow?

A

Face, chest and upper back. The distribution of sebaceous glands

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20
Q

What is the pathogenesis of acne vulgaris?

A

Increased androgens (during puberty) > increased sensitivity of sebaceous glands to androgen > keratin plugging of pilosebaceous units > infection with corynebacterium acnes > bursting causes sebum leakage into the dermis which induces local inflammation

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21
Q

Are cornybacterium acnes aerobic or anaerobic?

A

Anaerobic

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22
Q

What are the two types of comedones? What is the difference between the two?

A

Blackheads and whiteheads. Blackheads are open and whiteheads are closed.

23
Q

How does rosacea present?

A

Recurrent facial flushing, telangiectasia, pustules, rhinopyma

24
Q

What is rhinopyma?

A

Fibrous thickening of the skin of the nose

25
Q

Who most commonly gets rosacea?

A

Women and white people

26
Q

Which factors can aggrevate rosacea?

A

Alcohol, sunlight, spicy food, stress

27
Q

Tetracycline medications can be used to treat rosacea. T/F

A

True - works in some cases

28
Q

What is the pathogenesis of rosacea?

A

Vascular ectasia
Patchy inflammation with plasma cells > perifollicular granulomas > pustule formation (follicular dermodex mites often found)

29
Q

Vesicules/bulla often occur as a secondary phenomenon in many skin diseases. T/F

A

True

30
Q

What is the primary feature of immunobullous diseases?

A

Blisters

31
Q

Which sex and age groups are most likely to develop pemphigus?

A

Equal across sexes. Middle aged individuals

32
Q

What is pemphigus?

A

An autoimmune bullous condition causing the loss of integrity of epidermal cell adhesion

33
Q

When is pemphigus most commonly fatal?

A

When affecting aerodigestive tract.

34
Q

Which type of autoantibody is involved in pemphigus? What is it made against?

A

IgG. Desmoglein 3

35
Q

What is the role of desmoglein 3?

A

Maintenance of dermosomal attachments

36
Q

What is the pathogenesis of pemphigus?

A

Immune complexes form > complement activation > protease release > disruption of desmosomes > acantholysis

37
Q

How does pemphigus vulgaris present?

A

Fluid filled blisters which burst to form shallow erosions. Distributed on the skin and mucosal surfaces.

38
Q

Where on the skin is pemphigus vulgaris most commonly found?

A

Scalp, face, axillae, groin & trunk

39
Q

Pemphigus blisters are fragile/strong

A

Fragile

40
Q

Which layer of the epidermis is involved in pemphigus vulgaris?

A

Prickle cell layer

41
Q

Desmosomes and hemidesmosomes are affected in pemphigus vulgaris. T/F

A

False - hemidesmosomes are not affected

42
Q

How can pemphigus be diagnosed? What is the characteristic appearance?

A

IgG immunofluorescence. Chickenwire pattern

43
Q

What is bullous pemphigoid?

A

An autoimmune blistering condition

44
Q

What is the pathogenesis of bullous pemphigoid?

A

Circulating IgG antibodies react with major ± minor hemidesmosome antigen > complement activation > local inflammation > subepidermal blistering

45
Q

A typical feature of bullous pemphigoid is acantholysis. T/F

A

False - this is a feature of pemphigus vulgaris

46
Q

How can bullous pemphigoid be diagnosed? What is the characteristic appearance?

A

IgG immunofluorescence. Linear deposition around the basement membrane

47
Q

When sending samples of bullous pemphigoid it must be early/late stage blisters. Why?

A

Early stage. This is because the blisters will mimic pemphigus vulgaris in their later stages

48
Q

What is dermatitis herpetiformis?

A

A rare autoimmune bullous disease

49
Q

What condition is dermatitis herpetiformis associated with?

A

Coeliac disease

50
Q

How does dermatitis herpetiformis present?

A

Highly itchy (often excoriated) symmetrical lesions. Distributed along the elbows, buttocks and knees

51
Q

Dermatitis herpetiformis is associated with HLA-DQ2 haplotype. T/F

A

True

52
Q

What is the characteristic histological feature of dermatitis herpetiformis?

A

Papillary dermal microabsesses

53
Q

How can dermatitis herpetiformis be diagnosed? What is the characteristic appearance?

A

IgA immunofluorescence. Deposits in dermal papilla

54
Q

What is the pathogenesis of dermatitis herpetiformis?

A

IgA antibodies target gliaden component of gluten > cross reaction with connective tissue matrix proteins > immune complexes form in dermal papilla > complement activated > neutrophil chemotaxins generated