Pathology of Rashes Flashcards

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1
Q

What cells does the epidermis mainly consist of?

A

Maturing squamous cells

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2
Q

Where is the mitotic pool of the epidermis?

A

Basal Layer

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3
Q

Where are melanocytes found in normal skin?

A

dermo-epidermal junction

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4
Q

Ratio of melanocytes: basal cells?

A

1:10

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5
Q

What kind of epithelium is the normal epidermis?

A

Stratified squamous epithelium

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6
Q

What is prominent in the prickle cell layer?

A

Desmosomes

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7
Q

What is the granular layer rich in?

A

Keratohyalin granules

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8
Q

What is the corneal layer rich in?

A

Differentiated keratinised cells

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9
Q

What do corneocytes turn into?

A

House dust

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10
Q

Where are melanocytes found in normal epidermis?

A

Basal layer

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11
Q

How do melanocytes transfer pigment?

A

Transfer pigment to keratinocytes via dendritic processes

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12
Q

Where are langerhans cells found?

A

Upper and mid-epidermis

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13
Q

What is the role of langerhans cells?

A

Sentinels monitoring environment for antigens, important in initiating inflammation

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14
Q

Describe the structure of the dermis

A
  • Matrix of type 1 and 111 collagen
  • Elastic fibres
  • ground substances; hyaluronic acid + chondroitin sulphate
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15
Q

Describe the structure and location of the papillary dermis

A

Thin, lies just beneath the epidermis

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16
Q

Describe the structure and location of the reticular dermis

A
  • Thicker bundles of type 1 collagen

- reticular dermis contains appendage structures

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17
Q

What does the epidermal BM consist of?

A

Laminin and collagen IV

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18
Q

Define hyperkeratosis?

A

Increased thickness of keratin layer

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19
Q

Define parakeratosis?

A

Persistence of nuclei in the keratin layer

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20
Q

Define acanthosis?

A

Increased thickness of epithelium

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21
Q

Define papillomatosis?

A

Irregular epithelial thickening

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22
Q

Define spongiosis?

A

Oedema fluid between squames appears to increase prominence of intercellular prickles.

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23
Q

What are the four patterns of inflammatory skin disease?

A
  1. Spongiotic
  2. Psoriasform
  3. Lichenoid
  4. Vesiculobullous
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24
Q

Describe a spongiotic condition?

A

Intraepidermal oedema e.g. eczema

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25
Q

Describe a psoriasform condition?

A

Elongation of the rete ridges e.g. psoriasis

26
Q

Describe a lichenoid condition?

A

Basal layer damage e.g. lichen plants and lupus

27
Q

Describe a vesiculobullous condition?

A

Blistering e.g. pemphigoid, pemphigus and dermatitis herpetiformis

28
Q

Describe the pathogenesis of psoriasis?

A
  • Epidermal hyperplasia
  • Increased epidermal turnover
  • Hereditary factors
  • Associated specific HLA types
  • New lesions at sites of trauma (koebner)
  • Complement mediated attack on keratin layer
29
Q

What is the prototypic lichenoid disorder?

A

Lichen planus

30
Q

Describe the lesions in lichen planus

A

Itchy flat topped violaceous papule

31
Q

Describe 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
32
Q

What other lichenoid disorders resemble lichen planus?

A

Discoid Lupus

Drug rashes

33
Q

What lichenoid disorders have a more marked vacuolar interface change?

A

Erythema multiforme, TEN

34
Q

When do vesicles and bullae occur?

A

Vesicles and bullae occur as a secondary phenomenon in many skin diseases e.g. eczema

35
Q

Name three examples of immunobullous diseases?

A

Pemphigus
Bullus pemphigoid
Dermatitis herpetiformis

36
Q

What is the cause of pemphigus?

A

Rare autoimmune disease with four subtypes

Loss of integrity of epidermal cell adhesion

37
Q

What does pemphigus respond to?

A

Steroids

38
Q

What is the most common form of pemphigus?

A

80% of cases are pemphigus vulgaris

39
Q

What is the cause of pemphigus vulgaris?

A

IgG auto-antibodies made against desmoglein 3

40
Q

What is the function of desmoglein 3?

A

Maintains desmosomal attachments

41
Q

Describe the pathogenesis of pemphigus vulgaris?

A

Immune complexes form on cell surface

Complement activation and protease release

Disruption of desmosomes

End result is acantholysis

42
Q

Where does pemphigus vulgaris affect?

A

Skin esp scalp, face, axillae, groin, trunk

May affect mucosal in mouth, resp tract

43
Q

What happens to the blisters in pemphigus vulgaris?

A

Rupture to form shallow erosions

44
Q

What is common to all variants of pemphigus?

A

Acantholysis= lysis of intercellular adhesion sites

45
Q

What is bullous pemphigoid?

A

Subepidermal blister formation

46
Q

Describe the pathogenesis of bullous pemphigoid?

A

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

47
Q

What is there no evidence of in bullous pemphigoid?

A

Acantholysis

48
Q

What is seen in immunofluorescence of bulgur pemphigoid?

A

Linear IgG + complement deposited about the BM

49
Q

What do old lesions of pemphigoid show?

A

Re-epithelialisation of their floor, mimicking pemphigus vulgarisms

50
Q

What is dermatitis herpetiformis?

A

Autoimmune bullous disease

51
Q

What is dermatitis herpetiformis associated with?

A

Coeliac disease (HLA-DQ2 haplotype)

52
Q

What is seen in dermatitis herpetiformis?

A

Intensely itchy lesions-symmetrical

Elbows, knees and buttocks often excoriated

Hallmark= papillary derma micro abscesses

53
Q

What is seen in DIF or dermatitis herpetiformis?

A

IgA in dermal papillae

54
Q

Describe the pathophysiology of dermatitis herpetiformis?

A

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

55
Q

Describe the aetiology of acne?

A

Increased androgens at puberty

Increased androgen sensitivity of sebaceous gland

Keratin plugging of pilosebaceous units

Infection with anaerobic bacterium corynebacterium acnes

56
Q

What does rupture of pilosebaceous unit cause?

A

Acute inflammation and foreign body granulomas

57
Q

What is seen in rosacea?

A

Recurrent facial flushing

Visible blood vessels

Pustules

Thickening of the skin-rhinophyma

58
Q

What trigger aggravate acne rosacea?

A

Sunlight
Alcohol
Spicy foods
Stress

59
Q

What does rosacea respond to?

A

Tetracyclines

60
Q

Describe the pathology of rosacea?

A
  • Vascular ectasia
  • Patchy inflammation with plasma cells
  • Pustules
  • Periofollicular granulomas
  • Follicular demodex mites often notes

Is it an allergic reaction to mites

61
Q

What is nikolsky’s sign?

A

The top layer of skin slips away from lower layer when slightly rubbed

Suggests plane of cleavage is within the epidermis