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Dermatology > Pathology > Flashcards

Pathology Flashcards

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Dermatology Board Prep flashcards
1
Q

name an endocrine function of the skin

A

UV stimulation of vit D

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2
Q

describe the cells making up the epidermis

A

stratified keratinising squamous epithelium

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3
Q

what does the germinal layer make

A

is the basal layer of the epidermis- makes epidermis

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4
Q

name a granule in the granular layer

A

keratohyalin granules

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5
Q

what cells make up the corneal layer

A

differentiated keratinised cells

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6
Q

what cells shed from skin surface creating house dust

A

corneocytes

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7
Q

where are melanocytes found

A

in basal layer

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8
Q

how is pigment transferred to keratinocytes

A

via dendritic processes

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9
Q

where are langerhans cells located

A

upper and mid epidermis

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10
Q

what do langerhan cells do

A

dendritic

monitor environment for antigens (sentinels- indicator of presence of a disease)

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11
Q

how do langerhans cells initiate inflammation

A

antigens taken up by dendritic cells and make them more immunogenic

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12
Q

what types of collagen make up the dermis

A

type 1 and type 111

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13
Q

describe the papillary dermis

A

thin, lies just beneath epidermis

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14
Q

what is the reticular dermis

A

thicker bundles of type 1 collagen containing appendage structures (sweat glands, pilosebaceous units)

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15
Q

what is the epidermal basement membrane made from

A

laminin and collagen IV

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16
Q

what are the components of the dermis

A

is a matrix of type 1 and type 111 collagen, elastic fibres and ground substances (hyaluronic acid and chondroitin sulphate)

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17
Q

what is hyperkeratosis

A

increased thickness of keratin layer

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18
Q

what is parakeratosis

A

persistence of nuclei in the keratin layer resulting in epidermis turning over too quickly

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19
Q

what is acanthosis

A

increased thickness of epithelium

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20
Q

what is papillomatosis

A

irregular epithelial thickening (causes diabetic thick, velvety plaques in axilla)

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21
Q

what is spongiosis

A

oedema fluid between squames (epithelial cells in the epidermis) appears to increase prominence of intercellular pricles

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22
Q

what is the pathological hallmark of eczema

A

spongiosis

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23
Q

what happens if spongiosis is severe

A

vesicles filled with oedema fluid appear

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24
Q

what are the four main reaction patterns of inflammatory skin diseases and the diseases they are associated with

A

spongiotic- intraepidermal oedema (eczema)

psoriasiform-
elongation of the rete ridges

lichenoid- basal layer damage (lichen plaus and lupus)

vesiculobullous - blistering (pemphigoid, pemphigus, dermatitis herpetiformis)

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25
Q

what common chronic inflammatory dermatosis has epidermal hyperplasia resulting in increased epidermal turnover causing thickened scales

A

psoriasis

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26
Q

what are munro micro abscesses seen in

A

psoriasis

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27
Q

describe the morphology of psoriasis

A

well defined plaques of erythema with prominent scales, very often symmetrical on the extensor surfaces (adults)

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28
Q

what is guttate psoriasis

A

psoriasis that presents as many small lesions over the upper trunk and proximal extremities

29
Q

what can psoriasis cause in the nails

A

nail dystrophy; pitting, onycholysis (separates from nail bed), subungual hyperkeratosis, colour change, fungal nail infections

30
Q

what is auspitz sign

A

when you pick a scale of a psoriasis plaque it may bleed due to the closeness of the vessels to the epidermis

31
Q

what is seen histologically in psoriasis

A

elongation of rete ridges, aggregates of neutrophils in the surface

32
Q

what are linchenoid disorders characterised by

A

damage to basal epidermis

33
Q

describe the morphology of lichen planus

A

itchy flat topped violaceous papules

34
Q

what is seen histologically in lichen planus

A

irregular sawtooth acanthosis

hypergranulosis and orthohyperatosis

band like upper dermal infiltrate of lymphocytes

basal damage with formation of cytoid bodies

35
Q

name 2 other lichenoid disorder that resemble lichen planus

A

discoid lupus, drug rashes

36
Q

name 2 other lichenoid disorders that have marked mvacuolar interface change

A

erythema multiforme, toxic epidermal necrolysis

37
Q

when do you get pigment in the dermis

A

when basal epidermis is damaged eg lichenoid disorders

38
Q

give examples if 3 skin diseases where vesicles and bullae occur as a secondary phenomenum

A

eczema, herpes virus infection, burns

39
Q

are blisters in immunobullous diseases a secondary or primary feature

A

primary

40
Q

give three examples of immunobullous diseases

A

pemphigus, bullous pemphigoid, dermatitis herpetiformis

41
Q

describe pemphigus

A

rare autoimmune bullous disease causing loss of integritity of of epidermal cell adhesion (desomosome attachments)

42
Q

what is the most common type of pemphigus

A

4 types, 80% of cases= pemphigus vulgaris

43
Q

what treatment does pemphigus respond to

A

steroids

44
Q

describe the pathophysiology of pemphigus vulgaris

A

IgG auto-antibodies made against desmoglein 3 (which maintains desmosomal attachments)

immune complexes form on cell surface

complement activation and protease immune mediator response

disruption of desmosomes

=ACANTHOLYSIS

45
Q

what is acantholysis

A

lysis of intercellular ahesions sites- resulting in loss of cohesion between keratinocytes

46
Q

describe the presentation of pemphigus vulgaris

A

fluid filled blisters which rupture to form shallow erosions

involves scalp, face, axillae, groin and trunk
- may affect mucosae in mouth, resp tract etc

47
Q

what is the common variable across all types of pemphigus

A

acantholysis- lysis of intercellular adhesion sites

48
Q

what is seen sticking to the dermis in pemphigus vulgaris

A

basal layer if epithelium as antibodies dont affect this connection

49
Q

describe the pathophsyiology of bullous pemphigoid

A

circulating antibodies IgG react with a major and/or minor antigen of the hemidesmosomes (which usually anchors basal cells to the basment membrane)

= local complement activation and tissue damage, basement membrane detaches from epidermis, space inbetween fills with fluid and inflammatory cells

50
Q

where are the blisters in skin in bullous pemphigoid

A

subepidermal blister

51
Q

what do the autoantibodies attack in bullous pemphigoid

A

hemidesmosomes and basement membrane

52
Q

what is the dermal papillae

A

small, nipple like projections of the dermis into the epidermis (create fingerprints)

53
Q

what does immunofluorescence show in bullous pemphigoid

A

linear IgG and complement depositied around the BM

54
Q

why do you always send early lesions of bullous pemphigoid to histology

A

as late lesions shoe re-epithelialisation of their floor mimicking pemphigus vulgaris

55
Q

difference between bullous pemphigoid and pemphigus vulgaris blisters

A

vulgaris burst very easily

pemphigoid tense and well defined, sub epidermal

56
Q

what is dermatitis herpetiformis

A

autoimmune bullous disease

57
Q

what other conditions is dermatitis herpetiformis associated with

A

coeliac disease

58
Q

what gene is associated with dermatitis herpetiformis

A

HLA-DQ2 haplotype

59
Q

describe the lesions in dermatitis herppetiformis

A

intensely itchy lesions, symmetrical, elbows knees and buttock

60
Q

what is the hallmark of dermatitis herpetiformis

A

papillary dermal microabscesses

61
Q

what seen histologically in dermatitis herpetiformis

A

papillary dermal microabscesses

neutrophils in upper dermis

deposits of IgA in dermal papillae

62
Q

why do 90% of dermatitis herpetiformis patients have gluten sensitive enteropathy

A

IgA in dermal papillae target gliadin component of gluten but cross react with connective tisse matrix proteins

immune complexes form in dermal papillae and activate complement and generate neutrophil chemotaxins

63
Q

what does the distribution of acne (face, upper back, anterior chest)

A

sebaceous glands

64
Q

describe the aetiology of acne vulgaris

A

increased androgens at puberty, keratin and sebum plugging of pilosebaceous units

keratin and sebum build up to produce comedones (black and white heads)

infection with anaerobic bacterium corynebacterium acnes

rupture causes inflammation and foreign body graulomas

65
Q

what is the presentation of rosacea

A

recurrent facial flushing

visible blood vessels

pustules

thickening of skin- rhinophyma

66
Q

what can trigger rosacea

A

sunlight, alcohol, spicy foods, stress, sometimes tetracyclines

67
Q

what is seen pathologically in roscaea

A

vascular ectasia (small, dilated blood vessels)

patchy inflammation with plasma cells

pustules

perifollicular granulomas

follicular demodex mites often noted

68
Q

where do demodex mites live

A

in sebaceous duct

Dermatology (23 decks)

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