Psthology of Rashes

Question 1

what is the endocrine function of the skin?

Answer 1

UV stimulation of vitamin D

Question 2

what happens when cells become corneocytes?

Answer 2

nuclei are lost

cells are then shed from the upper surface of skin

Question 3

what is contained within the granular layer?

Answer 3

keratohyalin granules

Question 4

what do melanocytes do and how?

Answer 4

synthesise melanin pigment and transfer it to keratinocytes via dendritic processes
found in basal layer

Question 5

what do Langerhans cells do?

Answer 5

found in upper and mid-dermis and act as sentinels monitoring environment for antigens and initiate inflammation through dendritic function

Question 6

what are the 2 parts of the dermis?

Answer 6

papillary dermis = thin superficial layer

reticular dermis = thicker deeper layer containing type 1 collagen and skin appendages

Question 7

what is the epidermal basement membrane made of?

Answer 7

laminin and collagen 4

Question 8

what holds the dermis onto the epidermis?

Answer 8

hemi-desmosomes at the dermo-epidermal junction

Question 9

what is parakeratosis?

Answer 9

persistence of nuclei in cells in the keratin layer - sign that epidermal turnover is too fast - psoriasis

Question 10

what is acanthosis?

Answer 10

increased thickness of epithelium

Question 11

what is papillomatosis?

Answer 11

irregular epithelial thickening

growth of dermal papilla upwards into the epidermis

Question 12

what is spongiosis?

Answer 12

oedema fluid between squamous cells of the epidermis, increasing the prominence of intracellular prickles
hallmark of eczema

Question 13

what are the 4 main reaction patterns of inflammatory skin disease?

Answer 13

spongiotic-intraepidermal oedema - eczema
psoriasiform - elongation of rete ridges - psoriasis
lichenoid - basal layer damage - lichen planus, lupus
vesiculobullous - blistering - pemphigoid, pemphigus, dermatitis herpatiformis

Question 14

describe the pathogenesis of psoriasis

Answer 14

increased epidermal turnover leads to epidermal hyperplasia
complement attracts neutrophils to keratin layer
koebner phenomenon
hereditary factors (specific HLA types)

Question 15

what are some features of psoriasis plaques?

Answer 15

well defined
erythematous as blood vessels run close to the top due to dermal papillae
symmetrical
on extensor surfaces

Question 16

what is guttate psoriasis?

Answer 16

lots of smaller coin sized plaques instead of few large ones

often after throat infection

Question 17

give 2 histological features of psoriasis

Answer 17

elongation/club shaped junction (dermal papillae)

accumulation of neutrophils in corneal layer

Question 18

how do lichenoid disorders develop?

Answer 18

damage to basal layer

lymphocytes attack the basal membrane cells when then start dropping into the dermis

Question 19

describe the histological appearance of lichen planus

Answer 19

irregular sawtooth acanthosis
formation of cytoid bodies
band-like infiltration of lymphocytes in the upper dermis
orthohyperkeratosis with hypergranulosis

Question 20

name 4 other types of lichenoid disorders

Answer 20

discoid lupus
erythema multiforme
toxic epidermal necrolysis
some drug rashes

Question 21

how does lichen planus present?

Answer 21

very itchy small papules with flat plaque topped surfaces
buccam striae (white lacey appearance in mouth)

Question 22

what are immunobullous disorders?

Answer 22

where an underlying immune disease causes blisters (bullae/vesicles)appear on the skin
pemphigus
pemphigoid
dermatitis herpatiformis

Question 23

what is pemphigus vulgaris?

Answer 23

rare autoimmune bullous disease where IgG auto-antibodies are made against desmoglein 3 which is important in maintaining desmosomal attachment between prickle cells

Question 24

how are desmosomes destroyed in pemphigus vulgaris?

Answer 24

immune complexes form on cell surfaces (auto IgG etc)

complement activated and proteases released which disrupt desmosomes resulting in acantholysis

Question 25

how does pemphigus vulgaris present? is this the same with all pemphigus?

Answer 25

fluid filled blisters which can rupture to form erosions

common on scalp, face, axillae, groin, trunk and mucosa (e.g mouth)

Question 26

what does pemphigus vulgaris look like histologically?

Answer 26

basal layer still attached to dermis

destruction between cells of suprabasal epidermis

Question 27

how is pemphigus vulgaris tested for?

Answer 27

immunoflouresence

chickenwire pattern as antibodies between squamous epidermal cells light up

Question 28

what are the differences between pemphigus and pemphigoid?

Answer 28

pemphigoid = subepidermal blisters with no evidence of acantholysis
pemphigus = epidermal blisters with acantholysis

Question 29

what happens in bullous pemphigoid?

Answer 29

IgG antibodies react with a major antigen of hemidesmosomes which anchor basal cells of epidermis to the dermis at the junction
results in complement activation and tissue damage causing the epidermis to detach from the dermis and fluid to build up in between

Question 30

how is bullous pemphigoid tested for?

Answer 30

immunoflouresence

IgG deposited around the basal layer

Question 31

what is dermatitis herpatiformis?

Answer 31

relatively rare autoimmune bullous disease associated with HLA-DQ2 haplotype and occurs with coeliac disease

Question 32

how does dermatitis herpatiformis present?

Answer 32

intensely itchy symmetrical lesions on the elbows, knees and buttocks

Question 33

what is the histological appearance of dermatitis herpatiformis?

Answer 33

lots of neutrophils in the upper dermis causing micro abscesses

Question 34

what happens in dermatitis herpatiformis?

Answer 34

IgA in dermal papillae target gliadin in gluten but also cross react with connective tissue proteins, activating complement and generating neutrophil chemotaxins

Question 35

how is dermatitis herpatiformis tested for?

Answer 35

immunoflouresence shows IgA deposits in dermal papillae

Question 36

how does acne vulgaris develop?

Answer 36

increase in androgens at puberty
increased androgen sensitivity of sebaceous glands causes excess sebum production and blockage of pilosebaceous units, this results in inflammation and infection