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hypersensitivity, allergy and inflammation Flashcards

inflammatory dermatoses: summarise the biology and significant clinical manifestations of specific inflammatory dermatoses including acne, eczema, psoriasis, bullous pemphigoid and pemphigus vulgaris (57 cards)

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1
Q

microanatomy of skin (layers from superficial to deep)

A

epidermis (including stratum cornea) -> dermis -> hypodermis (containing subcutaneous tissue)

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2
Q

contents of dermis and hypodermis

A

sweat gland, sebaceous gland, hair follicle, blood vessels

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3
Q

2 layers of dermis (superficial to deep)

A

papillary dermis -> reticular dermis

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4
Q

what is present in hair bearing skin

A

apocrine glands, hair follicle, sebaceous gland

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5
Q

4 important cells of epidermis

A

keratinocytes, Langerhans cells, Merkel cells, melanocytes

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6
Q

structure of epidermis (from young at bottom, old at top)

A

dermis -> stratum basale -> stratum spinosum -> stratum granulosum -> stratum lucidum -> stratum corneum

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7
Q

what is present in dermis

A

sensory nerve ending

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8
Q

what is present in stratum basale

A

dividing keratinocyte (stem cell), tactile cell

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9
Q

what is present in stratum spinosum

A

melanocyte, dendritic cell, living keratinocytes

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10
Q

what is present in stratum corneum

A

dead keratinocytes (those on surface flake off)

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11
Q

keratinocyte differentiation pathway

A

basal cell -> prickle cell -> granular cell -> keratin

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12
Q

structure of stratum corneum

A

protein and lipids in between corenocyte layers (dead keratinocytes - flat and no nuclei)

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13
Q

function of stratum corneum

A

barrier

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14
Q

what do defects in stratum corneum lead to

A

eczema

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15
Q

common gene mutation in eczema patients (intrinsic factor), meaning more suscpetible to other atopic diseases

A

filagrin, as protein in between corenocyte layers, so defect allows allergens entry

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16
Q

define atopy

A

tendency to develop hypersensitivity

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17
Q

3 atopic diseases

A

eczema, asthma, hayfever

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18
Q

3 features of atopic eczema

A

common (typical as baby but most grow out of it), relapsing, remitting

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19
Q

describe atopic march: sequence of atopic diseases and when they typically come about

A

eczema -> food allergies -> asthma -> rhinitis; typically rise as child, peak at teens, reduce as adult

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20
Q

extrinsic factors of atopic eczema

A

penetration of exogenous agents e.g. allergens, irritants, pathogens (usually due to intrinsic factor causing defect first)

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21
Q

describe acute form of atopic eczema

A

activation of CD4+ lymphocytes and Th2 response

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22
Q

describe chronic form of atopic eczema

A

activation of CD4+ and CD8+ lymphocytes and Th1 response

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23
Q

what is a sign of a filagrin gene mutation

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A

palmar hyperlinearity (palms on hands are more prominent)

24
Q

common sites of infantile atopic eczema

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A

affected on face, elbows and knees (irritable areas where able to rub themselves)

25
common sites of adult atopic eczema
hands, back of knees, elbows, neck, face (flexures)
26
acute vs chronic eczema appearance
acute: very red with crusty appearing skin; chronic: less red but more lichenified (thickened with extenuated skin marks), with poor cut off between affected and unaffected skin
27
describe eczema herpecitum
cold sore virus which can spread over eczema area (appear as ulcers and vesicles)
28
3 other types of eczema (not atopic)
seborrhoeic, allergic contact dermatitis, discoid
29
describe seborrhoeic eczema appearance, location and susceptibility
red and greasy scale (similar to dandruff), affecting nose, eyebrows, chest, back; appears at times of stress
30
describe process of allergic contact dermatitis
when patient becomes sensitised to specific allergen antigens, causing eczema
31
describe discoid eczema appearance and predisposition
disc like patches of eczema (appears like coins), related to dryness (e.g. overwashing)
32
describe psoriasis cause and appearance
inflamed skin with overproduction of immature keratinocytes (due to polygenic inflammatory susceptibility, and possible triggers e.g. stress, infections), with scales and plaques which are well defined and symmetrical
33
5 histological features of psoriasis
hyperkeratosis (thick keratin layer), parakeratosis (keratinocytes at top have not lost nuclei), acanthosis (thickening of epidermis), inflammation (lymphocytes in dermis, neutrophils in epidermis), dilated blood vessels
34
common locations of psoriasis
scalp, face, armpit, trunk, elbows, buttocks, groin, nails, knees (extensor surfaces), feet
35
features of psoriasis vulgaris on soles of feet
well-demarcated, symmetrical, erythematous plaques with thick, yellowish scale and desquamation on sites of pressure arising on plantar feet (similar lesions present on palms)
36
psoriasis nail changes: subungual hyperkeratosis
build up of debris under nail
37
psoriasis nail changes: dystrophic nail and loss of cuticle
dystrophy of nail of bacteria and fungi can enter and cause infection
38
psoriasis nail changes: onycholysis
splitting of nail (lifts off of nail plate) - can also cause pitting of nail
39
describe guttate psoriasis susceptible patients and appearance
teenagers and young adults, where small papules (2-4mm) - same as plaques just small
40
describe location and appearance of palmoplantar pustulosis
just affects hands and feet, with small pustules
41
describe appearance of generalised pustular psoriasis
extensive involvement of skin with small pustules (sterile neutrophils in epidermis; also caused by infection and drug reaction)
42
what is acne a disorder of
disorder of pilosebacceous unit (hair follicle and sebaceous gland)
43
describe acne formation
genetic predisposition causing accumulation of dead cells and sebum in hair follicle pore by androgens -> bacteria (propionibacteria acnes) proliferate (pimple - comedone formation) -> rupture of follicular canal (inflammation)
44
5 clinical features of acne (usually all present at same time), and 3 possible treatments
whitehead (closed comedones), blackhead (open comedones), papule, pustule, nodule; treat by: sterilising skin, administering topical antibiotics (lipophilic), using contraceptive pill to reduce androgen concentration
45
conditions causing blistering: describe blisters in bullous pemphigoid
blisters are deep
46
location of basement membrane zone in skin
between epidermis and dermis, so different embryological orgins
47
what proteins anchor basement membrane
tonofilaments in epidermis, anchoring fibrils in dermis
48
causes of blistering due to attack of basement membrane proteins
genetically defective proteins, or proteins e.g. BPAg1, BPAg2 are a target of auto-antibodies
49
conditions causing blistering: epidermolysis bullosa
genetically defective protein where small traumas cause skin to blister and sheer off
50
conditions causing blistering: pathology of bullous pemphigoid
autoantibody against BPAg1 and 2 causing split in basement membrane
51
conditions causing blistering: location and appearance of bullous pemphigoid
tense blisters (bullae) all over body, including mouth, with blisters arising in inflamed areas (tense blisters) as well as normal appearing skin
52
conditions causing blistering: treatment of bullous pemphigoid
immunosuppressants to suppress auto-antibody formation
53
conditions causing blistering: pempigus vulgaris
flaccid blisters which break easily and arise in normal appearing skin
54
connections between keratinocytes
between plasma membranes; attachment plaque; keratin intermediate filaments
55
connections between keratinocytes: between plasma membranes
desmogleins and desmocollins
56
connections between keratinocytes: in attachment plaque to keratin intermediate filaments
plakophilin, plakoglobin, desmoplakin
57
pephigus vulgaris pathology
auto-antibodies (vs desmogleins antigen) causing split between epidermis keratinocytes

Y2 MCD Immunology (14 decks)

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