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
microanatomy of skin (layers from superficial to deep)
epidermis (including stratum cornea) -> dermis -> hypodermis (containing subcutaneous tissue)
contents of dermis and hypodermis
sweat gland, sebaceous gland, hair follicle, blood vessels
2 layers of dermis (superficial to deep)
papillary dermis -> reticular dermis
what is present in hair bearing skin
apocrine glands, hair follicle, sebaceous gland
4 important cells of epidermis
keratinocytes, Langerhans cells, Merkel cells, melanocytes
structure of epidermis (from young at bottom, old at top)
dermis -> stratum basale -> stratum spinosum -> stratum granulosum -> stratum lucidum -> stratum corneum
what is present in dermis
sensory nerve ending
what is present in stratum basale
dividing keratinocyte (stem cell), tactile cell
what is present in stratum spinosum
melanocyte, dendritic cell, living keratinocytes
what is present in stratum corneum
dead keratinocytes (those on surface flake off)
keratinocyte differentiation pathway
basal cell -> prickle cell -> granular cell -> keratin
structure of stratum corneum
protein and lipids in between corenocyte layers (dead keratinocytes - flat and no nuclei)
function of stratum corneum
barrier
what do defects in stratum corneum lead to
eczema
common gene mutation in eczema patients (intrinsic factor), meaning more suscpetible to other atopic diseases
filagrin, as protein in between corenocyte layers, so defect allows allergens entry
define atopy
tendency to develop hypersensitivity
3 atopic diseases
eczema, asthma, hayfever
3 features of atopic eczema
common (typical as baby but most grow out of it), relapsing, remitting
describe atopic march: sequence of atopic diseases and when they typically come about
eczema -> food allergies -> asthma -> rhinitis; typically rise as child, peak at teens, reduce as adult
extrinsic factors of atopic eczema
penetration of exogenous agents e.g. allergens, irritants, pathogens (usually due to intrinsic factor causing defect first)
describe acute form of atopic eczema
activation of CD4+ lymphocytes and Th2 response
describe chronic form of atopic eczema
activation of CD4+ and CD8+ lymphocytes and Th1 response
what is a sign of a filagrin gene mutation
palmar hyperlinearity (palms on hands are more prominent)
common sites of infantile atopic eczema
affected on face, elbows and knees (irritable areas where able to rub themselves)
common sites of adult atopic eczema
hands, back of knees, elbows, neck, face (flexures)
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
describe eczema herpecitum
cold sore virus which can spread over eczema area (appear as ulcers and vesicles)
3 other types of eczema (not atopic)
seborrhoeic, allergic contact dermatitis, discoid
describe seborrhoeic eczema appearance, location and susceptibility
red and greasy scale (similar to dandruff), affecting nose, eyebrows, chest, back; appears at times of stress
describe process of allergic contact dermatitis
when patient becomes sensitised to specific allergen antigens, causing eczema
describe discoid eczema appearance and predisposition
disc like patches of eczema (appears like coins), related to dryness (e.g. overwashing)
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
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
common locations of psoriasis
scalp, face, armpit, trunk, elbows, buttocks, groin, nails, knees (extensor surfaces), feet
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)
psoriasis nail changes: subungual hyperkeratosis
build up of debris under nail
psoriasis nail changes: dystrophic nail and loss of cuticle
dystrophy of nail of bacteria and fungi can enter and cause infection
psoriasis nail changes: onycholysis
splitting of nail (lifts off of nail plate) - can also cause pitting of nail
describe guttate psoriasis susceptible patients and appearance
teenagers and young adults, where small papules (2-4mm) - same as plaques just small
describe location and appearance of palmoplantar pustulosis
just affects hands and feet, with small pustules
describe appearance of generalised pustular psoriasis
extensive involvement of skin with small pustules (sterile neutrophils in epidermis; also caused by infection and drug reaction)
what is acne a disorder of
disorder of pilosebacceous unit (hair follicle and sebaceous gland)
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)
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
conditions causing blistering: describe blisters in bullous pemphigoid
blisters are deep
location of basement membrane zone in skin
between epidermis and dermis, so different embryological orgins
what proteins anchor basement membrane
tonofilaments in epidermis, anchoring fibrils in dermis
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
conditions causing blistering: epidermolysis bullosa
genetically defective protein where small traumas cause skin to blister and sheer off
conditions causing blistering: pathology of bullous pemphigoid
autoantibody against BPAg1 and 2 causing split in basement membrane
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
conditions causing blistering: treatment of bullous pemphigoid
immunosuppressants to suppress auto-antibody formation
conditions causing blistering: pempigus vulgaris
flaccid blisters which break easily and arise in normal appearing skin
connections between keratinocytes
between plasma membranes; attachment plaque; keratin intermediate filaments
connections between keratinocytes: between plasma membranes
desmogleins and desmocollins
connections between keratinocytes: in attachment plaque to keratin intermediate filaments
plakophilin, plakoglobin, desmoplakin
pephigus vulgaris pathology
auto-antibodies (vs desmogleins antigen) causing split between epidermis keratinocytes
