Dermatitis and Eczema Flashcards

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1
Q

in cornification where is the nucleus lost from cells

A

at the granular layer

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2
Q

what is seen histologically in eczema

A

spongiosis (oedema between keratinocytes)

inflammatory cell infiltrate (acute or chronic; lymphocytes and/or neutrophils)

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3
Q

what is a common symptom in ALL types of eczema

A

itching

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4
Q

what is eczema a form of

A

dermatitis

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5
Q

describe the acute phase of eczema

A

papulovesicular erthematous (red) lesion, oedema (spongiosis), ooze or scaling and crusting

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6
Q

describe the chronic phase of eczema

A

thickening (lichenification), elevated plaques, increased scaling

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7
Q

what are the key words to remember for the presentation of eczema

A

itchy, ill defined, erythematous and scaley

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8
Q

what is seen histologically in ALL types of dermatitis

A

spongiotic dermatitis

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9
Q

what causes contact irritant dermatitis

A

trauma (eg soap, water)

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10
Q

what causes atopic dermatitis

A

genetic and environmental factors resulting in inflammation

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11
Q

what causes lichen simplex dermatitis

A

physical trauma to skin (e.g. scratching)

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12
Q

what causes stasis dermatitis

A

physical trauma to skin (hydrostatic pressure - peripheral oedema)

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13
Q

what extra feature is seen histologically in drug related dermatitis

A

eosinophils

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14
Q

what extra feature is seen histologically in lichen simplex dermatitis

A

external trauma

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15
Q

what extra feature is seen histologically in stasis dermatitis

A

extravasation of RBS’c (leakage into surrounding tissue)

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16
Q

what are common causes of contact allergic dermatitis

A

nickle, chemicals, topical therapies, plants

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17
Q

why can weeping occur in eczema

A

due to acute oedema of the skin, liquid weeps out

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18
Q

what is the difference between a vesicle and a bullae

A

vesicle- small

bullae-big

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19
Q

describe the immunopathology of contact allergic dermatitis

A

langerhans cells in epidermis processes antigen (increased immunogenicity) anf present it to Th cells in the dermis.

sensitised Th cells migrate into lymphatics and then to regional nodes where antigen presentation is amplified

on subsequent antigen challenge, sensitised T cells proliferate and migrate to infiltrate skin = dermatitis

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20
Q

how long are skin patch batteries left in place and when are the reactions checked

A

left for 48 hours

checked after 96 hours

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21
Q

what is the difference between irritant contact dermatitis and contact allergic dermatitis

A

irritant contact dermatitis is a non specific physical irritation rather than a specific allergic reaction

22
Q

what are features commonly seen in contact irritant dermatitis

A

erythema, scaling, fissuring, lichenification, nail dystrophy, crusting, erosions

23
Q

is nappy rash irritant or allergic contact dermatitis- how can you tell

A

irritant- to urine, as flexures usually spared

24
Q

what is and causes ‘lip-lick’ chilitis

A

lip irritant contact dermatitis to saliva

25
Q

what is the difference between atopic eczema and atopic dermatitis

A

none same thing

26
Q

why does atopic eczema have such a big impact on childrens QOL

A

pruritus= sleep disturbance= neurocognitive impairment

affects whole family

27
Q

what mutation is associated with atopic eczema

A

filaggrin mutation

28
Q

what is seen on the palms of chldren with atopic eczema

A

extra linear palm

29
Q

what ‘cycle’ is seen in eczema

A

the itch- scratch cycle

30
Q

how does atopic eczema present

A

pruritus, ill-defined erythema and scaling, generalised dry skin, flexural distrubution

31
Q

what atopic diseases is atopic eczema associated with

A

asthma, allergic rhinitis (hay fever), food allergy,

32
Q

what ONLY happens in ATOPIC eczema

A

eczema beneath the earlobe- is pathognomonic

33
Q

how does eczema present in darker skin

A

papules, erythema (harder to see), extensive lichenification, prurigo-like nodules, hypertrophic scarring and keloid formation

34
Q

what are the chronic changes of atopic eczema

A

lichenification
excoriation
secondary infection

35
Q

what does (gold) crusting of eczema mean

A

secondary staph aureus infection

36
Q

what is eczema herpeticum

A

when eczema becomes infected with herpes simplex virus- systemic and potentially life threatening

37
Q

describe the presentation of eczema herpeticum

A

extremely painful, monomorphic punched out lesions

38
Q

how do you treat eczema herpeticum

A

anti viral e.g. acyclovir

39
Q

the uk diagnostic criteria for atopic eczema; WHAT plus 3 or more;

A

ITCHING + 3 or more;

  • visible flexural* rash
  • history of flexural* rash
  • (cheeks and extensor in infants)
  • personal history of atrophy (or 1st degree relative if <4yo)
  • generally dry skin
  • onset before age of 2
40
Q

how do you treat eczema

A
  • lots of emollients
  • avoid irritants including shower gels and soaps
  • topical steroids
  • treat infection
  • phototherapy (mainly UVB)
  • systemic immunosuppressants (cyclosporin, methotrexate, azathioprine)
  • biologic agents
41
Q

what is the most important gene in skin barrier function

A

filaggrin

42
Q

what causes eczema

A

multifactoral; genes + environment + immunology

43
Q

describe discoid eczema

A

coin shaped lesions, patients often atopic too

44
Q

what is chronic actinic dermatitis

A

photosensitive eczema

45
Q

how does photosensitive eczema present

A

extensive lichenification and chronic erythema- cut off at collar

46
Q

what is the presentation of stasis eczema

A

eczema follows varicose veins

47
Q

how do you treat stasis eczema

A

treat hydrostatic pressure- compression stocking, surgery etc

48
Q

what is cradle cap

A

seborrhoeic dermatitis- can be atopic eczema often with co fungal or yeast infection

49
Q

what is pompholyx eczema

A

eczema where vesicles appear due to rapid onset of intercellular oedema

50
Q

what is lichen simplex

A

when normal skin has become thickened and scaley due to scratching

51
Q

how is lichen simplex treated

A

potent topical steroids