Dermatitis 2.0 Flashcards
1
Q
which layer of skin does dermatitis effect
A
epidermis
2
Q
outline the acute phase of dermatitis
A
- erythema, oedema, vesicular/bullois lesions and exudates
3
Q
signs of 2y infection
A
golden crusting - strep/staph, may exacerbate acute dermatitis
4
Q
what changes can skin inflammation have on skin colour
A
can cause disruption of skin pigmentation causing post inflammatory hyper/hypo pigmentation
5
Q
outline the histology of dermatitis
A
- characterised histologically by a spongiotic tissue reaction pattern - spongiotic dermatitis is oedema between epidermal kertainocytes which may progress to vesicles/bullae
6
Q
allergic contact dermatitis
A
- a type IV delayed hypersensitivity reaction to a material (allergen) in contact with the skin
- occurs 48-72 hours after exposure to allergen
7
Q
common contact allergens for allergic contact dermatitis
A
nickel, perfume, chrome (cement), latex
8
Q
outline the immunology of allergic contact dermatitis
A
- Specific antigens penetrate the epidermis and are picked up by Langerhans cells. This causes T cells to become sensitized to the antigen. Involves CD4+ T cells
- On subsequent exposure to antigen an allergic reaction occurs because of the accumulation of the accumulation of sensitized T cells with a resultant inflammatory response. This takes 48 hours and is amplified by interleukins.
9
Q
how much allergen is needed to cause a contact allergic dermatitis reaction?
A
- a small amount of allergen can cause a disproportionately large reaction
- note patient may have been exposed to allergen for years without it causing a reaction
10
Q
who is more prone to contact allergic dermatitis reaction
A
those with impaired skin barrier eg leg ulcer, chronic irritant contact dermatitis, atopic dermatitis with defective filaggrin gene
11
Q
how can specific substances be detected for contact allergic dermatitis reaction
A
patch testing
- pathches removed after 48 hours
- results are determined a further 48 hours later
12
Q
what can skin patch testing be used for
A
contact irritant and allergic dermatitis
13
Q
treatment of conact allergic dermatitis
A
topical steroids and emollients
14
Q
Irritant Contact Dermatitis
A
- non specific physical irritation that occurs when chemicals/physical agents damage the epidermis faster than the skin is able to repair damage
- there is no immune mechanism involved
15
Q
describe the appearance of Irritant Contact Dermatitis
A
dry, erythema, scaling, fissuring
16
Q
how does Irritant Contact Dermatitis relate to exposure and quantity of irritant
A
- occurs soon after exposure
- severity varies with quantitiy, concentration and length of exposure to substance
- a minimum exposure is necessary
17
Q
examples of skin irritatns that cause Irritant Contact Dermatitis
A
water, dry cold air, detergents, solvents, acids, alkalis, adhesives, metalworking fluids and friction
18
Q
in which situations can ICD have serious implications
A
for occupation
19
Q
name 2 characteristic ICD
A
- nappy rash due to urine - spares flexors
- around mouth from licking - saliva is alkaline
20
Q
can irritant and allergic contact dermaitits co exist?
A
yes
21
Q
testing for ICD
A
patch testing
22
Q
who is more likely to get atopic dermatitis
A
those who have an atopic tendency: atopic dermatitis, asthma, allergic rhinitis
23
Q
how does atopic dermatitis tend to present
A
- in infancy and early childhood - facial involvement initally (cheeks) and then later extensor limb
- infants have widely distributed eczema
- later on with flexural limb involvement
24
Q
describe the atopic dermatitis rash
A
intensely itchy, ill defined erythema and scaling
25
psychological impact of atopic dermatitis
intense itch can affect sleep - impacting the whole family and causing early neurocognitive impairement
26
chronic atopic dermatitis changes
* lichenification induces skin markings
* excoriation caused by scratching
* 2y infection
27
why are people with atopic dermatitis prone to skin infections
* breaks in skin from dry, split skin and from scratching itchy areas allows colonisation by micro organisms.
* 2y infections heralded by golden crusting -staph and strep
* also eczema herpeticum and molluscum contagiosum is more common (parapox)
28
UK diagnostic criteria for atopic dermatitis
29
treatment of atopic dermatitis
30
aetiology of atopic dermatitis
* multiple genetic and environemental factors
* **Filaggrin** **gene** defect leads to impaired skin barrier function - predisposing factor
* allowing access/sensitisation to allergen and promotes colonisation by micro organisms, and also water loss from skin
* associated with severe/early onset disease
31
which T cells are implicated in atopic dermatitis
Th2 and Th17
32
what condition does a filaggrin gene mutation cause
ichythosis vulgaris
* characterised by excessive dry, scaly skin
* mainly caused by water loss from the straum corneum
* skin doesnt shed its dead skin cells
33
discoid (nummular) eczema
* intensely pruitic coin shaped (nummular) lesions on limbs
34
what may discoid (nummular) eczema be mistaken for
ringworm
35
cause of discoid (nummular) eczema
unknown, may be associated with S Aureus, can also occur in atopic dermatitis etc
36
eczema herpeticum
* develops when HSV infects large areas of skin, rather than being confined to a small area eg in cold sore
* Disseminated viral infection characterised by fever and clusters of itchy blisters or punched-out erosions. Often seen as a complication of **atopic dermatitis**
37
what are most cases of EH due to
HSV 1, also 2
38
who tends to get EH
* infants and children with atopic dermatitis, or other reasons for skin barrier breakdown eg burns, pemphigus vulgaris
39
describe the appearance of EH
* Usually initially presents with a cluster of itchy and painful blisters
* Monomorphic (all appear similar to each other) punched out lesions
* Secondary bacterial infection with Staph or Strep may lead to impetigo and/or cellulitis
40
how serious is EH
can be life threatening
41
treatment of EH
IV acyclovir
42
who gets stasis eczema
* middle aged and elderly patients with venous insufficiency
* associated with history of DVT, history of cellulitis, chronic swelling, varicose veins and venous leg ulcers
43
describe the appearance of stasis eczema
* occurs usually on both legs of patients with venous insufficiency
* itchy, red blistered and crusted plaques, dry fissuring and scaly plaques
* there will also typically be peripheral oedema and ulceration
* other features include haemosiderin deposits, lipodermatosclerosis
44
pathophysiology of stasis eczema
* Due to fluid collecting in the tissues and activation of the innate immune response.
* Increased vascular hydrostatic pressure due to venous insufficiency leads to **extravasation of serum and RBCs.**
* Over time, increased haemosiderin and fibrin deposition in the extracellular space leads to pigmentary and fibrotic changes in the skin as well as tissue hypoxia and ulcer formation.
45
what can stasis eczema lead to
2y eczema in other areass of the body, cellulitis and contact allergy to treatments
46
treatment of stasis eczema
reduce swelling in leg (activity, elevate, bandage, graduated compression stockings once eczema has settled) and treat eczema
47
seborrhoeic dermatitis
* Common chronic or relapsing form of dermatitis that mainly affects sebaceous gland rich regions eg scalp, eyebrows, nasolabial folds, upper sternum and back
48
dandruff
* pityriasis capitis
* an uninflamed form of SD
49
what is SD associated with
* psoriasis - a FH of psoriasis predisposes one
* more common in those with HIV
50
what is seen on the eyes with SD
* seborrhoeic blepharitis - scaly, red eyelid margins
51
describe the SD lesions
* Fine, greasy scales on erythematous background. Flat patches (psoriasis tends to be raised plaques)
* disease is chronicl, relapsing and mild
52
management of SD
* *Treatment:* topical antifungal e.g. ketoconazole, mild steroids
53
pompholyx eczema
* **A form of hand/foot eczema characterised by vesicles/bullae (blisters)**
* there are itching spongiotic vesciles on fingers, palms and soles
54
cause of pompholyx eczema
unknown, there is an association with contact allergy
55
clinical course of pompholyx eczema
* Clinical course can range from self-limiting to chronic, severe, or debilitating
56
lichen simplex - cause
* localised area of lichenification produced from physical trauma from rubbing due to chronic localised itch
* Primary itch can be due to atopic eczema, contact eczema, venous eczema, psoriasis etc.
57
who is lichen simplex more common in
those with anxiety, OCD etc
58
photosensitive eczema
* reaction to UV light or drugs/substances
* can occur due to contact with plant material - chrysanthemum
59
what is a key factor in the immunology of atopic dermatitis
* impairement of skin barrier
* mutation in filaggrin gene predispoes one and is associated with severe/early onset disease
* decreased AMP may account for suscpetibility to infection
60
outline the immunology of atopic dermatitis
* Impaired skin barrier allows access and sensitisation to allergen and promotes colonisation by micro-organisms
* Mast cell degranulation releases molecules which dilate the blood vessels and make them leaky, and attracts more immune cells to the area
* Mast cells release IL-5: stimulates eosinophils, which degranulate and release toxins
* Negative cycle: The inflammation makes the skin barrier leakier and allows more allergen to enter. While the leaky barrier and blood vessels allows water to escape, the skin dry and itchy. This is itchy, and subsequently scratching makes this all worse
61
what is sensitisation
* Sensitisation is the mast cells binding to IgE on first exposure to allergen
* There is degranulation on 2nd exposure.
62
why is skin dry
lost water from stratum corneum
