Dermatitis 2.0 Flashcards
which layer of skin does dermatitis effect
epidermis
outline the acute phase of dermatitis
- erythema, oedema, vesicular/bullois lesions and exudates
signs of 2y infection
golden crusting - strep/staph, may exacerbate acute dermatitis
what changes can skin inflammation have on skin colour
can cause disruption of skin pigmentation causing post inflammatory hyper/hypo pigmentation
outline the histology of dermatitis
- characterised histologically by a spongiotic tissue reaction pattern - spongiotic dermatitis is oedema between epidermal kertainocytes which may progress to vesicles/bullae
allergic contact dermatitis
- a type IV delayed hypersensitivity reaction to a material (allergen) in contact with the skin
- occurs 48-72 hours after exposure to allergen
common contact allergens for allergic contact dermatitis
nickel, perfume, chrome (cement), latex
outline the immunology of allergic contact dermatitis
- 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.
how much allergen is needed to cause a contact allergic dermatitis reaction?
- 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
who is more prone to contact allergic dermatitis reaction
those with impaired skin barrier eg leg ulcer, chronic irritant contact dermatitis, atopic dermatitis with defective filaggrin gene
how can specific substances be detected for contact allergic dermatitis reaction
patch testing
- pathches removed after 48 hours
- results are determined a further 48 hours later
what can skin patch testing be used for
contact irritant and allergic dermatitis
treatment of conact allergic dermatitis
topical steroids and emollients
Irritant Contact Dermatitis
- 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
describe the appearance of Irritant Contact Dermatitis
dry, erythema, scaling, fissuring
how does Irritant Contact Dermatitis relate to exposure and quantity of irritant
- occurs soon after exposure
- severity varies with quantitiy, concentration and length of exposure to substance
- a minimum exposure is necessary
examples of skin irritatns that cause Irritant Contact Dermatitis
water, dry cold air, detergents, solvents, acids, alkalis, adhesives, metalworking fluids and friction
in which situations can ICD have serious implications
for occupation
name 2 characteristic ICD
- nappy rash due to urine - spares flexors
- around mouth from licking - saliva is alkaline
can irritant and allergic contact dermaitits co exist?
yes
testing for ICD
patch testing
who is more likely to get atopic dermatitis
those who have an atopic tendency: atopic dermatitis, asthma, allergic rhinitis
how does atopic dermatitis tend to present
- 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
describe the atopic dermatitis rash
intensely itchy, ill defined erythema and scaling
psychological impact of atopic dermatitis
intense itch can affect sleep - impacting the whole family and causing early neurocognitive impairement
chronic atopic dermatitis changes
- lichenification induces skin markings
- excoriation caused by scratching
- 2y infection
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)
UK diagnostic criteria for atopic dermatitis
treatment of atopic dermatitis
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
which T cells are implicated in atopic dermatitis
Th2 and Th17
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
discoid (nummular) eczema
- intensely pruitic coin shaped (nummular) lesions on limbs
what may discoid (nummular) eczema be mistaken for
ringworm
cause of discoid (nummular) eczema
unknown, may be associated with S Aureus, can also occur in atopic dermatitis etc
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
what are most cases of EH due to
HSV 1, also 2
who tends to get EH
- infants and children with atopic dermatitis, or other reasons for skin barrier breakdown eg burns, pemphigus vulgaris
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
how serious is EH
can be life threatening
treatment of EH
IV acyclovir
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
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
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.
what can stasis eczema lead to
2y eczema in other areass of the body, cellulitis and contact allergy to treatments
treatment of stasis eczema
reduce swelling in leg (activity, elevate, bandage, graduated compression stockings once eczema has settled) and treat eczema
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
dandruff
- pityriasis capitis
- an uninflamed form of SD
what is SD associated with
- psoriasis - a FH of psoriasis predisposes one
- more common in those with HIV
what is seen on the eyes with SD
- seborrhoeic blepharitis - scaly, red eyelid margins
describe the SD lesions
- Fine, greasy scales on erythematous background. Flat patches (psoriasis tends to be raised plaques)
- disease is chronicl, relapsing and mild
management of SD
- Treatment: topical antifungal e.g. ketoconazole, mild steroids
pompholyx eczema
- A form of hand/foot eczema characterised by vesicles/bullae (blisters)
- there are itching spongiotic vesciles on fingers, palms and soles
cause of pompholyx eczema
unknown, there is an association with contact allergy
clinical course of pompholyx eczema
- Clinical course can range from self-limiting to chronic, severe, or debilitating
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.
who is lichen simplex more common in
those with anxiety, OCD etc
photosensitive eczema
- reaction to UV light or drugs/substances
- can occur due to contact with plant material - chrysanthemum
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
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
what is sensitisation
- Sensitisation is the mast cells binding to IgE on first exposure to allergen
- There is degranulation on 2nd exposure.
why is skin dry
lost water from stratum corneum
