Allergic skin diseases Flashcards
Allergic contact dermatitis definition
- inflammatory skin disease caused by a delayed-type hypersensitivity reaction to material (the allergen) in contact with the skin
Irritant contact dermatitis definition
inflammation of the skin caused by contact with irritant materials, environmental factors (no immunological mechanism involved)
Photodermatitis definition
dermatitis caused by UV rays and delayed-type hypersensitivity reaction (photoallergic) or toxic damage of an epidermis (phototoxic)
Photodermatitis clinical manifestation
- burning
- itching
- stinging
- large blisters
caused by contact with the photosensitizing compounds found naturally in some plants and vegtables like parsley, citrus fruits, carrots
Allergic contact dermatitis can occur from…
2-3 years (rarely in infancy)
The most common contact allergens among children
- nickel
- chrome (is used in tanning)
- Cobalt
Acute Contact Dermatitis presentation
- clearly defined erythema, edema
- papules, vesicles
- oozing, crusts
- scaling
- itchign, burning
Chronic contact dermatitis presentation
- slght erythema
- scaling
- hyperpigmentation
- lichenification
- erosions
- itching
Diagnosis of allergic CD
- history and clinical presentation
- skin patch testing
Diaper dermatitis
- usually irritant CD
- may be allergic in these cases
- -> disperse dyes
- -> emulsifier
- -> rubber products
- -> fragnances
- -> preservatives (in wipes)
- -> resin (glue)
Dimethyl-glyoxime test
Nickel spot test
Natural remedies for CD
- balsam of peru (from myroxylon pereira)
- essential oils –> tea tree oil, lemon oil, eucalyptus oil
Tattoos
- in black henna: p-phenylenediamine (PDD)
Acute contact dermatitis management
- avoidance of allergens or irritant substances
- treatment of skin inflammation (local CCS, systemic CCs for severe cases)
- sensitive skin topical calcineurin inhibitors
- improvvement of skin’s barrier function (emollient)
- orevention if infections and treatment
Atopy
- genetic tendency to produce specific immunoglobulin E to small doses of environmental allergens
atopic diseases
- atopic dermatitis
- allergic bronchial asthma
- allergic rhinoconjunctivitis
Atopic dermatitis is characterized by:
- intensive pruritus
- typical symmetrical skin rash
- relapsing course
Endogenic causes of atopic dermatitis
- genetically impaired skin barrier function with increased transepidermal water loss (filaggrin deficiency)
- filaggrin is a protein that binds keratin fibers in epithelial cells
- individuals with mutations in the gene for filaggrin are predisposed to a severe form of dry skin, ichtyosis vulgaris and eczema
Pathophysiology of atopic dermatitis
- immune deviation towards the Th2 pathway in the initiation phase with consequent increased IgE production
- increased production of mediators from various inflammatory cells
- deficient skin barrier function due to abnormal lipid metabilism and epidermal structural protein formation of filaggrin and protease inhibitors
- an abnormal micorbial colonization with pathogenic organisms such as S. aureus and increased susceptibility to skin infection
Etiology of atopic dermatitis
- environmental allergens
- food allergens
- infections
- hormones
- climate
- season
- stress
- skin irritants
Fungal infections
- yeast malassezia or pityrosporum
- can be a trigger in AD
- patients with head-and-neck dermatitis
- antimycotic therapy can help (2-3 months of itraconazole or ketoconazole)
Infantile atopic dermatitis clinical manifestations
- face, neck, chest, scalp, extensor surfaces, flexor surfaces
- “wet eczema”: pruritic, red, scaly and crusted lesions
- acute lesions include vesicles, and there can be serous exudates and crusting in severe cases
Childhoof atopic dermatitis clinical manifestations
- neck, flexor surfaces: antecubital and popliteal fossa, wrists, ankles, periorbital erythema, eyelids, nipple area, lips
- “dry eczema”: symmetrical erythemic lichenified plaques, excoriation, scaling
Adolescent atopic dermatitis
- hyperlinear palms
Atopic dermatitis diagnosis
- anamnesis
- clinical signs
- lab. testing: blood test, IgE
- allergological examination:
- -> skin prick test, prick-to-ptick test
- -> skin patch test
- -> oral food challenge
- 3 major and 3 minor criteria
Major criteria in AD
- typical localization of skin lesioins
- pruritus
- chronic or relapsing course
- personal history of allergy
- family history of allergy
Minor cirteria in AD
- dry skin
- early age of onset
- cheilitis
- hyperlinear palms
- elevated serum IgE
- susceptibility to cutaneous infections
- course influenced by environment
- recurrent conjunctivitis
- white dermographism
- infraorbital folds
- pityriasis alba
- keratosis pilaris
White dermographism
- due to an abnormal vascular response in patients with AD
Pityriasis alba
stages:
- slighly scaly pink plaque with just palpable papular surface
- hypopigmented plaque with fine surface scale
- post-inflammatory hypopigmented macule without scale
- resolution
Keratosis pilaris
- common in children with AD
- autosomal dominant inheritance
- more prominent in winter
- due to abnormal keratinization of the linign of the upper portion of the hair follice
- both upper arms, thighs, buttocks and sides of the cheeks
Bacterial skin infection in atopic dermatiits
- S.aureus
- -> impetigo bullosa or non-bullous impetigo
Impetigo bullosa
- 4th day from the beginning of rash
- 2nd day: T>39°
Eczema herpeticum
- multiple umbilicated vesiculopustules
- mostly head, neck, trunk
- rapildy worsening, painful lesions
- possible fever, malaise, lymphadenopathy
- prone to secondary bacterial infection
- life-threatening dissemination
- heal within 2-6 weeks
SCORAD index
I Area - determine affected sites
II Objective assessment of skin lesions
III Assessment of subjective symtpoms (itch and sleeplessness)
SCORAD I (A)
from 0 to 96 points (children under 2)
from 0 to 100 points (in children over 2)
SCORAD II (B)
signs assessed are:
- erythema
- edema /papules
- oozing/ crust
- excoriation
- lichenification
- xerosis
intensity of ech sign is assessed from 0 to 3
SCORAD III (C)
- under 7 years old: parents should answer
- symptoms during last 3 days
- from 0 to 10 points each
SCORAD index evaluation
- using formula A/5 + 7 x B/2 + C
1-24 points: mild AD
25-50 pints: moderate AD
- over 50 points: severe AD
General management of AD
- avoidance of allergens and exacerbating factors
- skin care, emollients
- bath and bath oils for avoiding epidermal dehydration
- antiseptics and antimicrobial agents (against S.aureus)
- topical CCS or calcineurin inhibtors
- antihistamines (systemic)
wet wrap treatment in severe AD
two layers fo dressing
- moist dressing which is saturated with emdicaments directly on skin
- ovelying dry dressing
- cooling, anti-inflammatory and anti-pruritic effect
Allergen-specific immunotherapy (ASIT)
- not recommended as a general treatment for AD
Urticaria definition
- skin disease characterized by pruritis transient (up to 24 hours) superficial swellings of skin –> wheals
- angioedema
Angioedema in urticaria
- acute swelling of deeper skin layers, hypodermis
- painful rather than itchy
- often with swellign of mucosa
- lasts longer (up to 72 horus)
Classification of urticaria
CHRONIC SPONTANEOUS
INDUCIBLE
- symptomatic dermographism
- delayed pressure
- solar urticaria
- heat urticaria
- vibratory angioedema
- cholinergic urticaria
- contact urticaria
- aquagenic urticaria
Pathophysiology of urticaria
- mast cell degranulation adn liberation of histamine
- -> type I hyerpsensitivity reactions –> allergic urticaria
- .> Autoantibodies agains FcRI receptors or IgE –> autoimmune ruticaria
- -> Stimulation of nervous system: cholinergic urticaria
- -> direct liberation of histamine: contat urticaria
Role of histamine
- vasodilation and increased plasma extravasation
- -> swelling of superficial-mid dermis -wheals
- -> swelling of deep dermis –> angioedema
Stages of urticarial reactions
- Erythema: vasodilation
- wheal: due to edema
- Red flare around the whal: due to axon reflex
Classification of urticaria based on duration
- acute: under 6 weeks
- chronic: over 6 weeks, minimum 2 episodes per week
Spontaneous uritcaria diagnosis
- acute: diagnostic tests not recommended
- chronic: blood test, ESR, CRP, omission of suspected drugs
test for infectious diseases, allergy, Abs, thyroid hormones, phyiscal tests…
Cold urticaria
- after contact with cold or mosit air, after cold shower
- on not clothed skin sites
- patients may experience syncope due to generalized urticaria (in the sea)
- usually patients have other chronic diseases
Cold uritcaria diagnosis
- cold provocation test
- ESR, CRP, cryoglobulons
Delayed pressure urticaria
- type of dermographic urticaria
- deep and painful skin swelling after sustained pressure (after 1 hour)
Delayed pressure urticaria diagnosis
- pressure test (0.2-1.5 kg/cm2 or 10-20 min)
Heat uritcaria diagnosis
- heat provocation
Solar urticaria diagnosis
- UV and visible light of different wavelengths test
Symtpomatic dermographism
- rapidly occuring pruritic linear whealing after moderate scrathcing, stroking or rubbing
- after wearing tight clothes
- most common subtype of inducible ruticaria
Symtpomatic dermographism diagnosis
- elicit dermatographism
- ESR, CRP
Aquagenic urticaria
- after contact with water (shower, swimming)
Aquagenic urticaria diagnosis
wet clothes at bod temperature appllied for 20 min
Contact urticaria
after contact wiht allergen
Cholinergic urticaria
- small short-lived wheals
- after exercising, perpiration
- induced by an increase in the body core temperature, emotional distress
- main mediator: acetylcholine
Cholinergic urticaria diagnosis
- exercise and hot bath provocation
Contact urticaria diagnosis
- skin prick/ skin patch test
Assessming disease activity in urticaria
from 0 to 3 points
WHEALS
0: none
1: mild (under 20 per 24h)
2: moderate (20-50 in 24h)
3: intense (over 50 in 24 h)
PRURITUS
0: non
1: mild
2: moderate
3: intense
Management of urticaria
- first line: modern second generation antihistamines
if symtpoms persist after 2 weeks:
- second line: increased dosage up to fourfold of moder second generation antihistamines
if symptoms persist after 1-4 further weeks
- third line: add on to second line omalizumab or Cyclosporin A or Montelukast
- short couse (max 10 days) of CCS may also be used
