Allergy & The Skin Flashcards

1
Q

What mediates type 1 hypersensitivity/allergy

A

IgE

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2
Q

When does a type 1 hypersensitivity/allergy present with respect to allergen exposure

A

Immediate reaction - occurs within minutes & up to 2 hours after exposure to allergen

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3
Q

What route of exposure causes type 1 hypersensitivity/allergy

A

Skin contact e.g. latex
Inhalation e.g. pollen, house dust mite
Ingestion e.g. nuts, seafood
Injection e.g. bee sting, medications

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4
Q

Describe the pathophysiology of type 1 allergy

A
  • Sensation stage: production of specific IgE by B cells (helped by T cells) in response to initial allergen exposure, residual IgE antibodies bind to circulating mast cells via Fc receptors
  • Allergic stage: on re-exposure to allergen, the allergen will bind to IgE coated mast cells → cell degranulation (release of histamine and other inflammatory mediators)
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5
Q

Type 1 allergy clinical features

A
  • Urticaria (wheels & hives)
  • Angioedema (localised, non pitting oedema)
  • GI symptoms (N&V, abdominal pain, diarrhoea)
  • Respiratory (wheezing, sneezing, nasal itching, rhinorrhoea)
  • Anaphylaxis
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6
Q

Oedema in allergy vs swelling secondary to atopic dermatitis - how do you tell the difference

A

Atopic dermatitis is likely to be scaly, itchy, weeping etc with less pronounced swelling
Allergic oedema is likely to be accompanied by hives & other allergic symptoms

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7
Q

Type 1 Allergy investigations

A
  1. History
  2. Specific IgE (RAST) blood test
  3. Skin prick test (if IgE negative)
  4. Challenge test (only if SPT is negative)
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8
Q

Anaphylaxis investigation

A

Serum mast cell tryptase level (during anaphylaxis)

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9
Q

Type 1 allergy management

A
  • Allergy avoidance
  • Anti histamines (prevents effects of mast cells) (1st line)
  • Corticosteroids (anti inflammatory agent) (2nd line)
  • Adrenaline auto injector (for anaphylaxis)
  • Sodium cromoglicate (mast cell stabiliser/blocker)
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10
Q

When does a type IV hypersensitivity/allergy present with respect to allergen exposure

A

Delayed hypersensitivity - Onset of reaction typically after 12-24 hours

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11
Q

What mediates Type IV allergy

A

T Cell mediated, antigen specific

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12
Q

What is type IV allergy aka

A

Allergic contact dermatitis

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13
Q

What route of exposure causes type IV hypersensitivity/allergy

A

Direct skin contact e.g. cosmetic preservative, nickel in belt
Airborne contact e.g. fragrances, plants
Injection e.g. tattoo

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14
Q

Type IV Allergy investigations

A

Patch testing

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15
Q

What can be mistaken for allergic contact dermatitis

A

Irritant contact dermatitis
Endogenous dermatitis e.g. eczema
Infection

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16
Q

Irritant/ Allergic contact dermatitis management

A

•Allergen / Irritant avoidance
•Allergen / Irritant minimisation
•Emollients
•Topical steroids
•UV phototherapy
•Immunosuppressants

17
Q

Type IV allergy/ allergic contact dermatitis pathophysiology

A
  1. Sensation stage: generation of memory T cells following exposure to antigen (via Langerhans cells in epidermis and MHC-II)
  2. Allergic stage: activation of sensitised Th cells in response to antigen, causing release of inflammatory cytokines and cell-mediated cytotoxicity
18
Q

Allergic contact dermatitis clinical features

A

itchy, eczematous rash (vesicles, fissures, erythema)

19
Q

Allergic vs irritant contact dermatitis clinical features

A
  • In allergic contact dermatitis the rash may extend beyond the boundaries of immediate contact
  • This is unlike irritant contact dermatitis, where the skin changes are localised directly to the area of exposure
  • Allergic contact dermatitis requires a sensitisation phase whereas irritant contact dermatitis doesn’t
20
Q

Common irritants

A

Detergents, bleach, PPD, nappy rash (urine - flexures will be spared), ‘lip-lick’ chelitis