3. Allergens Flashcards
What is Atopy?
‘a personal &/or family tendency to become sensitised and produce antibodies in response to allergens
What is hypersensitivity?
‘objectively reproducible symptoms or signs,
initiated by exposure to a defined stimulus,
At a dose tolerated by normal subjects’
What is an allergy?
‘is a hypersensitivity reaction initiated by immunological mechanisms’
What is meant by ‘Atopic’
‘allergic symptoms in a person who has atopic constitution’. A state defined by the genetically determined disposition to develop atopic eczema, allergic rhinoconjunctivitis, and/or allergic asthma.
Factor predisposing to food allergy.
A genetic predisposition and environmental factors interplaying with the intrinsic properties of the particular food allergy.
What is the classification system for allergy severity? Describe it.
Gel and Coombes
Type I: Immediate Hypersensitivity. IgE (e.g. Anaphylaxis)
Type 2: Antibody Dependent, Cytotoxic. IgG, IgM (e.g. AI Haemolytic Amaenmia)
Type 3: Immune Complex Deposition. IgG (e.g. Vasculitis, Nephritis)
Type 4: Delayed Type Hypersensitivity T-Cells (e.g. Contact dermatitis, mantoux test)
What is a clinical allergy?
IgE antibody response to an environmental antigen
Where do clinical allergies manifest? Why?
Manifest on skin surfaces, nose, conjunctiva, airway & GI.
High levels of mast cells: IgE is affixed
What is sensitisation?
Prior exposure & immunological sensitisation
What are the possible routes of primary sensitiasation?
Acquired in utero
Unrecognised oral exposure
Non-oral routes (cutaneous or respiratory)
What are the two types of Cow’s Milk Protein Allergy?
Cow’s milk protein allergy (CMPA)
IgE mediated
Non-IgE mediated
What are some of the symptoms of IgE mediated CMP allergy?
Early reactions Urticaria Angioedema vomiting Acute flare of atopic dermatitis
What are some of the symptoms of Non-IgE mediated CMP allergy?
Blood/Mucous in Stools Loose/Freq Stools GERD Abdominal Pain Infantile Colic Food Refusal/Aversion Constipation Perianal Redness Pallor and Tiredness
What is the Tx for Non-IgE mediated CMPA?
Elimination (2-6 weeks) & then re-challenge
Hypoallergenic formula
Maternal avoidance of cow’s milk
What are common allergies in the infant/toddle/child?
Urticaria Angioedema Nasal drainage Sneezing Ocular itch Pruritis Abdominal pain
Acute severe allergic reactions (e.g. Nuts)
Asthma
What is childhood/adolescence allergic airway disease?
Asthma & Rhinitis co-existing
What is the pathophysiology of Allergic Airway Disease?
Close functional & anatomical relationship: upper & lower airways
What is important in the Management of Allergic Airway Disease?
Optimum control of allergic rhinitis improves asthma control
What are the clinical features of Allergic Rhinitis?
Sneezing/nasal congestion Rhinorrhoea Itching of nose, eyes & throat Cough Sinus pressure Epistaxis Nasal polyps
‘Allergic salute
What allergens can trigger allergic rhinitis?
Pollen (seasonal)
House dust mite
Animals (cat/dog/horse..mice)
What test results support a Dx of allergic rhinitis?
Positive serum IgE or
Skin Prick Testing (SPT) to allergen
What is the Tx for Allergic Rhinitis?
Avoidance Oral/nasal antihistamines Nasal steroids Cromoglycate Immunotherapy
Outline the approach to Dxing a skin disease?
Type of lesion
Distribution of lesions - characteristic
Time course – congenital, acute or chronic
What are the common skin lesions?
Macule Papule Vesicle Urticaria Pupura
What are the properties of macules?
Flat, small (<2-3cm)
Erythematous/pigmented
What are the properties of Papules?
Palpable (raised)
Small
What are the properties of Vesicles? What make them a pustule?
Palpable
Small (<5mm)
Clear fluid within
Pustule if cloudy fluid
What are the properties of Urticarias?
Red
Blanches to pressure
Raised lesion
Well demarcated edge
What are the properties of Purpuras? What makes them Petechiae?
Flat
Does not blanch
Bruise/ecchymosis if large
Petechiae if pinpoint
What is Atopic Dermatitis?
A common, chronically relapsing, pruritic inflammatory skin disease
What is a significant risk factor for atopic dermatitis?
Personal/family history of allergy
Strong Genetic Influence
What are the clinical features of Atopic Dermatitis?
Typically distributed lesions
Hallmark of AD: skin barrier dysfunction
Dryness, erythema, excoriation, lichenification
Periods of exacerbation/improvement
What is the typical distribution of atopic dermatitis?
Face in infants Extensor Surfaces < age 2 yr Flexor > age 2 yr May be generalised *Spares nappy area*
What are the causes/risk factors for an abnormal skin barrier leading to atopic dermatitis?
Abnormalities in epidermal structural proteins, filaggrin: mutated in 15% of patients with AD
Filaggrin mutations a major susceptibility factor in AD
Also lipids, proteases & protease inhibitors
What other conditions are commonly associated with Atopic Dermatitis?
Food allergy may be present in approx 30% children with AD
AD < 6 months of age associated with greater risk of egg, milk or peanut allergy
A strong link with severity of eczema
What is the dual allergen exposure hypothesis?
Tolerance occurs due to oral exposure to food & allergenic sensitisation results from cutaneous exposure
What is the Tx for Atopic Dermatitis?
1 Bathing 2 Emollients 3 Avoidance of trigger factors 4 Topical corticosteroids 5 Anti - histamines 6 Paste bandages or wet wraps
What are useful Tx for the combination of Food Allergy and Atopic Dermatitis?
Optimise management:
Topical emollients & steroid
Dietary exclusions rarely needed - Cow’s milk is an important source of calcium
*Dietician referral if restrictions considered
What are the potential complications of poorly controlled Atopic Dermatitis?
Sleeplessness Irritability Poor self esteem Effect on other sibs Stunting of growth Loss of school days Bullying Psychological Implications
What is a food alergy?
Adverse immune response to a food protein
What are the classifications of food allergy?
IgE mediated
non-IgE mediated
Also: mixed IgE & non IgE mediated
What is the incidence of food allergies amongst children?
5-6%
1-2% in older children/adults
How do the majority of food allergies present?
Majority of allergic reactions to food occur on first known exposure.
How do IgE mediated reactions typically present?
IgE mediated reactions usually occur within 20 minutes of exposure - almost all occur within 2 hours
Minor symptoms such as
Urticaria, angioedema (swelling of face, eyes ,lips)
Major
Anaphylaxis such as breathing difficulty, hypotension
How do Non-IgE mediated reactions tend to present?
Tend to be delayed
From one hour to several days after ingestion
Exacerbation of eczema &/or diarrhoea & abdominal discomfort.
What non-immunological reactions may result in food intolerance?
enzyme deficiencies
pharmacological agents
naturally occurring substances
Outline the approach to a child with a suspected food allergy?
SUSPECTED FOOD ALLERGY
Food exclusion diet
DIAGNOSIS Allergy focused history… Appropriate use of skin prick testing Serum specific IgE testing Component testing (eg Ara h2 – peanut) Oral food challenge Supervised elimination diets
What info should be elicited from the Allergen Hx?
Determine the allergen
Time from exposure to reaction
The nature of the reaction
What principles should govern investigations in possible allergies?
- High index of suspicion: (based on a good history)
tests are useful for confirming allergy - Low index of suspicion:
tests useful for ruling out a diagnosis of allergy - History & tests equivocal
confirmation by an open or blinded provocative challenge test required to make diagnosis
Investigations should only be performed if inferred by history
Beware of false positives in allergy tests
A negative test is reassuring that risk of serious allergy is negligible
What physical examinations should be performed on the child with suspected allergies?
General Inspection of the skin Nasal/ oral cavity/ pharynx Respiratory - lung fields Palpation & percussion abdomen
What is the purpose of SPT and Serum Testing? Limitations?
To detect specific IgE antibody
To confirm an allergen-specific immediate allergic reaction
Limitations:
- highly sensitive (generally >90%)
- moderately specific (50%)
What is the appropriate management for IgE positive food allergy?
- Allergen avoidance
For a clearly identified allergen
?Exclude allergen from diet without risk of malnutrition - The dietary approach: earlier introduction, which may assist in the acquisition of tolerance
Eg Baked egg, Baked milk - Written action plan for accidental exposure
- Anti-histamine for mild reaction; Salbutamol inhaler
- Adrenaline auto-injector x2 for severe reaction
What is the appropriate management for Non-IgE positive food allergy?
Supervised exclusion and reintroduction
Time defined (4-6 weeks duration) & exclude no more than 4 foods
What are Red-Flags for IgE mediated reactions?
Immediate
Reproducible
Multi-system (Skin plus, Gut plus)
What are red flags for anaphylaxis?
Asthma
Airway signs
Wheezing
Collapse
A ‘sense of doom’
Severe abdominal pain
What are high risk settings for anaphylaxis?
school
daycare
friends/relative homes
restaurants
What are the clinical features of Anaphylaxis?
Majority - IgE mediated: (Food allergen: 30 mins)
Cutaneous symptoms w anaphylaxis – in children
Respiratory compromise
- Bronchoconstriction (wheeze)
- Laryngeal oedema (airway obstruction)
Hypotension & shock : less commonly seen early in children
*Asthma - a major risk factor for life-threatening food related anaphylaxis
What conditions might mimic anaphylaxis?
Vasovagal syncope Cardiogenic & hypovolaemic shock Status asthmaticus Seizure disorder Systemic mastocytosis Hereditary or acquired angioedema Panic attacks Drug overdose ‘Red man syndrome’ following iv Vancomycin
Describe the management of anaphylaxis?
Mild Reaction: Oral Antihistamines, Monitor
Severe: ABCDE
ACT: Adrenaline Autoinjector, 112, Monitor
What is SCIT? Efficacy? Risks?
Subcutaneous Immunotherapy
Well documented clinical & long term efficacy in Hymenoptera venom allergy, allergic asthma & rhinitis.
Anaphylaxis risk.
What is SLIT?
S/L immunotherapy documented for pollen rhinitis
How might tolerance of an allergen be promoted/induced?
Desensitisation:
A temporary tolerant state
Increased threshold for the allergen is achieved
Maintenance exposure essential
Threshold may be reduced by exercise, stress, illness
Long term Tolerance:
Persistent state after cessation of immunotherapy
