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Paediatrics > 3. Allergens > Flashcards

3. Allergens Flashcards

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1
Q

What is Atopy?

A

‘a personal &/or family tendency to become sensitised and produce antibodies in response to allergens

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2
Q

What is hypersensitivity?

A

‘objectively reproducible symptoms or signs,
initiated by exposure to a defined stimulus,
At a dose tolerated by normal subjects’

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3
Q

What is an allergy?

A

‘is a hypersensitivity reaction initiated by immunological mechanisms’

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4
Q

What is meant by ‘Atopic’

A

‘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.

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5
Q

Factor predisposing to food allergy.

A

A genetic predisposition and environmental factors interplaying with the intrinsic properties of the particular food allergy.

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6
Q

What is the classification system for allergy severity? Describe it.

A

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)

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7
Q

What is a clinical allergy?

A

IgE antibody response to an environmental antigen

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8
Q

Where do clinical allergies manifest? Why?

A

Manifest on skin surfaces, nose, conjunctiva, airway & GI.

High levels of mast cells: IgE is affixed

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9
Q

What is sensitisation?

A

Prior exposure & immunological sensitisation

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10
Q

What are the possible routes of primary sensitiasation?

A

Acquired in utero

Unrecognised oral exposure

Non-oral routes (cutaneous or respiratory)

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11
Q

What are the two types of Cow’s Milk Protein Allergy?

A

Cow’s milk protein allergy (CMPA)
IgE mediated
Non-IgE mediated

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12
Q

What are some of the symptoms of IgE mediated CMP allergy?

A 
Early reactions 
Urticaria 
Angioedema
vomiting 
Acute flare of atopic dermatitis
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13
Q

What are some of the symptoms of Non-IgE mediated CMP allergy?

A 
Blood/Mucous in Stools
Loose/Freq Stools
GERD
Abdominal Pain
Infantile Colic
Food Refusal/Aversion
Constipation
Perianal Redness
Pallor and Tiredness
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14
Q

What is the Tx for Non-IgE mediated CMPA?

A

Elimination (2-6 weeks) & then re-challenge
Hypoallergenic formula
Maternal avoidance of cow’s milk

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15
Q

What are common allergies in the infant/toddle/child?

A 
Urticaria
Angioedema
Nasal drainage
Sneezing
Ocular itch
Pruritis
Abdominal pain

Acute severe allergic reactions (e.g. Nuts)
Asthma

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16
Q

What is childhood/adolescence allergic airway disease?

A

Asthma & Rhinitis co-existing

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17
Q

What is the pathophysiology of Allergic Airway Disease?

A

Close functional & anatomical relationship: upper & lower airways

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18
Q

What is important in the Management of Allergic Airway Disease?

A

Optimum control of allergic rhinitis improves asthma control

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19
Q

What are the clinical features of Allergic Rhinitis?

A 
Sneezing/nasal congestion
Rhinorrhoea
Itching of nose, eyes & throat
Cough
Sinus pressure
Epistaxis
Nasal polyps

‘Allergic salute

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20
Q

What allergens can trigger allergic rhinitis?

A

Pollen (seasonal)
House dust mite
Animals (cat/dog/horse..mice)

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21
Q

What test results support a Dx of allergic rhinitis?

A

Positive serum IgE or

Skin Prick Testing (SPT) to allergen

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22
Q

What is the Tx for Allergic Rhinitis?

A 
Avoidance
Oral/nasal antihistamines
Nasal steroids 
Cromoglycate
Immunotherapy
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23
Q

Outline the approach to Dxing a skin disease?

A

Type of lesion
Distribution of lesions - characteristic
Time course – congenital, acute or chronic

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24
Q

What are the common skin lesions?

A 
Macule 
Papule
Vesicle 
Urticaria
Pupura
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25
What are the properties of macules?
Flat, small (<2-3cm) | Erythematous/pigmented
26
What are the properties of Papules?
Palpable (raised) | Small
27
What are the properties of Vesicles? What make them a pustule?
Palpable Small (<5mm) Clear fluid within Pustule if cloudy fluid
28
What are the properties of Urticarias?
Red Blanches to pressure Raised lesion Well demarcated edge
29
What are the properties of Purpuras? What makes them Petechiae?
Flat Does not blanch Bruise/ecchymosis if large Petechiae if pinpoint
30
What is Atopic Dermatitis?
A common, chronically relapsing, pruritic inflammatory skin disease
31
What is a significant risk factor for atopic dermatitis?
Personal/family history of allergy | Strong Genetic Influence
32
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
33
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* ```
34
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
35
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
36
What is the dual allergen exposure hypothesis?
Tolerance occurs due to oral exposure to food & allergenic sensitisation results from cutaneous exposure
37
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 ```
38
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
39
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 ```
40
What is a food alergy?
Adverse immune response to a food protein
41
What are the classifications of food allergy?
IgE mediated non-IgE mediated Also: mixed IgE & non IgE mediated
42
What is the incidence of food allergies amongst children?
5-6% | 1-2% in older children/adults
43
How do the majority of food allergies present?
Majority of allergic reactions to food occur on first known exposure.
44
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
45
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.
46
What non-immunological reactions may result in food intolerance?
enzyme deficiencies pharmacological agents naturally occurring substances
47
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 ```
48
What info should be elicited from the Allergen Hx?
Determine the allergen Time from exposure to reaction The nature of the reaction
49
What principles should govern investigations in possible allergies?
1. High index of suspicion: (based on a good history) tests are useful for confirming allergy 2. Low index of suspicion: tests useful for ruling out a diagnosis of allergy 3. 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
50
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 ```
51
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%)
52
What is the appropriate management for IgE positive food allergy?
1. Allergen avoidance For a clearly identified allergen ?Exclude allergen from diet without risk of malnutrition 2. The dietary approach: earlier introduction, which may assist in the acquisition of tolerance Eg Baked egg, Baked milk 3. Written action plan for accidental exposure - Anti-histamine for mild reaction; Salbutamol inhaler - Adrenaline auto-injector x2 for severe reaction
53
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
54
What are Red-Flags for IgE mediated reactions?
Immediate Reproducible Multi-system (Skin plus, Gut plus)
55
What are red flags for anaphylaxis?
Asthma Airway signs Wheezing Collapse A ‘sense of doom’ Severe abdominal pain
56
What are high risk settings for anaphylaxis?
school daycare friends/relative homes restaurants
57
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
58
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 ```
59
Describe the management of anaphylaxis?
Mild Reaction: Oral Antihistamines, Monitor Severe: ABCDE ACT: Adrenaline Autoinjector, 112, Monitor
60
What is SCIT? Efficacy? Risks?
Subcutaneous Immunotherapy Well documented clinical & long term efficacy in Hymenoptera venom allergy, allergic asthma & rhinitis. Anaphylaxis risk.
61
What is SLIT?
S/L immunotherapy documented for pollen rhinitis
62
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

Paediatrics (7 decks)

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