3. Allergens Flashcards

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
Q

What are the properties of macules?

A

Flat, small (<2-3cm)

Erythematous/pigmented

26
Q

What are the properties of Papules?

A

Palpable (raised)

Small

27
Q

What are the properties of Vesicles? What make them a pustule?

A

Palpable
Small (<5mm)
Clear fluid within
Pustule if cloudy fluid

28
Q

What are the properties of Urticarias?

A

Red
Blanches to pressure
Raised lesion
Well demarcated edge

29
Q

What are the properties of Purpuras? What makes them Petechiae?

A

Flat
Does not blanch
Bruise/ecchymosis if large
Petechiae if pinpoint

30
Q

What is Atopic Dermatitis?

A

A common, chronically relapsing, pruritic inflammatory skin disease

31
Q

What is a significant risk factor for atopic dermatitis?

A

Personal/family history of allergy

Strong Genetic Influence

32
Q

What are the clinical features of Atopic Dermatitis?

A

Typically distributed lesions
Hallmark of AD: skin barrier dysfunction
Dryness, erythema, excoriation, lichenification
Periods of exacerbation/improvement

33
Q

What is the typical distribution of atopic dermatitis?

A
Face in infants
Extensor Surfaces < age 2 yr
Flexor > age 2 yr
May be generalised
*Spares nappy area*
34
Q

What are the causes/risk factors for an abnormal skin barrier leading to atopic dermatitis?

A

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
Q

What other conditions are commonly associated with Atopic Dermatitis?

A

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
Q

What is the dual allergen exposure hypothesis?

A

Tolerance occurs due to oral exposure to food & allergenic sensitisation results from cutaneous exposure

37
Q

What is the Tx for Atopic Dermatitis?

A
1 	Bathing
2 	Emollients
3 	Avoidance of trigger factors
4 	Topical corticosteroids
5 	Anti - histamines
6 	Paste bandages or wet wraps
38
Q

What are useful Tx for the combination of Food Allergy and Atopic Dermatitis?

A

Optimise management:
Topical emollients & steroid
Dietary exclusions rarely needed - Cow’s milk is an important source of calcium

*Dietician referral if restrictions considered

39
Q

What are the potential complications of poorly controlled Atopic Dermatitis?

A
Sleeplessness
Irritability
Poor self esteem
Effect on other sibs
Stunting of growth
Loss of school days
Bullying
Psychological Implications
40
Q

What is a food alergy?

A

Adverse immune response to a food protein

41
Q

What are the classifications of food allergy?

A

IgE mediated
non-IgE mediated
Also: mixed IgE & non IgE mediated

42
Q

What is the incidence of food allergies amongst children?

A

5-6%

1-2% in older children/adults

43
Q

How do the majority of food allergies present?

A

Majority of allergic reactions to food occur on first known exposure.

44
Q

How do IgE mediated reactions typically present?

A

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
Q

How do Non-IgE mediated reactions tend to present?

A

Tend to be delayed

From one hour to several days after ingestion

Exacerbation of eczema &/or diarrhoea & abdominal discomfort.

46
Q

What non-immunological reactions may result in food intolerance?

A

enzyme deficiencies
pharmacological agents
naturally occurring substances

47
Q

Outline the approach to a child with a suspected food allergy?

A

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
Q

What info should be elicited from the Allergen Hx?

A

Determine the allergen
Time from exposure to reaction
The nature of the reaction

49
Q

What principles should govern investigations in possible allergies?

A
  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
Q

What physical examinations should be performed on the child with suspected allergies?

A
General
Inspection of the skin
Nasal/ oral cavity/ pharynx
Respiratory - lung fields
Palpation & percussion abdomen
51
Q

What is the purpose of SPT and Serum Testing? Limitations?

A

To detect specific IgE antibody

To confirm an allergen-specific immediate allergic reaction

Limitations:

  • highly sensitive (generally >90%)
  • moderately specific (50%)
52
Q

What is the appropriate management for IgE positive food allergy?

A
  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
Q

What is the appropriate management for Non-IgE positive food allergy?

A

Supervised exclusion and reintroduction

Time defined (4-6 weeks duration) & exclude no more than 4 foods

54
Q

What are Red-Flags for IgE mediated reactions?

A

Immediate
Reproducible
Multi-system (Skin plus, Gut plus)

55
Q

What are red flags for anaphylaxis?

A

Asthma
Airway signs
Wheezing

Collapse
A ‘sense of doom’
Severe abdominal pain

56
Q

What are high risk settings for anaphylaxis?

A

school
daycare
friends/relative homes
restaurants

57
Q

What are the clinical features of Anaphylaxis?

A

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
Q

What conditions might mimic anaphylaxis?

A
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
Q

Describe the management of anaphylaxis?

A

Mild Reaction: Oral Antihistamines, Monitor
Severe: ABCDE

ACT: Adrenaline Autoinjector, 112, Monitor

60
Q

What is SCIT? Efficacy? Risks?

A

Subcutaneous Immunotherapy

Well documented clinical & long term efficacy in Hymenoptera venom allergy, allergic asthma & rhinitis.

Anaphylaxis risk.

61
Q

What is SLIT?

A

S/L immunotherapy documented for pollen rhinitis

62
Q

How might tolerance of an allergen be promoted/induced?

A

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