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allergies in children Flashcards

1
Q

IgE mediate allergy - diagram

A
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2
Q

pathophysiology of IgE mediated allergy

A
  1. presentation of allergen to class II MHC molecule
    1. release of various interleukins and messenger compounds - direct effects on cells and influence B cells
  3. class switching and production of specific immunoglobulin E
  4. IgEs bind to mast cells - sensitisation to a particular allergen
  5. subsequent exposure to allergen - cross binding of 2 IgE molecules, degranulation, release of mediators from mast cells
  6. direct effects on epithelial cells, fibroblasts, smooth muscles and blood vessels
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3
Q

what is a class II MHC molecule

A

APC which binds to T helper cells

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4
Q

which interleukins released by T cells affect B cells

A

T2 helper cells via IL 4 and IL 13 affect the B cell

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5
Q

mast cell degranulation leads to

A

release of inflammatory mediators

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6
Q

mast cell degranulation - clinical relevance

A

rapid release and onset of symptoms:

  • histamine, tryptase, hydrolase

later release w/ subsequent effects:

  • secreted inflammatory mediators - prostaglandins, leukotrienes, platelet activating factors, cytokines
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7
Q

what does histamine induce

A
  • bronchial smooth muscle contraction
  • vasodilation → flushing, hypotension if sustained
  • separation of endothelial cells → hives, subcutaneous oedema
  • activation of nerve endings → pain and itching
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8
Q

what is the genetic influence to allergy

A
  • paternal atopy (maternal)
  • concordance for allergy in twins
  • neither parent w/ atopy - 14% risk of atopy in child, one 30% and two 60%
  • hygiene hypothesis
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9
Q

how to tell if it is an allergy

A
  • rapid onset
  • histamine mediated reactions
  • urticaria, erythema, angioedema, pallor/sweating, wheeze
  • improvement w/ antihistamines
  • relatively quick resolution of symptoms
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10
Q

possible triggers for allergic reaction

A

food

environmental allergen - pollen, house dust mites etc

drug

sting/bite

idiopathic

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11
Q

common food allergens (>90%)

A
  • milk
  • hen’s egg
  • peanut
  • tree nuts
  • soya
  • wheat
  • fish
  • sesame
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12
Q

which allergies are more common in which countries

A

cow’s milk - 8x more common in UK and US than in Israel

peanut allergy - 0.2% in israel vs 2.2% in US, UK and canada

shellfish allergy more common in singapore than UK

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13
Q

determining severity of reaction

A

mild/mod: angioedema (not involving airway), urticaria and rash

severe: angioedema of airway (stridor), bronchospasm, peripheral vascular dilation → hypotension

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14
Q

supporting evidence to an episode being an allergy

A

previous reactions

atopy

Fhx - allergy, atopy (siblings and other first degree relatives)

response to treatment

co-existing asthma

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15
Q

investigations for allergies

A

skin prick testing

specific IgE

oral food challenge

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16
Q

why is skin prick testing first line investigation

A

easy to perform

non-invasive

immediate results (20 mins)

cheap

-ve SPT is an excellent predictor for a -ve IgE mediated food reaction in pts w/ anaphylaxis (>95%)

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17
Q

negatives of SPT

A

must stop antihistamines 48hrs prior - importance of +ve control

broken skin

theoretical risk of anaphylactic reactions

dermatographism - all results would be +ve, importance of -ve control

over-interpretation of +ve results - sensitisation and therefore false +ve response

avoid random tests

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18
Q

pros and cons to specific IgE testing

A

pros:

  • no need to stop antihistamines
  • no risk of reactions

cons:

  • expensive and invasive
  • delay in obtaining results
  • less sensitive and specific than SPT
  • highly unreliable results in eczema
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19
Q

strong +ve predictive values on specific IgE testing

A
  • less clearly established in younger children
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20
Q

SPT vs specific IgE testing

A
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21
Q

oral food challenge

A

day case procedure

gold standard

exposure to allergen in controlled environment - tells you what actually happens upon contact or ingestion

  • done in stepwise manner with close observation
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22
Q

making a diagnosis of allergy

A

clear hx

worst reaction - guides treatment options

supporting evidence from investigations

identify and advise on allergen avoidance

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23
Q

how common is urticaria and angioedema

A

lifetime prevalence of 8.8%

chronic in 30-45%

urticaria alone 50%

urticaria and angioedema 40% (up to 85%)

angioedema alone 10%

up to 20% of those referred to hospital remain symptomatic after 10yrs

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24
Q

types of urticaria and angioedema and different triggers

25
investigations for urticaria and angioedema
urticaria only w/ no trigger - no investigation consider SPT/IgE is suspected food/environmental trigger angioedema only (most commonly in teenagers w/ new presentation) - look for hereditary angioedema, C4 and C1 esterase inhibitor rarely: FBC, urinalysis, ESR, LFT, coeliac screen, TFT, antithyroid Ab, ANA * only investigate when troublesome, recurrent or not responding to treatments
26
treatments for urticaria
avoidance of triggers H1 antihistamine (2nd or 3rd gen) high dose antihistamines +/- 2nd antihistamine leukotriene antagonist e.g. montelukast corticosteroids (3-5 days) TXA - esp for angioedema anti IgE monoclonal ab (omalizumab) in children \>7
27
prognosis for urticaria and angioedema
rarely severe usually remits w/ treatment and avoidance of triggers - 25% after 3yrs and 96% asymptomatic after 7yrs physical urticarias resolve after 2-3yrs
28
features of anaphylaxis
laryngeal oedema → upper airway obstruction, stridor hypotension/collapse → pallor, faint, CV collapse bronchospasm → acute wheeze feeling of impending doom onset usually in minutes (symptoms begin within 60 mins, later onset → less severe attack)
29
biphasic anaphylactic reaction
20% have a biphasic reaction 1-8hrs later need steroids and hospital admission to prevent 2nd attack due to secretion of inflammatory mediators following mast cell degranulation
30
prevalence of anaphylaxis
unknown 5.6-10.2 cases per 100 000 from 1991-1995 hospital admissions 7x increase over last 10yrs, 20 deaths p/a UK
31
anaphylaxis fatalities in children
5yr study - children's hospital philadelphia 7 cases of fatal anaphylaxis in 16/12 6/7 had unwittingly ingested a food that had provoked a previous reaction
32
risk factors for anaphylaxis
asthma - poorly controlled stress - emotional or physical w/ acute infection or co-existing illness → lower threshold to developing anaphylaxis exercise viral infection alcohol
33
adrenaline pen for anaphylaxis doses
adult 0.3mg - \>30kg junior 0.15mg - \<30kg
34
adrenaline pens for anaphylaxis
education on use at home/school - have 2 available incase one doesn't work/2nd dose required 1st line treatment for anaphylaxis early use is associated w/ better outcomes potential interaction w/ beta blockers and tricyclics
35
what does adrenaline do
* reverses peripheral vasodilation * increases peripheral vascular resistance * improves BP and coronary perfusion * decreases angioedema * causes bronchodilation * decreases release of inflammatory mediators
36
who needs an adrenaline pen
* have suffered a severe systemic reaction * where the allergen cannot be easily avoided * allergic to high risk allergens e.g. nuts, w/ other risk factors e.g. asthma * even if the reaction was relatively mild * reaction in response to trace amounts of allergen/trigger * continuing risk of anaphylaxis e.g. food dependent, exercise induced * idiopathic anaphylaxis
37
management of allergies
* allergen avoidance * anti-histamine * adrenaline injectors - asthma, anaphylaxis * dietary advice * optimise asthma control * allergy action plan
38
questions re. dietary advice - may contain labels
* use common sense - e.g if it contains nuts but doesn't specify, avoid * if you've had it previously w/o reaction, likely safe to continue * new foods - take care * in general most foods can be eaten safely
39
how common is peanut allergy
rapid rise in 1990s ~2% UK prevalence (children)
40
types of nuts
peanuts = legume, related to peas, chickpeas, beans lentils, lupin tree nuts - hazelnut, almond, **walnut - pecan, cashew - pistachio**, macadamia (bold = cross reactivity) sesame other nut - pine nut, coconut, nutmeg, chestnut peanut oil - refined, likely safe
41
prognosis for nut allergy
20% grow out of peanut allergy 10% grow out of tree nut allergy * takes a long time, if you don't grow out of it by teenage years you will usually have it for life
42
risk factors to developing nut allergy
* eczema - transcutaneous sensitisation * filaggrin mutation * eczema creams containing peanut oil (arachis) * egg allergy * asthma - 78% of fatal peanut anaphylaxis also had asthma * teenagers and young adults - risk taking, alcohol, not carrying epi pen
43
immunotherapy for nut allergies
in phase 3 trials oral immunotherapy 67% able to tolerate 600mg at exit challenge - 2 peanuts 50% able to tolerate 1000mg - 3-4 peanuts asthma or chronic GI excluded from trial SE - 98.7% adverse event (4.3% severe, 59.7% mod, 34.7% mild) limited data on long term maintenance
44
why do fruit and veg allergies occur
oral allergy syndrome cross reactivity of tree/plant pollens and foods causes mainly oral symptoms - itching, mouth swelling, tongue discomfort **birch** - kiwi, apple, pear, nectarines **alder** - celery, pear, apple, cherry **ragweed** - watermelon, banana, cucumber **mugwort** - celery, fennel, carrots **grass pollen** - melon, tomato, orange
45
management of oral allergy syndrome
peeling or cooking often reduces symptoms antihistamine avoidance highly unlikely to cause anaphylaxis
46
prevalence of egg allergy
2% prevalence in children and 0.1% in adults most common presentation to allergy clinic in infancy 67% grow out of it by 5y/o
47
severity of egg allergy
usually mild and benign but can be severe tolerate well cooked egg first and raw egg last
48
management of egg allergy
avoidance re-introduction egg ladder
49
how common is milk allergy and what is the prognosis
common food allergy in infancy prognosis - IgE cow's milk allergy - 50% grow out by 1yr, 70% by 2yrs and 85% by 3yrs often causes confusion
50
IgE mediated cow's milk allergy
rapid onset histamine based reactions symptoms may include vomiting and occasionally diarrhoea can be identified by SPT or IgE
51
typical presentation of IgE mediated cow's milk allergy
exclusively BF infant who is then given formula ~4-6m/o rapid onset urticaria and angioedema
52
non IgE mediated cow's milk allergy
not histamine based no diagnostic test other than dietary management improves w/ withdrawal of milk protein
53
presentations of non IgE mediated cow's milk allergy
diarrhoea vomiting irritability infantile eczema bloating PR bleeding
54
investigations for milk allergy
hx SPT specific IgE therapeutic trial of exclusion under dietetic review * withdrawal of cow's milk from diet, reintroduce after 6wks to see if symptoms are still there * sometimes ask BF mothers to remove all cow's milk from their diet (Ca and Vit D supplementation is important)
55
types of milk formulas
cow's milk EHF (exclusively hydrolysed) w/ or w/o lactose PHF (partially hydrolysed) - not currently commercially available lactose free formulas AA soya, wheat, coconut, almond, hazelnut
56
what milks to use for different cow's milk allergies
57
management of cow's milk proteins allergy
* almost identical for IgE mediated and non IgE mediated * maternal avoidance of cow's milk (supplement calcium and vit D) * EHF formula * AA formula if not tolerated * soya milk \>1y/o or if not tolerated above
58
prognosis of cow's milk allergy
most children better by 3 (IgE mediated) early introduction of CMP

Y3 paediatrics (45 decks)

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