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Y3 paediatrics > allergies in children > Flashcards

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

A
25
Q

investigations for urticaria and angioedema

A

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
Q

treatments for urticaria

A

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
Q

prognosis for urticaria and angioedema

A

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
Q

features of anaphylaxis

A

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
Q

biphasic anaphylactic reaction

A

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
Q

prevalence of anaphylaxis

A

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
Q

anaphylaxis fatalities in children

A

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
Q

risk factors for anaphylaxis

A

asthma - poorly controlled

stress - emotional or physical w/ acute infection or co-existing illness → lower threshold to developing anaphylaxis

exercise

viral infection

alcohol

33
Q

adrenaline pen for anaphylaxis doses

A

adult 0.3mg - >30kg

junior 0.15mg - <30kg

34
Q

adrenaline pens for anaphylaxis

A

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
Q

what does adrenaline do

A
  • reverses peripheral vasodilation
  • increases peripheral vascular resistance
  • improves BP and coronary perfusion
  • decreases angioedema
  • causes bronchodilation
  • decreases release of inflammatory mediators
36
Q

who needs an adrenaline pen

A
  • 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
Q

management of allergies

A
  • allergen avoidance
  • anti-histamine
  • adrenaline injectors - asthma, anaphylaxis
  • dietary advice
  • optimise asthma control
  • allergy action plan
38
Q

questions re. dietary advice - may contain labels

A
  • 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
Q

how common is peanut allergy

A

rapid rise in 1990s

~2% UK prevalence (children)

40
Q

types of nuts

A

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
Q

prognosis for nut allergy

A

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
Q

risk factors to developing nut allergy

A
  • 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
Q

immunotherapy for nut allergies

A

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
Q

why do fruit and veg allergies occur

A

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
Q

management of oral allergy syndrome

A

peeling or cooking often reduces symptoms

antihistamine

avoidance

highly unlikely to cause anaphylaxis

46
Q

prevalence of egg allergy

A

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
Q

severity of egg allergy

A

usually mild and benign but can be severe

tolerate well cooked egg first and raw egg last

48
Q

management of egg allergy

A

avoidance

re-introduction

egg ladder

49
Q

how common is milk allergy and what is the prognosis

A

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
Q

IgE mediated cow’s milk allergy

A

rapid onset

histamine based reactions

symptoms may include vomiting and occasionally diarrhoea

can be identified by SPT or IgE

51
Q

typical presentation of IgE mediated cow’s milk allergy

A

exclusively BF infant who is then given formula ~4-6m/o

rapid onset urticaria and angioedema

52
Q

non IgE mediated cow’s milk allergy

A

not histamine based

no diagnostic test other than dietary management

improves w/ withdrawal of milk protein

53
Q

presentations of non IgE mediated cow’s milk allergy

A

diarrhoea

vomiting

irritability

infantile eczema

bloating

PR bleeding

54
Q

investigations for milk allergy

A

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
Q

types of milk formulas

A

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
Q

what milks to use for different cow’s milk allergies

A
57
Q

management of cow’s milk proteins allergy

A
  • 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
Q

prognosis of cow’s milk allergy

A

most children better by 3 (IgE mediated)

early introduction of CMP

Y3 paediatrics (45 decks)

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