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allergy Flashcards

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1
Q

usual progression of atopic diseases age wise

A

eczema (<12months) > asthma > allergic rhinitis

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2
Q

distinguish between the different types of hypersensitvity

A

type 1 = IgE = allergy (seconds if previously exposed / delayed 2-12h)

type 2 = Ab dependent cytotoxic (mins-hours)
- antigen attaches to a self-cell > IgM/G/A complexes with Ag> complement system (chemotaxins/MAC/opsonised)

type 3 = immune complex (1-3weeks after exposure)
- Ag-Ab complex deposits in walls

type 4 = T cell mediated (delayed; 2-7 days)
- APC display antigen to T cell > destruction from CD8 and macros

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3
Q

main diff between type 2 and 3 hypersensitivity reaction

A

type II: Ag is bound to cell surface, then Ab binds to that. complement is activated in small amoumts
type III: Ag is soluble i.e. just floating, and Ab binds so it forms a complex. complement is activated in large amounts, so complement can be used to track disease progression

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4
Q

examples of each type of hypersensitivity reaction

A

type 1 = anaphylaxis, urticaria, atopy
type 2 = goodpasture’s, AIHA, myasthenia gravis, graves
type 3 = SLE, GN, HSP, serum-sickness e.g. 2nd cefaclor
type 4 = T1DM, mantoux test, contact dermatitis, SJS

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5
Q

small vs large immune complex: which is more immunogenic

A

the larger the complex, the more immunogenic it is

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6
Q

GVHD is what kind of hypersensitivity reaction

A

type IV

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7
Q

heritability of atopy if one vs both parents have atopy

A

one parent - 25% risk

both parents - 50-75%

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8
Q

describe process of type I hypersensitivity

A

sensitisation phase: antigen + APC presented to naive T cell > Th2 cell –> makes IL-4 to IgM class switch to IgE, IL-5 to stimulate eosinophils

so, with second exposure: Ag binds to IgE (that are already on mast cells_–> cross-linking of IgE on mast cell > degranulation e.g. histamine, tryptase

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9
Q

why are first gen anti-histamines so sedating?

A

lipophilic and cross BBB

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10
Q

allergen immunotherapy - allowed in which age group

A

5 or above only

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11
Q

normal level of eosinophils

A

3-10% total WCC

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12
Q

some differentials for eosinophilia

A 
allergy 
ABPA 
gi - esoinophilic GI, IBD
helminths 
neoplastic
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13
Q

some differentials for high IgE total

A 
atopy 
helminths 
ABPA 
Wiskott Aldrich
hyper IgE syndrome
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14
Q

how do we conduct the SPT test and interpret the result

A

no oral anti-histamines 4-5 days prior
allergen pricked into skin (back&raquo_space;> arm)
read after 15min
positive: >3mm above control. size of wheal says how likely a reaction will occur NOT how severe the reaction will be

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15
Q

SPT vs patch test

A

SPT for allergy/IgE mediated

patch test - contact dermatitis and type 4 reaction… not allergy!

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16
Q

when to use intra-dermal testing over SPT?

A

higher risk of anaphylaxis, so only for high yield:

  • venom allergy
  • immediate allergy to drugs (esp. penicillin) or some vaccines
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17
Q

contra-indications for SPT

A 
diffuse derm problem (skin should be intact) 
severe dermatographism (obvs) 
unable to cease anti-histamines

relative CI:

  • bad asthma
  • beta-blockers
  • recent anaphylaxis
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18
Q

serum allergen specific IgE test measures what?

A

detects free antigen-specific IgE in serum

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19
Q

SPT vs ssIGE - pros and cons

A 
SPT: 
quick, multiple allergens tested at once
better range, inc. fruits/vegs 
but can't do it if - recent anaphylaxis, broken skin, anti-histamines
positive = 3mm+

ssIGE:
more standardised and can do in IgE-problem people
but slower, range of allergens not as big (no fruit/veg)
false positive with high total IgE
positive = >0.35 KuA/L

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20
Q

specificity vs sensitivity

  • what is the difference
  • SPT
A
  • sensitivity: identifies most who have the condition
  • specificity: identifies most who don’t have the condition

SPT: high sensitivity, low specificity

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21
Q

most common cause of IgE food allergy vs anaphylaxis

A

IgE food allergy = milk

anaphylaxis = nut

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22
Q

risk factors for fatal anaphylaxis

A

a. Adolescence
b. Nut and shellfish allergy, drugs, insect stings
c. Poorly controlled asthma
d. Delays to administration of adrenaline or emergency services
e. pre-existing cardiac/resp conditions

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23
Q

Mx for anaphylaxis

A

remove allergen if present
DO NOT let them stand/walk, supine only
IM Adr 10mcg/kg or 0.01ml/kg of 1:1000 every 5 mins

consider: Adr infusion, O2, fluid boluses, salbutamol, anti-histamines
observe for at least 4h

LT:
update medical record, refer to allergy/paed, confirm with SPT/ssIgE, action plan, epipen script

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24
Q

time frame of anaphylaxis

A

30min-4h

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25
dx of anaphylaxis made by...?
skin + one or more system typical of anaphylaxis OR Hypotension, bronchospasm or upper airway obstruction where anaphylaxis is possible
26
risk factors for biphasic anaphylaxis reaction
>1 dose adrenaline and/or need for IV fluids
27
how does adrenaline work in anaphylaxis?
Alpha-1 receptor: o Vasoconstriction + increased BP o Reduces mucosal edema Beta-2 receptor: o Broncho dilatation o Reduces mediator release Beta-1 receptor: o Increases HR o Increases cardiac contraction force
28
doses of epipen
7.5 - 20 kg = EpiPen Jnr® or Anapen® (150 microgram) | >20 kg = EpiPen® or Anapen® (300 microgram)
29
anaphylactoid reaction: what? example?
- Occurs due to direct mast cell activation eg. red man syndrome / contrast - Ie. Non-IgE mediated activation of mast cells/basophils
30
three 'allergic' exam findings to look out for in atopy
1. Allergic ‘salute’ – line from rubbing nose 2. Allergic ‘gape’ – mouth open breathing 3. Allergic ‘shiners’ – dark circles under eyes
31
most common cause of seasonal allergic rhinitis
grass pollens most common
32
types of Rx for allergic rhinitis
1. IN steroids 1st line: 2-4 weeks until effect reached, continue for 3-6mo. - for sneezing/eye symptoms 2. anti-histamine: if itch/sneeze - not for nasal congestion 3. nasal irrigation decongestant not recommended
33
peri-oral dermatitis vs eczema
peri-oral dermatitis: zone of sparing, variant of rosacea, rebound from topical steroids peri-oral eczema: continuous with lips
34
genetics of atopic dermatitis - two mutations to know
50% severe AD have filaggrin mutation - structural epidermal protein Spink 5 – protease inhibit defect (Netherton's!)
35
factors influencing atopic dermatitis
``` genetics - esp defective barrier irritants - heats, abrasion, dryness airborne - mites infection food - 40% co-existing food allergy ```
36
types of steroids for eczema
Face a. 1% hydrocortisone E.g. DermAid, Sigmacort, Cortic b. Pimecrolimus – E.g. Elidel – for moderate facial eczema Trunk and limbs – avoid face + genitals a. Methylprednisolone 0.1% - E.g. Advantan fatty ointment b. Mometasone furoate 0.1% - E.g. elocon
37
pimecrolimus AE
burning irritation skin infection slightly increased rare - desquamation
38
pimecrolimus MOA
calcineurin inhibitor
39
how much steroid could you use for eczema?
1 tube of potent steroids/week on 6 month old is safe
40
troubleshooting if no response to your eczema management
``` ECxEMA: Existing Dx correct? Co-existent disease? infection, immune deficiency Environment Medication adequate Allergy/intolerance ```
41
types of reactions to insect stings
1. local: 1-5cm swelling within mins. remove stinger, cold compress 2. large local: swelling peaks 48h, lasts up to a week, 10cm. conservative, anti-HA, pred 3. Generalised cutaneous: urticaria, angioedema, pruritus (systemic non-life threatening) 4. anaphylaxis: as soon as there is vom/abdo pain = anaphylaxis!! 5. Serum sickness
42
risk factors for insect stings
a. Elevated tryptase b. Absence of cutaneous signs c. Latency < 5 minutes d. Age e. Honey bee venom f. Concurrent beta blocker/ ACE inhibitor use
43
Risk of anaphylaxis for those who experienced a large local reaction to an insect sting? generalised cutaneous?
LLR: 5-10% only, so no VIT indicated | generalised cutaneous: 10%
44
who should get venom immunotherapy?
generalised cutaneous reaction >17yo and SPT+ (risk 20%) | anaphylaxis (more evidence if SPT+ or ssIgE+) (risk 40%)
45
which kinds of conjunctivitis can cause eye damage? which can't?
``` Allergic conjunctivitis can't Vernal keratoconjunctivitis (Atopic conjunctivitis (atopic adolescent), Giant papillary conjunctivitis (FB) can ```
46
acute vs chronic urticaria timeline
acute <6 weeks | chronic > 6 weeks (persistent/recurrent) - kinin mediated
47
angioedema involving the throat, tongue or lips, WITHOUT urticaria should prompt consideration for ...?
can be due to allergy, but need to consider: | drug-induced angioedema (eg. seen with ACE), hereditary angioedema, or acquired C1 inhibitor deficiency
48
two important ddx for acute (just) urticaria
EM | urticaria vasculitis e.g. HSP (probably more unwell)
49
causes of chronic urticaria
NA PRIDE neoplastic angioedema: C1, ACEI, acquired physical: cold, pressure, heat (30%) rhem: SLE, JIA idiopathic: some relationship with anti-IgE (70% idiopathic) drug: ACE endo: thyroid!!
50
type I vs type II vs type III HAE and C4/C1 results
``` type I = C1 inh def - C4 low, C1 low, C1 function low type II = C1 inh dysfunction - C4 low, C1 normal, C1 function low type III = Hereditary angioedema with normal C1 - all normal ```
51
which molecule is directly responsible for the oedema in HAEt
bradykinin
52
what kind of attacks can you get with HAE?
1. cutaneous: usually hand/foot 2. GI: colic, N/V, diarrhoea 3. laryngeal/pharyngeal: usually starts with lump/tight throat. can kill.
53
triggers for HAE attack
i. Physical triggers ii. Medication = estrogen containing, tamoxifen, ACE-I iii. Hormonal change in women
54
timing of HAE attacks
- 40% have first attack by age 5 years - Repeated attacks in pre-adolescent children uncommon - Attack frequency increases in puberty - Diagnosis usually made in 2nd-3rd decade
55
test to differentiate HAE type I/II vs Acquired C1 esterase inhibitor deficiency
C1q normal in HAE type I/II, low in acquired
56
Tx of HAE attack
Does NOT respond to adrenaline, antihistamines or glucocorticoids severe: C1 inhibitor, icatibant (BK antag), ecallantide (kallikrein inhib) mild: tranexamic (partial BK inhib), danazol (inc hepatic production of C1 inhib)
57
serum sickness vs serum sickness like
both: fever, rash, arthralgia Serum sickness: 1-2 weeks after first exposure, low complement Serum sickness-like reaction (SSLRs): 5-10 days after, normal complement
58
SSLR most likely with what Rx? SS?
SS: anti-venom, ritux! SSLR: cefaclor - 15x more likely than other drugs in children
59
serum sickness - pathogenesis
type III hypersensitivity - Ig against Ab in serum: immune complex deposit in basement membrane of many organs > complement > neutrophils > inflammation
60
serum sickness: clinical features
1-2 weeks after initial exposure, ~24h after second ***fever, rash (flexures first, then generalised), polyarthralgia *** also itch, lymphadenopathy, proteinuria Low C3 + C4 (nadir day 10) + total haemolytic complement (CH50) proteinuria
61
DDx of SS/SSLRs
1. EM 2. SJS 3. KD 4. RF 5. JIA
62
differentiate between IgE, mixed and non-IgE mediated food allergy: timing, examples, triggers
IgE-mediated: immediate onset <60min, allergy/anaphylaxis - uncommon to have cow's milk/soy trigger (5%), usually nuts mixed: 1-48h, atopic dermatitis, eos oesophagitis non-IgE: 1-48h, FPIES, non-IgE cow's milk allergy - uncommon to be nut trigger, usually cow's milk/soy 50%
63
FPIES - key features
- usually <2yo (1 in 7000)- repetitive profuse vomiting 1-4h post ingestion +/- diarrhoea / hypotension - no skin manifestations - often misdiagnosed as gastro - usually formula fed
64
FPIES: key triggers
* * cow's milk/soy ** * *rice** * *oats**
65
lab findings FPIES
- hypoalbuminaemia - methaemoglobinaemia in 1/3 cases! - metabolic acidosis - neutrophilia - faecal blood
66
FPIES and atopy relationship
30% FPIES will develop atopy
67
what do you do to retest a FPIES kid?
1. repeat SPT prior to challenge - could have had IgE transformation 2. FPIES is only non-IgE mediated FA needing hospital challenge
68
risk factors for IgE mediated food allergy
``` PHx atopy FHx atopy other IgE food allergy 2x asian parents, kid born here severe eczema ```
69
food allergy affects how many Aus/NZ infants?
10%!!
70
which food allergies are more likely to persist into adulthood
nuts and seafood – 75% persist
71
nuts and cross reactivity - more likely to have reaction with which nut groups
cashew + hazelnut almond + hazelnut walnut + pecan
72
pollen-associated allergy syndrome: key features
IgE mediated older children with birch/ragweed allergic rhinitis immediate symptoms with raw fruit/vegetable (cross-reactivity) usually just tingling, pruritus, angioedema at oropharynx
73
usual age at onset of allergy: - egg/milk - peanuts/tree nuts - wheat/soybean - fish - kiwi
- egg/milk: 0-1yo - peanuts/tree nuts: 1-2yo - wheat/soybean: 6mo-24mo - fish: late childhood/adulthood - kiwi: any age (other fruits are later)
74
allergic proctocolitis (FPIAP): key features for exams
- inflammation of distal colon - rectal bleeding only +/- mild diarrhoea (rule out outher causes of rectal bleeding) - no bad features e.g. FTT, vomiting, fever - cow's milk 75%, so usually formula fed - present 2-8 weeks old, resolve by 12mo after removal of trigger
75
food protein enteropathy: key features
- same pathology as coeliac - T cell activation - cow's milk most common - chronic non-bloody diarrhoea with other enteropaty issues - present in first 12mo, resolves 2-3yo - avoid allergy (EHF if no FTT, AA formula if FTT)
76
most common trigger for eosinophilic oesophagitis
cow's milk
77
what kind of systems can be impacted in a IgE cow's milk allergy
GI: v/d derm: urticaria, angioedema, dermatitis resp: cough, asthma, OM, rhinitis anaphylaxis
78
which formulas are recommended and not recommended in IgE mediated cow's milk allergy? non-IgE?
not anaphylactic: 1st line - soy or novalac rice formula 2nd line - extensively hydrolysed 3rd - AAF Anaphylactic: continue breastfeeding (exclude CMP) 1st line - AAF Not recommended: - partially hydrolysed (cross reactivity 60%) - sheep / goat (75%) non-IgE: - exclude CMP breastfeed - 1st line: extensively hydrolysed - 2nd line: AAF
79
when cow's milk allergy resolves?
80% resolve by 3-5yo
80
vernal keratoconjunctivitis - key features
horner dots and trantus dots (those gross spots) Giant papillae upper tarsal plate – cobblestoning ropey discharge corneal shield ulcer - warrants urgent ophthal review
81
chronic urticaria vs urticarial vasculitis
urticarial vasculitis: lesions last longer (up to a week) - chronic urticaria usually don't last past 24h often residual bruising more likely to have arthralgia / systemic problems
82
EM vs urticaria multiforme vs pityriasis rosea
``` EM: a/w HSV, 10-14 days after Target lesions Not pruritic! Typically acral distribution, more hands/feet ``` Urticaria multiforme: Annular urticaria, doesn’t leave bruising like EM often does Often mistaken for EM Should resolve within 24h Pityriasis rosea: Self-limiting rash within 6-8weeks, common adolescents Herald patch before spreading Slightly raised, oval, salmon pink with peripheral scale no clear cause
83
risk factors for allergic rhinitis
FHx, male birth during pollen season, firstborn early abx, maternal smoking in first year, exposure to indoor allergens very high IgE before 6yo
84
test for penicillin allergy if low vs high risk
low = OPC with penicillin/amoxicillin high (=rash in last year / angioedema/systemic)= SPT not tryptase or ssIgE

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