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immunology > allergy > Flashcards

allergy Flashcards

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
Q

dx of anaphylaxis made by…?

A

skin + one or more system typical of anaphylaxis
OR
Hypotension, bronchospasm or upper airway obstruction where anaphylaxis is possible

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26
Q

risk factors for biphasic anaphylaxis reaction

A

> 1 dose adrenaline and/or need for IV fluids

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27
Q

how does adrenaline work in anaphylaxis?

A

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

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28
Q

doses of epipen

A

7.5 - 20 kg = EpiPen Jnr® or Anapen® (150 microgram)

>20 kg = EpiPen® or Anapen® (300 microgram)

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29
Q

anaphylactoid reaction: what? example?

A
  • Occurs due to direct mast cell activation eg. red man syndrome / contrast
  • Ie. Non-IgE mediated activation of mast cells/basophils
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30
Q

three ‘allergic’ exam findings to look out for in atopy

A
  1. Allergic ‘salute’ – line from rubbing nose
  2. Allergic ‘gape’ – mouth open breathing
  3. Allergic ‘shiners’ – dark circles under eyes
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31
Q

most common cause of seasonal allergic rhinitis

A

grass pollens most common

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32
Q

types of Rx for allergic rhinitis

A
  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

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33
Q

peri-oral dermatitis vs eczema

A

peri-oral dermatitis: zone of sparing, variant of rosacea, rebound from topical steroids

peri-oral eczema: continuous with lips

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34
Q

genetics of atopic dermatitis - two mutations to know

A

50% severe AD have filaggrin mutation - structural epidermal protein
Spink 5 – protease inhibit defect (Netherton’s!)

35
Q

factors influencing atopic dermatitis

A 
genetics - esp defective barrier 
irritants - heats, abrasion, dryness 
airborne - mites 
infection 
food - 40% co-existing food allergy
36
Q

types of steroids for eczema

A

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
Q

pimecrolimus AE

A

burning
irritation
skin infection slightly increased
rare - desquamation

38
Q

pimecrolimus MOA

A

calcineurin inhibitor

39
Q

how much steroid could you use for eczema?

A

1 tube of potent steroids/week on 6 month old is safe

40
Q

troubleshooting if no response to your eczema management

A 
ECxEMA:
Existing Dx correct?
Co-existent disease? infection, immune deficiency 
Environment 
Medication adequate 
Allergy/intolerance
41
Q

types of reactions to insect stings

A
  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
Q

risk factors for insect stings

A

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
Q

Risk of anaphylaxis for those who experienced a large local reaction to an insect sting? generalised cutaneous?

A

LLR: 5-10% only, so no VIT indicated

generalised cutaneous: 10%

44
Q

who should get venom immunotherapy?

A

generalised cutaneous reaction >17yo and SPT+ (risk 20%)

anaphylaxis (more evidence if SPT+ or ssIgE+) (risk 40%)

45
Q

which kinds of conjunctivitis can cause eye damage? which can’t?

A 
Allergic conjunctivitis can't 
Vernal keratoconjunctivitis (Atopic conjunctivitis (atopic adolescent), Giant papillary conjunctivitis (FB) can
46
Q

acute vs chronic urticaria timeline

A

acute <6 weeks

chronic > 6 weeks (persistent/recurrent) - kinin mediated

47
Q

angioedema involving the throat, tongue or lips, WITHOUT urticaria should prompt consideration for …?

A

can be due to allergy, but need to consider:

drug-induced angioedema (eg. seen with ACE), hereditary angioedema, or acquired C1 inhibitor deficiency

48
Q

two important ddx for acute (just) urticaria

A

EM

urticaria vasculitis e.g. HSP (probably more unwell)

49
Q

causes of chronic urticaria

A

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
Q

type I vs type II vs type III HAE and C4/C1 results

A 
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
Q

which molecule is directly responsible for the oedema in HAEt

A

bradykinin

52
Q

what kind of attacks can you get with HAE?

A
  1. cutaneous: usually hand/foot
  2. GI: colic, N/V, diarrhoea
  3. laryngeal/pharyngeal: usually starts with lump/tight throat. can kill.
53
Q

triggers for HAE attack

A

i. Physical triggers
ii. Medication = estrogen containing, tamoxifen, ACE-I
iii. Hormonal change in women

54
Q

timing of HAE attacks

A
  • 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
Q

test to differentiate HAE type I/II vs Acquired C1 esterase inhibitor deficiency

A

C1q normal in HAE type I/II, low in acquired

56
Q

Tx of HAE attack

A

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
Q

serum sickness vs serum sickness like

A

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
Q

SSLR most likely with what Rx? SS?

A

SS: anti-venom, ritux!

SSLR: cefaclor - 15x more likely than other drugs in children

59
Q

serum sickness - pathogenesis

A

type III hypersensitivity - Ig against Ab in serum: immune complex deposit in basement membrane of many organs > complement > neutrophils > inflammation

60
Q

serum sickness: clinical features

A

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
Q

DDx of SS/SSLRs

A
  1. EM
  2. SJS
  3. KD
  4. RF
  5. JIA
62
Q

differentiate between IgE, mixed and non-IgE mediated food allergy: timing, examples, triggers

A

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
Q

FPIES - key features

A
  • 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
Q

FPIES: key triggers

A
    • cow’s milk/soy **
  • *rice**
  • *oats**
65
Q

lab findings FPIES

A
  • hypoalbuminaemia
  • methaemoglobinaemia in 1/3 cases!
  • metabolic acidosis
  • neutrophilia
  • faecal blood
66
Q

FPIES and atopy relationship

A

30% FPIES will develop atopy

67
Q

what do you do to retest a FPIES kid?

A
  1. repeat SPT prior to challenge - could have had IgE transformation
  2. FPIES is only non-IgE mediated FA needing hospital challenge
68
Q

risk factors for IgE mediated food allergy

A 
PHx atopy 
FHx atopy 
other IgE food allergy 
2x asian parents, kid born here 
severe eczema
69
Q

food allergy affects how many Aus/NZ infants?

A

10%!!

70
Q

which food allergies are more likely to persist into adulthood

A

nuts and seafood – 75% persist

71
Q

nuts and cross reactivity - more likely to have reaction with which nut groups

A

cashew + hazelnut
almond + hazelnut
walnut + pecan

72
Q

pollen-associated allergy syndrome: key features

A

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
Q

usual age at onset of allergy:

  • egg/milk
  • peanuts/tree nuts
  • wheat/soybean
  • fish
  • kiwi
A
  • 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
Q

allergic proctocolitis (FPIAP): key features for exams

A
  • 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
Q

food protein enteropathy: key features

A
  • 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
Q

most common trigger for eosinophilic oesophagitis

A

cow’s milk

77
Q

what kind of systems can be impacted in a IgE cow’s milk allergy

A

GI: v/d
derm: urticaria, angioedema, dermatitis
resp: cough, asthma, OM, rhinitis
anaphylaxis

78
Q

which formulas are recommended and not recommended in IgE mediated cow’s milk allergy? non-IgE?

A

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
Q

when cow’s milk allergy resolves?

A

80% resolve by 3-5yo

80
Q

vernal keratoconjunctivitis - key features

A

horner dots and trantus dots (those gross spots)
Giant papillae upper tarsal plate – cobblestoning
ropey discharge
corneal shield ulcer - warrants urgent ophthal review

81
Q

chronic urticaria vs urticarial vasculitis

A

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
Q

EM vs urticaria multiforme vs pityriasis rosea

A 
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
Q

risk factors for allergic rhinitis

A

FHx, male
birth during pollen season, firstborn
early abx, maternal smoking in first year, exposure to indoor allergens
very high IgE before 6yo

84
Q

test for penicillin allergy if low vs high risk

A

low = OPC with penicillin/amoxicillin
high (=rash in last year / angioedema/systemic)= SPT

not tryptase or ssIgE

immunology (3 decks)

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