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MD2 Rheumatology > Allergy Diagnosis and Treatment > Flashcards

Allergy Diagnosis and Treatment Flashcards

1
Q

What is allergy?

A

An inappropriate or harmful immune response to foreign substances that are otherwise not harmful to the body, mediated largely (though not exclusively) by IgE

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2
Q

What are allergens?

A

Generally proteins that elicit an IgE response in allergic individuals

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3
Q

Give some examples of allergens

A

Allergic rhinitis and asthma: grass pollens, dust mite proteins, animal proteins (e.g. cat dander), moulds
Food allergy: peanuts, tree-nuts, eggs, milk, fish, crustaceans

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4
Q

How is a “clinical allergy” defined?

A

Symptoms + demonstration of specific IgE response (either by skin test or RAST)

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5
Q

RAST

A

Radioallergosorbent test

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6
Q

What are the symptoms of allergy?

A

Dependent on route of exposure
Inhaled: rhinitis, asthma
Skin: acute contact urticaria
Mouth: oral allergy syndrome (local swelling only), cramping/vomiting/diarrhoea, can lead to anaphylaxis

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7
Q

When do allergic symptoms come on?

A

Classically immediately related to allergen exposure (within 1 hour, usually secs/mins)

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8
Q

What patient demographic is more likely to have an atypical allergy presentation?

A

Young children

Elderly

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9
Q

List 3 types of diagnostic tests for allergy

A

Skin prick tests (SPTs)
Serologic assays (RAST, EAST, CAP-FEIA)
Challenge testing

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10
Q

What is the criteria for a positive SPT?

A

≥3mm wheal

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11
Q

List 3 advantages of the SPT

A

Highly sensitive (usually >99%)
In vivo exposure to allergen
Convenient and results obtained within 20 mins

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12
Q

List 3 disadvantages of SPT

A

Potential (small) for anaphylaxis (mainly with SPT for latex, penicillin, venom)
May lack specificity either because of sensitised but asymptomatic individuals or through irritant false positive reactions (seen particularly with foods)
Usually require specialist clinic

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13
Q

What do serologic assays measure?

A

Allergen-specific IgE

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14
Q

What is RAST?

A

Radio-allergosorbent test

Now redundant but commonly used nomenclature for other serologic tests (i.e. CAP-FEIA, EAST, ELISA)

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15
Q

CAP-FEIA

A

Fluro-enzymatic immunoassay

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16
Q

EAST

A

Enzyme allergosorbent test

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17
Q

ELISA

A

Enzyme-linked immunosorbent assay

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18
Q

Describe the principles of in vitro IgE assays

A

Allergen and serum added to dish, allergen specific IgE will bind allergen
Wash out, only bound IgE remains (or only bound anti-human IgE fluoresces)
Fluorochrome-labelled mouse anti-human IgE added, binds the allergen-specific IgE
Light detector used to get a quantitative readout

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19
Q

List 4 advantages of in vitro assays

A

Availability (GPs can do)
Safety
Specific particularly at a high level (class II or above; around 80-90% specific)
Standardised

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20
Q

List 3 disadvantages of in vitro assays

A

Interpretation dependent on pre-test probability (FP rate usually 5-10%)
May get FPs with elevated total IgE (e.g. eczema)
Medicare only subsidises 4 tests at a time

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21
Q

What is the gold standard for allergy diagnosis?

A

Challenge tests

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22
Q

Where are challenge tests usually performed?

A

Only in specialised allergy clinics

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23
Q

When are challenge tests usually performed?

A

Potentially risky, so usually used when RAST and SPT are negative or discordant, but there is a good clinical story

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24
Q

What % of Australian children report wheeze?

A

~20%

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25
Q

Describe the role of genetics and environment in the rise of childhood food allergy

A

Genetic factors, FHx of atopy, parental age and maternal exposure (e.g. to Abx, probiotics, vitamin supplements, smoking, diet and food allergens) and fetal epigenetic modification all contribute to food allergy “programming” pre- and perinatally
Environmental factors including initiation of breast-feeding, exposure to sunlight (vit D) and exposure to pollutants, as well as infant dietary factors and factors associated with the “hygiene hypothesis” contribute to onset of food allergy postnatally

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26
Q

Describe 5 factors associated with the “hygiene hypothesis”

A

Increased sanitation, immunisation, Abx use
Decreased infections
Exposure to farm animals, domestic pets and endotoxins
Decreased microbial load in food and water
Presence of siblings

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27
Q

What symptoms are seen in an acute vs chronic allergic reaction? What mediates these responses?

A

Acute (related to mast cell activation): wheeze, urticaria, sneezing, rhinorrhoea, conjunctivitis
Chronic (related to mast cell activation, neuropeptide release from TH2 cells and eosinophils): further wheeze, sustained blockage of the nose, eczema

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28
Q

List 2 allergen-specific treatments for allergy

A

Allergen avoidance

Allergen specific immunotherapy

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29
Q

List 5 non-specific medical therapies for allergy

A 
Antihistamines
Corticosteroids
Adrenaline
Leukotriene antagonists
Anti-IgE Abs (e.g. omalizumab)
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30
Q

Describe the typical course of subcutaneous allergen immunotherapy

A

Increasing doses of allergen extract given subcutaneously initially weekly and then monthly for 3-5 years

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31
Q

What allergy therapy is the only one to provide prolonged improvement or cure?

A

Immunotherapy

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32
Q

What is the major risk in injection immunotherapy?

A

Small but important risk of anaphylaxis with SC immunotherapy (reported death rate from US data 1 in 2,000,000 injections)

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33
Q

Who should provide injection immunotherapy?

A

Generally recommended to be initiated and/or supervised by an allergy specialist

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34
Q

What is the main indication for SC injection immunotherapy?

A 
Venom allergy (e.g. bee, European wasp)
Allergic rhinitis +/- mild, well controlled allergic asthma (stable symptoms and FEV1 >70% predicted)
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35
Q

Why must allergic asthma be mild and well controlled for injection immunotherapy to be considered as a treatment option?

A

Level 1 evidence that it works in allergic rhinitis and allergic asthma, but risk of adverse reactions is higher in asthmatics (must have STABLE symptoms and FEV1 >70% predicted)

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36
Q

Name one contraindication to allergy immunotherapy

A

Co-existent B blockade

37
Q

Describe the proposed mechanism of allergy immunotherapy

A

Allergen presented by APC to Th0
Th0 releases IL-4, stimulates Th2 to release IL-4 and IL-5 which results in the production of IgE by activated B cells (the ALLERGIC response)
Following immunotherapy, Th0 releases IL-12 when stimulated by APCs; IL-12 induces release of IFN-y from Th1 cells, which acts on B cells to stimulate production of IgG (the NON-ALLERGIC response)

38
Q

Describe some practical aspects of injection allergen immunotherapy

A

Always wait at least 30 mins in surgery after injection
Usually antihistamine prior is advisable
Always check the dose and extract
Adrenaline and O2 must be available for treatment of anaphylaxis if it occurs

39
Q

Which is more effective: sublingual or subcutaneous immunotherapy?

A

Appear to be equally effective

40
Q

What are the advantages of sublingual immunotherapy?

A

Minimal risk of anaphylaxis (no deaths reported with use)

Can be administered at home by patient

41
Q

What is the limitation of sublingual immunotherapy?

A

Extracts are more expensive

42
Q

Describe the method of sublingual immunotherapy

A

Dose of allergen extract self-administered daily by patient sublingually, held for 2 mins under the tongue and then swallowed

43
Q

Define anaphylaxis

A

No clear consensus on definition; “serious allergic reaction that may cause death”
Generally implies IgE-mediated (as opposed to anaphylactoid which is non-IgE mediated)
Is a generalised serious IgE-mediated allergic reaction which usually involves CV (hypotension) and/or respiratory tract (asthma/laryngeal oedema)
Atypical presentations (e.g. without rash) are not uncommon, particularly in the very old or very young

44
Q

Describe the proposed mechanism of anaphylaxis

A

Massive mediator release primarily from mast cells and circulating basophils
Vasodilation, fluid extravasation, bronchial smooth muscle contraction and mucosal oedema
Death due to shock and/or hypoxaemia

45
Q

Describe some “mild” anaphylactic symptoms

A 
Pruritis (particularly in hand and groin)
Urticaria
Flushing
Vomiting
Diarrhoea
46
Q

Describe some moderate and severe anaphylactic symptoms

A

Angioedema (particularly of lips, tongue and larynx)
Wheeze, asthma
Hypotension
LOC

47
Q

Describe the death rate from anaphylaxis

A

One death per 3 million population per annum

48
Q

What are the main causes of fatal anaphylaxis?

A

Food allergy (especially nuts)
Insect venom
Drugs

49
Q

What is the risk of death per nut allergic person per year?

A

2.3/100,000 risk of death per nut allergic person per year

50
Q

What medications are most commonly associated with fatal anaphylaxis?

A

Anaesthetics
Abx
Contrast

51
Q

What foods are commonly associated with allergy?

A 
Peanuts
Tree-nuts
Eggs
Milk
Fish
Crustaceans
52
Q

Does anaphylaxis ever remit?

A

Anaphylaxis is often life-long, except for egg and milk allergy which frequently remit (cf peanut, only ~30% of children remit)

53
Q

How is food allergy causing anaphylaxis managed?

A

Avoidance

Mx of inadvertent exposure (adrenaline)

54
Q

List 5 risk factors for fatal food-related anaphylaxis

A 
Associated asthma
Lack of self-injectable adrenaline (Epipen, Anapen)
Young adults
Alcohol
Extreme sensitivity
55
Q

List the 3 main insect venom allergies

A

Bee
European wasp
Jumper ants

56
Q

How do bee deposit their venom? How much venom is deposited per sting?

A

Via a barbed modified ovipositor which is left in the skin (sting only once)
Each sting deposits 35-200 mcg of venom

57
Q

How do European wasps deposit their venom? How much venom is deposited per sting? When are stings most commonly acquired?

A

Can sting multiple times
10-20 mcg of venom per sting
Nests in concealed locations (underground, logs, wall cavities); single queen starts a new colony each spring, and wasps become most aggressive towards the end of summer

58
Q

Where are jumper ants most prevalent? How can jumper ant venom allergy be treated?

A

Unique to Australia; prevalent in Tas, Northern suburbs of Melbourne and Bellarine Peninsula
Immunotherapy effective but availability currently limited in Victora

59
Q

What is the efficacy of immunotherapy for insect venom allergy?

A

Efficacy 95% with vespid, 75-80% with bee venom

60
Q

What protocols are available for immunotherapy for insect venom allergy?

A

Standard
Cluster “rush”
“Ultrarush”

61
Q

How long should immunotherapy protocols last for insect venom allergy?

A

5 years

62
Q

What precautions should be taken with immunotherapy for insect venom allergy?

A

Epipen should be available until negative sting reaction is achieved

63
Q

Mr SM, 38 year old postie, stung at work by a bee (confirmed as left a stinger - no other insects do)
Experienced generalised urticaria, breathlessness
Ambulance called
Administered IM adrenaline 0.5mg, hydrocortisone and phenergan en route to ED
Dx?
Ix?
Mx?

A

Dx: honeybee venom allergy
Ix: RAST (was strongly positive, Class 3 out of 4, to honeybee)
Mx: desensitisation to honey bee recommended and Epipen and anaphylaxis plan provided

64
Q

In what populations is latex allergy typically seen?

A

Healthcare workers

Spina bifida patients

65
Q

What symptoms are commonly seen in latex allergy?

A

Irritant or contact dermatitis

Can be associated with urticaria, rhinitis, asthma and even anaphylaxis

66
Q

Why is latex allergy less of a problem now?

A

Has decreased in importance due to reduction in protein content of latex gloves

67
Q

What other things are cross reactive with latex allergens?

A

Banana
Avocado
Kiwi fruit

68
Q

What Abx are the main causes of allergy?

A

Penicillins

Cephalosporins

69
Q

What is the mechanism of allergy to radiocontrast agents?

A

Anaphylactoid (non-IgE mediated)

70
Q

What anaesthetic agents are more strongly associated with allergy?

A

Muscle relaxants

71
Q

What medication is a common cause of serious anaphylaxis but is often not thought of as a “medicine” but patients?

A

NSAIDs

72
Q

Give an example of a natural medicine which is associated with allergy

A

Echinacea

73
Q

How is anaphylaxis diagnosed?

A

Clinical diagnosis; broad differential including CV and other disorders
RAST testing, skin prick testing (when safe) and measurement of mast cell tryptase may aid diagnosis

74
Q

What is mast cell tryptase and how is it associated with anaphylaxis?

A

An enzyme released during degranulation of mast cells

Peaks around 4-6 hours post-anaphylaxis

75
Q

Describe the current Australian guidelines for emergency management of anaphylaxis

A

Stop administration of causative agent (if relevant), assess reaction severity and treat accordingly: call for assistance, give adrenaline IM (lateral thigh, 0.1 mg/kg to max dose of 0.5 mg), set up IV access, lay patient flat (elevate legs if tolerated), give high flow O2 + airway/ventilation support if needed, if hypotensive also set up additional wide-bore IV access and give IV normal saline bolus 20 mL/kg over 1-2 min under pressure
If there is inadequate response, an immediate life-threatening situation, or deterioration: start an IV adrenaline infusion OR repeat IM adrenaline injection every 3-5 min, as needed

76
Q

Describe the principles of long-term allergy therapy

A

Avoidance
Education on action plan: recognise symptoms, when to seek help, adrenaline injection, antihistamine tablets, desensitisation if relevant
Medical alert bracelet
“Action plan” for anaphylaxis

77
Q

Describe the typical appearance of urticaria

A

Circumscribed, slightly elevated, intensely pruritic skin lesions
Initially erythematous but can develop central pallor as oedema develops in the dermis
Can occur anywhere including face and scalp
Individual lesions rarely last longer than 24 hours
No residual skin staining

78
Q

Describe the typical appearance and presentation of urticaria

A

Non-pruritic, less erythematous and less clearly defined swelling occurring in the deep dermis or subcutaneous tissues
Can occur anywhere under skin or mucous membranes but frequently involves face including eyelids, lips or tongue
Often associated with a burning sensation or pain
Can last for up to 3 days

79
Q

What is chronic urticaria and angioedema indicative of? How can it be distinguished from acute allergy-related urticaria and angioedema?

A

Commonly not due to allergy

Clue is in the Hx: recurring lesions with no obvious temporally related allergic trigger

80
Q

How is chronic urticaria and angioedema managed?

A

Antihistamines are mainstay of treatment

81
Q

In the case of chronic urticaria and angioedema, what other diagnoses must be excluded?

A

AI disease (e.g. SLE) and other rare diseases (e.g. hereditary angioedema) may need to be excluded (amongst other Ix) if symptoms are severe or persistent

82
Q

What allergens are typically associated with allergic rhinitis?

A 
Perennial (year round allergens) include dust mite, pets (principally cats) and moulds
Seasonal rhinitis (springtime hayfever) usually due to grass pollen
83
Q

How is allergic rhinitis managed?

A

Nasal corticosteroids and/or antihistamines

Allergen specific immunotherapy is useful if medical therapy is inadequate/not tolerated (level 1 evidence)

84
Q

Master AK, 10 year old boy
PHx: eczema since 6/12 old, asthma since 6 years old, rhinorrhoea and nasal obstruction since 8 years old
Eczema and rhinitis have worsened recently
Mother is concerned regarding food allergies
Further Qs?

A

More detail regarding Hx and severity of atopic disorders, particularly regarding severity and possible hospitalisation for asthma
Previous treatments and efficacy
Qs regarding allergen exposure (e.g. dust, moulds, pets, seasonal variation, foods)
FHx

85
Q

Master AK, 10 year old boy
PHx: eczema since 6/12 old, asthma since 6 years old, rhinorrhoea and nasal obstruction since 8 years old
Eczema and rhinitis have worsened recently
Mother is concerned regarding food allergies
O/E: widespread chronic eczema esp face, cheeks and eyelids, flexural areas of arms and legs and hands, swollen pale boggy nasal turbinates with reduced nasal airflow bilaterally (polyps not present), clear chest examination
Mx?

A

Allergen avoidance: no efficacy demonstrated for primary prevention, greater evidence for allergen avoidance in ESTABLISHED allergic disease
Allergy Dx can direct avoidance of SPECIFIC allergens only (e.g. animals, occupational, etc)
I.e. does not need to avoid potential food allergens unless there is a proven Hx of food allergy

86
Q

Mr UD, 61 year old cotton goods importer and non-smoker, developed severe SOB during springtime thunderstorm
PHx: asthma since childhood, springtime hayfever
Required intubation in ED for acute respiratory failure and transferred to ICU for mechanical ventilation
Commenced budesonide/eformoterol (Symbicort) inhaler and oral prednisolone
Extubated, mobilised, discharged after 1 week
At follow up he feels well and is on inhaled corticosteroids (Symbicort), intranasal steroids (Nasonex) but his lung function still shows severe airflow obstruction (FEV1 30%)
Dx?
Ix?
Mx?

A

Dx: acute exacerbation of asthma due to springtime allergy
Ix: RAST (results were strongly positive for grass pollen)
Mx: immunotherapy not appropriate as he has severe asthma and FEV1

87
Q

What is a negative RAST result?

A

Less than 0.35kU/L of specific IgE

88
Q

Describe the proposed mechanism of thunderstorm asthma

A

Whole pollen grains get swept up into cloud as storm matures
Moisture in the cloud fragments the pollen into smaller pieces
Dry, cold outflows carry pollen fragments to ground level, where people breathe them into their lungs

89
Q

What is the mainstay of acute anaphylaxis Mx?

A

IM adrenaline

MD2 Rheumatology (5 decks)

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