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Flashcards in Allergy Deck (23)
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1
Q

What is meant by the term atopy?

A

Atopy is the tendency to produce an exaggerated IgE immune response to otherwise harmless environmental substances, while an allergic disease can be defined as the clinical manifestation of this inappropriate IgE immune response.

2
Q

What is the pathophysiology of allergic disease?

A

The immune system does not normally respond to the many environmental substances to which it is exposed on a daily basis. In allergic individuals, however, an initial exposure to a normally harmless exogenous substance (known as an allergen) triggers the production of specific IgE antibodies by activated B cells. These bind to high-affinity IgE receptors on the surface of mast cells, a step that is not itself associated with clinical sequelae. However, re-exposure to the allergen binds to and cross-links membrane-bound IgE, which activates the mast cells, releasing a variety of vasoactive mediators. This type I hypersensitivity reaction forms the basis of an allergic reaction, which can range from sneezing and rhinorrhoea to anaphylaxis.

In some individuals, the early phase response is followed by persistent activation of mast cells, manifest by ongoing swelling and local inflammation. This is known as the late phase reaction and is mediated by mast cell metabolites, basophils, eosinophils and macrophages. Long-standing or recurrent allergic inflammation may give rise to a chronic inflammatory response characterised by a complex infiltrate of macrophages, eosinophils and T lymphocytes, in addition to mast cells and basophils. Once this has been established, inhibition of mast cell mediators with antihistamines is clinically ineffective in isolation.

3
Q

What are the clinical features of allergic rhinitis?

A

Rhinorrhoea, nasal blockage, postnasal drip, excessive sneezing, nasal itch
Loss of smell and taste
Nasal polyps complicate rhinitis in 2% of cases
Allergic conjunctivitis (papillae)
Nasal polyps are more common in young males with asthma, aspirin intolerance and sinusitis (Samter’s triad)

4
Q

What is the pathophysiology of allergic rhinitis?

A

IgE antibodies bound to mast cells are cross-linked by allergen, leading to the degranulation of mast cells.

Mast cell mediators are chemotactic, especially for eosinophils, which release further vasoactive and toxic mediators.

The response is regulated by T cells of the Th2 subtype.

5
Q

What causes allergic rhinitis?

A

Seasonal allergens: grass, tree, weed pollens

Perennial allergens: animal danders including house dust mite, cat, moulds

6
Q

How is allergic rhinitis managed?

A

Identify offending allergens by skin prick testing or RAST.
Avoid offending allergens where possible
Intranasal corticosteroids
Oral antihistamines
Specific immunotherapy in selected cases

7
Q

What drugs cause type I hypersensitivity reactions?

A

Beta lactams

Antibiotics

8
Q

What drugs cause anaphylactoid reactions?

A

Anaphylactoid = non IgE dependent mast cell degranulation

Aspirin, NSAIDs, radio-contrast mediators

9
Q

What drugs cause type II hypersensitivity reactions?

A

These are rare and are antibody-dependent.

Penicillin induced haemolytic anaemia is probably the best example

10
Q

What drugs cause type III hypersensitivity reactions?

A

These are immune complex-mediated, serum sickness.

E.g. antibiotics, propylthiouracil

11
Q

What drugs cause a type IV hypersensitivity reaction?

A

These are delayed type and include topical preparations

12
Q

How are drug allergies managed?

A

Avoidance is desirable in all cases of known drug allergy.
Rapid desensitization is possible in a hospital setting, when a drug is urgently needed and there is no viable alternative.

13
Q

What is birch oral allergy syndrome?

A

This syndrome is characterised by the combination of birch pollen hay fever and local oral symptoms, including itch and angioedema, after contact with certain raw fruits, raw vegetables and nuts. Cooked fruits and vegetables are tolerated without difficulty. It is due to shared or cross-reactive allergens that are destroyed by cooking or digestion, and can be confirmed by skin prick testing using fresh fruit. Severe allergic reactions are unusual.

14
Q

How are suspected allergies diagnosed?

A

When assessing a patient with a complaint of allergy, it is important to identify what the patient means by the term, as up to 20% of the UK population describe themselves as having a food allergy; in fact, less than 1% have true allergy, as defined by an IgE-mediated hypersensitivity reaction confirmed on double-blind challenge.

The nature of the symptoms should be established and specific triggers identified, along with the predictability of a reaction, and the time lag between exposure to a potential allergen and onset of symptoms. An allergic reaction usually occurs within minutes of exposure and provokes predictable, reproducible symptoms such as angioedema, urticaria and wheezing.

Specific enquiry should be made about other allergic symptoms, past and present, and about a family history of allergic disease. Potential allergens in the home and workplace should be identified. A detailed drug history should always be taken, including details of adherence to medication, possible adverse effects and the use of over-the-counter or complementary therapies.

15
Q

Investigating suspected allergic disease?

A

1) Skin prick testing
2) Specific IgE tests
3) Supervised exposure to allergen
4) Mast cell tryptase
5) Serum total IgE
6) Eosinophilia

16
Q

What is skin prick testing?

A

This is the “gold standard” of allergy testing.
A droplet of diluted standardised allergen solution is placed on the forearm and the skin is superficially punctured through the droplet with a sterile lancet. After 15 minutes, a positive response is indicated by a local weak and flare response >2mm larger than the negative control.

17
Q

What are the main advantages and disadvantages of skin prick testing in allergy?

A

The major advantage is that the patient can see the results which improves compliance with avoidance measures.

Disadvantages include the remote risk of severe allergic reaction, so resuscitation measures need to be available. Results are unreliable in patients with extensive skin disease. Antihistamines inhibit the magnitude of the response and should be discontinued for at least 4 days before testing; steroids do NOT influence the results.

18
Q

What are specific IgE tests?

A

This is an alternative to skin prick testing and is the quantitation of IgE directed against the suspected allergen.

The sensitivity and specificity of specific IgE tests (previously known as radioallergosorbent tests or RAST) are lower than skin prick tests, hence why they are second line.

IgE testing may be very useful if skin testing is inappropriate; for example, in patients taking antihistamines or those who have severe skin disease or dermatographism.

19
Q

What is a challenge test?

A

This is a supervised exposure to an allergen. Allergen challenges are usually performed in specialist centres, and include bronchial provocation testing, nasal challenge and food challenge.

These are particularly useful in the investigation of occupational asthma or food allergy.

20
Q

When is mast cell tryptase measured?

A

After a systemic allergic reaction, the circulating level of mast cell mediators increases dramatically. Tryptase is the most stable of these and serum levels peak at 1-2 hours, remaining elevated for 24 hours.

Measuring serum mast cell tryptase is extremely useful in investigating a possible anaphylactic event. Ideally measurement should be made at the time of the reaction, and then 3 and 24 hours later.

21
Q

Are total serum IgE levels and eosinophil levels used in the assessment of suspected allergy?

A

Peripheral blood eosinophilia is common in atopic individuals. An eosinophil count >20% or an absolute count >1.5 should initiate a search for a non atopic cause.

Atopy is the most common cause of elevated total IgE in developed countries. But there are many other causes including parasite and helminth infections, lymphoma, drug reactions and Churg-Strauss vasculitis. Significant allergic disease can also occur without eosinophilia. So total IgE quantitation is not usually indicated in the routine investigation of allergic disease.

22
Q

How is allergic disease managed?

A

1) Avoidance of allergen
2) Antihistamines
3) Corticosteroids
4) Sodium cromoglicate (mast cell membrane stabiliser)
5) Antigen-specific immunotherapy
6) Omalizumab (monoclonal antibody against IgE)
7) Preloaded self-injectable adrenaline

23
Q

What is antigen-specific immunotherapy?

A

This involves the sequential administration of escalating amounts of dilute allergen over a prolonged period of time.

Its mechanism of action is unknown, but it is highly effective in the prevention of insect venom anaphylaxis, and allergic rhinitis secondary to grass pollen.

The traditional route of administration is via subcutaneous injections, which carry a risk of anaphylaxis and should only be performed in specialist centres.