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Paeds SAQsallergy-and-immunology

Paeds SAQs · allergy-and-immunology

Allergic rhinitis and rhinoconjunctivitis — short-answer questions

Two short-answer questions on the ARIA classification, IgE pathophysiology and stepwise management of allergic rhinitis in a school-aged child.

20 marks30 min3 min readVerification in progress

Target exams

RACP DWEMRCPCH Theory
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Study tools

Target exams

RACP DWEMRCPCH Theory
Prompt
An 8-year-old boy presents each spring with paroxysms of sneezing, a clear runny nose, itchy eyes and night-time nasal congestion that disturb his sleep and school concentration. He rubs his nose upwards repeatedly. He has a history of eczema in infancy and his mother has asthma. Skin-prick testing is positive to grass pollen and house-dust mite.

This stem concerns a typical seasonal allergic rhinoconjunctivitis presentation in an atopic school-aged child, illustrating classification, mechanism and stepwise management. [1]

Question 1 (10 marks)

a) Give the most likely diagnosis, classify it using the ARIA framework, and outline the IgE-mediated pathophysiology. (6 marks) [1]

The most likely diagnosis is seasonal allergic rhinoconjunctivitis — an IgE-mediated inflammation of the nasal and conjunctival mucosa driven by grass-pollen exposure, supported by the classic quartet of sneezing, itch, rhinorrhoea and congestion, the itchy eyes, and the positive grass-pollen skin-prick test. [1]

By the ARIA framework, the duration is persistent because symptoms occur on most days of the week for the duration of the pollen season (more than four consecutive weeks), and the severity is moderate-to-severe because sleep and school concentration are disturbed. The trigger pattern is seasonal, with a perennial dust-mite sensitisation likely contributing background symptoms. [1]

The pathophysiology has two phases. In sensitisation, inhaled pollen is taken up by antigen-presenting cells, presented to naïve CD4-positive T cells, which polarise to a T-helper-2 phenotype and release interleukin-4 and interleukin-13; these cytokines drive B-cell immunoglobulin class-switching to grass-pollen-specific IgE, which coats mast cells via Fc-epsilon-RI receptors. On re-exposure, pollen cross-links adjacent IgE complexes, triggering mast-cell degranulation with release of histamine and leukotrienes that produce immediate sneeze, itch and rhinorrhoea, followed by a late-phase eosinophil infiltration that sustains congestion. [3]

b) Describe four characteristic physical signs and state how you would confirm sensitisation. (4 marks) [3]

The four characteristic signs are the allergic salute with a transverse nasal crease, pale violaceous boggy inferior turbinates with clear rhinorrhoea, allergic shiners with Dennie-Morgan infraorbital folds, and conjunctival injection with watery discharge. [3]

Sensitisation is confirmed by skin-prick testing — a wheal at least 3 mm larger than the negative control at 15 to 20 minutes demonstrates allergen-specific IgE bound to skin mast cells — with serum-specific IgE reserved for when skin-prick testing is contraindicated or uninterpretable. [3]

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References4ShowHide
  1. [1]Sousa-Pinto B, Bousquet J, Vieira RJ Allergic Rhinitis and Its Impact on Asthma (ARIA)-EAACI Guidelines-2024-2025 Revision: Part I-Guidelines. Allergy, 2026.PMID 41324154
  2. [3]Skoner DP Allergic rhinitis: definition, epidemiology, pathophysiology, detection, and diagnosis. J Allergy Clin Immunol, 2001.PMID 11449200
  3. [5]Li Y, Xiong J, Zhang Z Efficacy and safety of various corticosteroids in the treatment of children with allergic rhinitis. J Evid Based Med, 2024.PMID 39313999
  4. [10]Paller AS, Spergel JM, Mina-Osorio P, et al. The atopic march and atopic multimorbidity: Many trajectories, many pathways. J Allergy Clin Immunol, 2019.PMID 30458183
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