Allergic rhinitis and rhinoconjunctivitis — viva

Opening (2 minutes)

The candidate should recognise the classic clinical picture of allergic rhinitis in an atopic school-aged child and classify it using the ARIA framework while committing to exclude alternative diagnoses. The symptoms of morning sneezing, persistent congestion, mouth breathing and impaired school performance in a child with a personal history of eczema and a family history of asthma make allergic rhinitis the leading diagnosis. [1]

Branch 1 — classification and pathophysiology

Examiner: "How would you classify this child's rhinitis and what is the underlying mechanism?" The expected answer applies the ARIA framework: symptoms are persistent because they occur daily for three months (more than four consecutive weeks) and moderate-to-severe because school performance is impaired. The mechanism is a type I IgE-mediated hypersensitivity with a sensitisation phase (Th2-driven IgE class-switching) and an effector phase (mast-cell degranulation producing immediate and late-phase symptoms). [1]

A strong candidate links the atopic history to the United Airway Disease concept, noting that this child's risk of developing asthma is roughly threefold higher than a non-atopic child and that aggressive rhinitis control is part of asthma prevention. [1]

Branch 2 — assessment and differential diagnosis

Examiner: "What will you look for on examination and what else could this be?" Expected findings include the allergic salute and transverse nasal crease, pale violaceous boggy inferior turbinates, clear rhinorrhoea, allergic shiners and Dennie-Morgan lines, cobblestoning of the oropharyngeal mucosa from post-nasal drip, and signs of coexisting asthma on chest examination. [12]

The candidate should articulate the key differentials and the features that separate them: viral upper-respiratory infection is acute, febrile and self-limiting; bacterial rhinosinusitis produces purulent discharge and facial pain beyond ten days; a nasal foreign body is unilateral and foul-smelling; and bilateral nasal polyps in a child should prompt cystic-fibrosis testing. The absence of fever, purulence and unilateral signs supports an allergic aetiology. [12]

Branch 3 — management and escalation

Examiner: "What is your stepwise management plan and how would you counsel about intranasal corticosteroid safety?" The plan follows the ARIA ladder: allergen avoidance and saline irrigation, an oral second-generation antihistamine, and — because this is moderate-to-severe persistent disease — an intranasal corticosteroid such as mometasone or fluticasone as the most effective single therapy. [5]

On safety, the candidate should state that intranasal corticosteroids have minimal systemic bioavailability at recommended paediatric doses, no clinically meaningful effect on the hypothalamic-pituitary-adrenal axis, and local side effects limited to mild epistaxis and dryness that are minimised by correct spray technique. Sedating first-generation antihistamines and topical decongestants beyond five days should be avoided. If symptoms remain uncontrolled, the next step is combination therapy and referral for allergen immunotherapy. [5]

Closing (1 minute)

Summarise the plan: classify as moderate-to-severe persistent allergic rhinitis, start an intranasal corticosteroid with an oral antihistamine and saline, arrange skin-prick testing, assess and co-manage asthma, and review in two to four weeks with escalation to combination therapy or allergist referral if control is inadequate. [12]