PE28.1-5 | Allergy and Asthma — Glossary

Structural changes in chronic uncontrolled asthma including subepithelial fibrosis, smooth muscle hypertrophy, goblet cell hyperplasia, and angiogenesis, driven by TGF-β and IL-13; causes partially irreversible airflow obstruction.

The only disease-modifying treatment for allergic rhinitis; involves graded exposure to the causative allergen (subcutaneous SCIT or sublingual SLIT) over 3–5 years to induce allergen tolerance via immune reprogramming.

Serum measurement of IgE antibodies directed against a specific allergen (reported via ImmunoCAP as kUA/L); class ≥2 (≥0.35 kUA/L) is positive; not affected by antihistamine use.

The sequential or overlapping progression of IgE-mediated atopic diseases: atopic dermatitis (early infancy) → allergic rhinitis → asthma, reflecting epithelial barrier dysfunction and systemic Th2 polarisation.

IgE-mediated Type I hypersensitivity inflammation of the nasal mucosa characterised by rhinorrhoea, nasal pruritus, sneezing, and congestion, classified by ARIA criteria as intermittent or persistent and mild or moderate-severe.

The characteristic gesture of children with AR who repeatedly rub the nose upward with the palm of the hand to relieve itch; over months this produces a transverse nasal crease across the lower nasal bridge.

Bilateral dark periorbital discolouration (infraorbital venous congestion) in children with allergic rhinitis, caused by impaired venous drainage secondary to nasal mucosal oedema.

Allergic Rhinitis and its Impact on Asthma (2001/2008) evidence-based classification system using a two-dimensional grid of duration (intermittent vs persistent) and severity impact (mild vs moderate-severe) to guide treatment decisions.

A chronic inflammatory disorder of the airways characterised by variable, reversible airflow obstruction, bronchial hyperreactivity, and episodic symptoms (wheeze, breathlessness, chest tightness, cough) triggered by allergens, exercise, or irritants.

A clinical prediction rule for persistent asthma in preschool wheezers: ≥3 episodes of wheeze in a year PLUS ≥1 major criterion (parental asthma or atopic dermatitis in the child) or ≥2 minor criteria (eosinophilia ≥4%, wheeze apart from colds, allergic rhinitis); positive API predicts persistent asthma.

Exaggerated bronchoconstrictor response to stimuli (allergens, cold air, exercise, irritants, pharmacological agents) that would not cause bronchospasm in normal airways; a cardinal feature and consequence of chronic asthma inflammation.

Lipid mediators (LTC₄, LTD₄, LTE₄) produced by mast cells and eosinophils that cause nasal congestion and bronchospasm; blocked by leukotriene receptor antagonists such as montelukast.

A breath-actuated inhaler device (Turbuhaler, Rotahaler, Accuhaler) that delivers drug as a fine powder requiring an inspiratory flow rate of ≥30–60 L/min for adequate dispersion; suitable for children ≥6–8 years with coaching; not suitable in acute severe exacerbation.

The immediate (0–60 min) mast cell degranulation response after allergen re-exposure, mediated by histamine and tryptase, causing itch, sneezing, and watery rhinorrhoea.

Transient bronchospasm occurring during or within 10–15 minutes after sustained exercise, caused by airway cooling and hyperosmolarity from increased ventilation; confirmed by >12% fall in FEV₁ post-exercise challenge.

Ratio of forced expiratory volume in 1 second to forced vital capacity; the primary spirometric indicator of airflow obstruction; <0.80 (or below lower limit of normal) indicates obstruction, as seen in asthma and COPD.

An international evidence-based asthma management programme producing annual guidelines; the GINA severity classification (intermittent/mild/moderate/severe persistent) and control classification (well/partial/uncontrolled) are the standard frameworks for paediatric asthma management.

The most prevalent perennial allergen in India (Dermatophagoides pteronyssinus and D. farinae); thrives in bedding, carpets, and soft furnishings in warm, humid environments; the dominant trigger for both AR and asthma in Indian children.

Topically acting corticosteroid (budesonide, beclomethasone, fluticasone) that suppresses eosinophilic airway inflammation in asthma; the cornerstone controller and most effective preventive therapy; systemic bioavailability is low at recommended doses.

Topically applied corticosteroid (budesonide, mometasone, fluticasone) that suppresses both early and late-phase nasal inflammation; first-line pharmacotherapy for persistent moderate-severe allergic rhinitis.

A short-acting muscarinic antagonist (SAMA) that blocks cholinergic bronchoconstriction; used as an add-on to SABA in acute moderate-severe asthma exacerbations; NOT a maintenance controller for asthma.

The delayed (4–8 h) inflammatory response driven by leukotrienes, cytokines, and recruited eosinophils, causing persistent nasal congestion and mucosal oedema that characterises chronic AR.

Beta-2 agonist (formoterol, salmeterol) with duration of action ≥12 hours; add-on controller for moderate-severe asthma; NEVER used as monotherapy in asthma — must always be combined with an ICS due to risk of masking worsening inflammation.

A smooth-muscle relaxant that antagonises calcium-mediated bronchospasm; given as 25–75 mg/kg (maximum 2.5 g) by slow IV infusion over 20 minutes in severe acute asthma not responding to SABA + ipratropium + systemic corticosteroids.

A selective cysteinyl leukotriene receptor-1 (CysLT₁) antagonist used for allergic rhinitis and mild-moderate asthma; given once nightly (4 mg <5 yr, 5 mg 6–14 yr, 10 mg ≥15 yr); FDA black-box warning for neuropsychiatric effects.

Microscopic examination of cells collected from the nasal mucosa by scraping or lavage; >10–20% eosinophils supports allergic rhinitis; predominantly neutrophils indicate infectious rhinitis; eosinophils with negative sIgE suggests NARES.

Topical application of isotonic or hypertonic saline (350–400 mOsm/L) to the nasal passages to wash out allergens, inflammatory mediators, and crusts; an effective, safe adjunct to pharmacotherapy that improves mucociliary clearance.

The most severe category of acute asthma exacerbation characterised by silent chest, cyanosis, fatigue, bradycardia or extreme tachycardia, and altered consciousness; requires immediate intensive care intervention including preparation for intubation.

An anti-IgE monoclonal antibody that binds free serum IgE, preventing its attachment to FcεRI receptors on mast cells; approved as add-on therapy for severe allergic asthma in children ≥6 years with confirmed sensitisation and inadequate control on high-dose ICS/LABA.

The maximum expiratory flow measured by a portable peak flow meter; expressed as % predicted for height and sex; used in acute exacerbation to grade severity (>70% mild; 40–69% moderate; <40% severe) and to monitor home asthma control.

Progressive reduction in the threshold for mast cell activation following repeated allergen exposure during an allergy season, explaining why AR symptoms worsen progressively despite the same allergen load.

A ≥12% increase in FEV₁ after inhaled SABA (salbutamol 400 µg via spacer); confirms variable airflow obstruction in the diagnosis of asthma; the 200 mL absolute criterion is less reliable in young children.

Rebound nasal congestion caused by overuse of topical decongestants (xylometazoline, oxymetazoline) beyond 3–5 days, due to paradoxical adrenergic desensitisation and rebound vasodilation.

H₁-receptor antagonists (cetirizine, loratadine, fexofenadine) that do not cross the blood–brain barrier at therapeutic doses and therefore lack the sedation, cognitive impairment, and anticholinergic effects of first-generation agents; preferred in paediatric AR.

The initial allergen exposure phase in which dendritic cells activate Th2 lymphocytes, driving B-cell class switching to produce allergen-specific IgE that binds mast cell FcεRI receptors — no symptoms occur at this stage.

Bronchodilator (salbutamol/albuterol) that activates beta-2 adrenergic receptors on bronchial smooth muscle, increasing cAMP and causing rapid bronchodilation (onset 5 min, duration 4–6 h); the reliever medication for all severities; chronic use without ICS signals inadequate control.

The primary allergy diagnostic test in which standardised allergen extracts are introduced through the epidermis; a wheal ≥3 mm above the negative saline control at 15–20 minutes constitutes a positive result.

A holding device attached between the pMDI and the patient that slows the aerosol cloud, allows propellant evaporation, and converts inhaler actuation into a breath-coordinated (or tidal breathing) delivery; essential in children <5–6 years to maximise lower-airway drug deposition.

A framework for asthma management that escalates (step-up) or reduces (step-down) treatment intensity based on GINA control classification; ensures that the minimum effective medication is used while maintaining well-controlled status.

Immune response dominated by Th2 helper T-cells that secrete IL-4, IL-5, and IL-13, driving IgE class switching and eosinophil survival; the hallmark of atopic disease including allergic rhinitis, asthma, and atopic dermatitis.