IgE-mediated nasal mucosal inflammation from inhaled allergens, producing congestion, rhinorrhea, sneezing, and itch.
Also known as: allergic rhinitis, hay fever, seasonal allergies, perennial rhinitis
Overview
IgE-mediated inflammation of the nasal mucosa triggered by inhalation of environmental allergens. Classified by pattern (seasonal vs perennial), frequency (intermittent vs persistent), and severity (mild vs moderate-severe).
Epidemiology
Affects 10-30% of US adults and up to 40% of children. Often coexists with asthma, atopic dermatitis, and food allergy ('atopic march'). Onset usually in childhood or adolescence; can persist or develop in adults.
Try two board-style Allergic Rhinitis questions
Real questions from the FirstPassPA bank, with the full explanation. Pick an answer — no signup, no email.
Question 1EENTMedium
A 24-year-old woman reports 3 years of recurrent springtime sneezing fits, clear watery rhinorrhea, and itching of the nose and eyes. Symptoms recur every April and resolve by July. On exam she has pale, boggy nasal turbinates with clear discharge and dark infraorbital circles. She wants to know precisely which allergens she should avoid and is considering immunotherapy. She has no eczema, no dermatographism, and is willing to stop her antihistamine for a week. Which of the following is the most appropriate next diagnostic test to identify her specific triggers?
ASerum total IgE blood level
BAllergen skin prick testing
CSinus computed tomography scan
DPeripheral eosinophil count
Reveal answer & full explanation
Correct answer: B — Allergen skin prick testing
ASerum total IgE blood level
BAllergen skin prick testing✓
CSinus computed tomography scan
DPeripheral eosinophil count
Why Allergen skin prick testing is correct
Skin prick testing is the most sensitive method to identify the specific environmental allergens driving IgE-mediated allergic rhinitis, which is exactly what this patient needs before allergen-avoidance counseling and immunotherapy.
It is the preferred allergen-identification study when the patient has no contraindication and can hold antihistamines for 5-7 days, both of which are true here.
Why the others are wrong
Serum total IgE blood level: a total IgE is nonspecific; it neither identifies which allergens the patient reacts to nor is routinely needed. Allergen-specific serum IgE (ImmunoCAP) is the alternative only when skin testing is not feasible.
Peripheral eosinophil count: eosinophilia is a nonspecific marker of atopy and does not pinpoint individual triggers, so it cannot guide avoidance or immunotherapy selection.
Sinus computed tomography scan: sinus imaging is reserved for suspected complicating rhinosinusitis or structural disease; it adds nothing to typical seasonal allergic rhinitis and does not identify allergens.
Question 2EENTMedium
A 9-year-old boy is brought to the clinic for several months of sneezing fits, clear watery rhinorrhea, and itchy, watery eyes that worsen each spring. Exam shows pale, boggy nasal turbinates, dark circles beneath both eyes, and a transverse crease across the lower nose. He has a history of eczema, and his mother has asthma. Of the features in this child's history, which of the following is the strongest risk factor for his condition?
AEarly-life exposure to indoor dust mites
BPersonal and family history of atopy
CHigher household socioeconomic status
DLiving in a densely populated urban area
Reveal answer & full explanation
Correct answer: B — Personal and family history of atopy
AEarly-life exposure to indoor dust mites
BPersonal and family history of atopy✓
CHigher household socioeconomic status
DLiving in a densely populated urban area
Why Personal and family history of atopy is correct
Allergic rhinitis is the IgE-mediated arm of the atopic march, and a personal or family history of atopic disease (asthma, eczema, food allergy) is the single strongest predictor, carrying the highest relative risk.
This child already has eczema and a mother with asthma, placing him squarely in the atopic phenotype that drives Th2-skewed IgE production.
Why the others are wrong
Early-life exposure to indoor dust mites is a genuine sensitizing exposure and a recognized risk factor, but it confers far less risk than the underlying atopic predisposition that determines whether sensitization occurs at all.
Living in a densely populated urban area is associated with higher rates (along with maternal smoking), yet it is a modest environmental contributor, not the dominant driver.
Higher household socioeconomic status is linked to allergic rhinitis through the hygiene hypothesis, but the association is weak and indirect compared with a family and personal history of atopy.
🔒 Free preview limit reached
Keep reading — start your free trial
You've read your 2 free diagnosis previews. Create your free account to unlock the full Allergic Rhinitis outline — plus all 514 diagnoses, 6,500+ board-style questions, flashcards, and an AI tutor. Your 7-day free trial includes everything, and there's no credit card required.
Personal or family history of atopy (asthma, eczema, food allergy)
Early-life exposure to allergens (dust mites, pets, pollen, cockroach, mold)
Maternal smoking, urban environment
Higher socioeconomic status (hygiene hypothesis association)
Pathophysiology
First exposure: APCs present allergen → Th2 differentiation → IL-4/IL-13 drive B-cell IgE production → IgE binds mast cells. Re-exposure: allergen crosslinks IgE on mast cells → degranulation with histamine, tryptase, leukotrienes → early-phase sneezing, itch, rhinorrhea (minutes). Late-phase 4-8 h later: eosinophil and Th2 infiltrate → congestion and hyperresponsiveness.
Clinical presentation
Symptoms
Sneezing, especially in paroxysms
Clear watery rhinorrhea
Nasal congestion / obstruction (often the most bothersome)
Itching of nose, eyes, palate, ears
Postnasal drip with throat clearing or chronic cough
Decreased smell/taste; sleep disturbance
Signs / physical exam
Allergic shiners — dark infraorbital circles from venous stasis
Dennie-Morgan lines — infraorbital folds
Allergic salute (transverse nasal crease in children)
Pale, bluish, boggy turbinates with clear discharge
Cobblestoning of posterior oropharynx
Conjunctival injection, tearing if concurrent allergic conjunctivitis
Classic findings
Pale boggy turbinates with clear watery rhinorrhea plus allergic shiners and a transverse nasal crease in an atopic child.
Differential diagnosis
Viral rhinitis (common cold) — Acute onset, self-limited 7-10 days, sore throat/cough, no itching, no triggers; supportive care
Nonallergic rhinitis (vasomotor) — Triggered by odors, temperature changes, foods; no itching, negative allergy testing; intranasal steroid or ipratropium
Acute bacterial sinusitis — Symptoms >10 days or worsening after initial improvement, facial pain/pressure, purulent discharge, fever
Rhinitis medicamentosa — Rebound congestion from prolonged topical decongestant (oxymetazoline) use >3-5 days; taper and replace with intranasal steroid
Nasal polyps — Persistent obstruction, anosmia, asthma + aspirin sensitivity (Samter triad); pale gray grape-like masses on rhinoscopy
Deviated septum / structural — Unilateral fixed obstruction, no allergic features
Foreign body (children) — Unilateral foul purulent discharge in a young child; remove
CSF rhinorrhea — Unilateral clear watery discharge after trauma or surgery; halo sign, beta-2 transferrin positive
Diagnostic workup
Diagnostic criteria
ARIA: based on temporal pattern (intermittent <4 days/week or <4 weeks; persistent ≥4 days/week AND ≥4 weeks) and severity (mild = normal sleep/activities; moderate-severe = impaired sleep, school/work, or troublesome symptoms).
Labs
Clinical diagnosis in most cases — history of trigger-related symptoms with characteristic findings
Skin prick testing (allergist) — most sensitive; identifies specific allergens; antihistamines must be held 5-7 days prior
Serum specific IgE (ImmunoCAP) — when skin testing not feasible (severe eczema, antihistamine dependence, dermatographism)
Total IgE and eosinophil count are nonspecific and not routinely needed
Imaging
Not required for typical allergic rhinitis
Nasal endoscopy if structural disease (polyps, deviated septum) or chronic sinusitis suspected
CT sinus only if complicating rhinosinusitis
Diagnostic algorithm
Severity / Pattern
Step Therapy
Mild intermittent
Oral 2nd-gen antihistamine PRN OR intranasal antihistamine
Moderate-severe intermittent
Intranasal corticosteroid ± 2nd-gen antihistamine
Mild persistent
Intranasal corticosteroid daily
Moderate-severe persistent
Intranasal corticosteroid + intranasal antihistamine; reassess in 2-4 weeks
Stepwise management of allergic rhinitis by severity and persistence (ARIA framework).
Treatment
First-line
Allergen avoidance: dust mite-impermeable bedding covers, HEPA filters, pet dander reduction, pollen avoidance and showering after exposure
Intranasal corticosteroid — fluticasone propionate/furoate, mometasone, budesonide, or triamcinolone — most effective single agent for moderate-severe or persistent symptoms; takes days for full effect, weeks for peak
Second-generation oral H1 antihistamine — loratadine, cetirizine, fexofenadine, or levocetirizine — first-line for mild/intermittent symptoms
Intranasal antihistamine — azelastine or olopatadine — fast onset (minutes); can replace or add to oral agents
Saline nasal irrigation (neti pot, sinus rinse) as adjunct
Second-line / adjunct
Combination intranasal corticosteroid + intranasal antihistamine (fluticasone/azelastine) for moderate-severe symptoms
Leukotriene receptor antagonist — montelukast — particularly if concurrent asthma; FDA boxed warning for neuropsychiatric effects
Short course oral corticosteroids only for severe refractory exacerbations
Topical decongestant — oxymetazoline — for short-term congestion (≤5 days) to avoid rhinitis medicamentosa
Allergen immunotherapy — subcutaneous (SCIT) or sublingual (SLIT, e.g., grass, ragweed, dust mite tablets) — disease-modifying; consider for inadequate response, side effects to medications, or desire to reduce medication burden
Complications
Sleep disturbance with daytime fatigue and impaired school/work performance
Acute and chronic rhinosinusitis
Otitis media with effusion in children
Asthma exacerbations (unified airway)
Nasal polyposis with chronic disease
PANCE pearls
Intranasal corticosteroids outperform oral antihistamines for nasal congestion and overall symptom control.
First-generation antihistamines (diphenhydramine, chlorpheniramine) cause sedation and cognitive impairment — avoid as first-line; especially avoid in elderly (Beers criteria).
Oxymetazoline use >5 days causes rhinitis medicamentosa — treat by stopping the topical, replacing with intranasal steroid, and counseling.
Allergic rhinitis plus asthma — treating the upper airway improves lower-airway control.
Unilateral nasal obstruction, epistaxis, or anosmia is NOT classic allergic rhinitis — evaluate for polyp, tumor, or foreign body.
References
AAAAI/ACAAI 2017 — Wallace DV et al. Joint Task Force Practice Parameter Update: Allergic Rhinitis. Ann Allergy Asthma Immunol 2017
ARIA 2020 — Bousquet J et al. Next-generation ARIA care pathways for allergic rhinitis. Allergy 2019;74(11):2087-2102
AAO-HNS 2015 — Seidman MD et al. Clinical Practice Guideline: Allergic Rhinitis. Otolaryngol Head Neck Surg 2015;152(1S):S1-S43
Practice EENT questions on FirstPassPA
Turn this outline into retention. 6,500+ board-style questions with an AI tutor that explains every answer — free to start, no card required.
Educational use only. This outline is a study aid for PA students and is not medical advice or a substitute for clinical judgment. FirstPassPA is an independent study tool and is not affiliated with, endorsed by, or sponsored by NCCPA or PAEA. PANCE® and PANRE® are registered trademarks of the National Commission on Certification of Physician Assistants; End of Rotation™ is a program of the Physician Assistant Education Association.