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Summary Table

Category	Details
Risk Factors	Personal or family history of atopy (asthma, eczema, food allergy); early childhood exposure to indoor allergens (dust mites, pet dander, mold); genetic predisposition (polygenic inheritance)
Etiology	IgE-mediated Type I hypersensitivity to inhaled allergens (pollen, dust mites, animal dander, mold spores, cockroach antigens)
Patient Presentation	Chronic or episodic sneezing, rhinorrhea (watery, clear), nasal congestion, nasal pruritus; often with ocular symptoms (itching, tearing, redness)
Classic Physical Exam	Allergic shiners (infraorbital darkening), Dennie-Morgan lines (infraorbital creases), allergic salute (transverse nasal crease from habitual upward rubbing), boggy/pale/bluish nasal turbinates, conjunctival injection, cobblestoning of posterior pharynx
Key Diagnostic Results	Elevated serum IgE; positive skin prick test (gold standard for allergen identification); peripheral eosinophilia; nasal smear with eosinophils
Management	Allergen avoidance; intranasal corticosteroids (first-line pharmacotherapy); second-generation oral antihistamines; allergen immunotherapy for refractory cases
Keywords	"Watery rhinorrhea," "pale boggy turbinates," "allergic shiners," "sneezing paroxysms," "seasonal pattern," "atopic triad"

1. Pathophysiology

Allergic rhinitis is a Type I (IgE-mediated) hypersensitivity reaction occurring at the nasal mucosa. Understanding the two-phase immune response is critical for exam purposes.

On initial exposure to an inhaled allergen, antigen-presenting cells process the allergen and present it to Th2 helper T cells. Th2 cells release IL-4 and IL-13, which drive B-cell class switching to produce allergen-specific IgE antibodies. These IgE molecules bind to high-affinity FcεRI receptors on the surface of mast cells residing in the nasal mucosa. This is the sensitization phase, and no symptoms occur here.

Upon re-exposure, the allergen cross-links two adjacent IgE molecules on the mast cell surface, triggering mast cell degranulation. This is the early phase (occurring within minutes), releasing preformed mediators including histamine, tryptase, and newly synthesized mediators such as leukotrienes (LTC4, LTD4) and prostaglandin D2. Histamine acts on H1 receptors in the nasal mucosa, directly causing the hallmark triad of sneezing, pruritus, and watery rhinorrhea. Vascular permeability increases, glandular secretion ramps up, and sensory nerve endings are stimulated. This is why antihistamines are effective against sneezing and itching but less so against congestion.

The late phase follows 4 to 8 hours later and is driven by recruited inflammatory cells, particularly eosinophils, basophils, and Th2 lymphocytes. Eosinophils release major basic protein and eosinophilic cationic protein, perpetuating mucosal inflammation and edema. This late-phase inflammation accounts for the persistent nasal congestion that does not respond well to antihistamines alone but does respond to corticosteroids, which broadly suppress the inflammatory cascade at the transcriptional level. This is the mechanistic reason intranasal corticosteroids are superior to antihistamines for overall symptom control, particularly congestion.

With chronic allergen exposure, the nasal mucosa undergoes a process called nasal priming, where progressively lower doses of allergen trigger progressively stronger responses. This explains why patients notice worsening symptoms as the allergy season progresses even without increased allergen exposure.

2. Classification and Clinical Manifestation

The classification follows the ARIA (Allergic Rhinitis and its Impact on Asthma) framework, which replaced the older "seasonal vs. perennial" terminology. Exam questions may use either system.

ARIA Classification by Duration

Classification	Criteria
Intermittent	Symptoms present < 4 days/week OR < 4 consecutive weeks
Persistent	Symptoms present ≥ 4 days/week AND ≥ 4 consecutive weeks

ARIA Classification by Severity

Classification	Criteria
Mild	None of the following: sleep disturbance, impaired daily activities/sports/leisure, impaired work or school performance, bothersome symptoms
Moderate-Severe	One or more of the above present

By Allergen Trigger (Traditional Classification)

Type	Common Triggers	Timing
Seasonal (hay fever)	Tree pollen (spring), grass pollen (late spring/summer), weed/ragweed pollen (fall), mold spores (fall)	Predictable annual pattern
Perennial	Dust mites, cockroach allergen, animal dander, indoor molds	Year-round, may fluctuate
Episodic	Sporadic exposure to allergens not in the patient's usual environment	Irregular, exposure-dependent

Clinical Manifestations by Mediator

Symptom	Mediator/Mechanism	Phase
Sneezing	Histamine stimulating sensory nerves (trigeminal)	Early
Rhinorrhea (clear, watery)	Histamine and parasympathetic glandular stimulation	Early
Nasal pruritus	Histamine on sensory nerve endings	Early
Ocular itching/tearing	IgE-mediated conjunctival mast cell degranulation	Early
Nasal congestion	Eosinophilic infiltration, mucosal edema, venous engorgement	Late
Hyposmia/anosmia	Chronic mucosal edema obstructing olfactory cleft	Late/Chronic
Post-nasal drip, throat clearing	Mucus overproduction, posterior drainage	Both

The critical exam point: sneezing, itching, and rhinorrhea are early-phase, histamine-driven symptoms (respond to antihistamines). Nasal congestion is predominantly a late-phase, eosinophil-driven symptom (responds best to intranasal corticosteroids).

3. Diagnostic Workup

Test	Role	Key Findings
Clinical history + physical exam	Best initial step	Pattern of symptoms, triggers, allergic facies, pale/boggy turbinates
Skin prick test (SPT)	Gold standard for allergen identification	Wheal-and-flare reaction ≥ 3 mm greater than negative control within 15-20 minutes
Serum allergen-specific IgE (ImmunoCAP)	Alternative when SPT cannot be performed	Elevated specific IgE to suspected allergens
Total serum IgE	Supportive but nondiagnostic	Often elevated; low sensitivity and low discriminatory value
Nasal smear cytology	Supportive	Eosinophils on nasal secretion smear
CBC	Supportive	Peripheral eosinophilia
Nasal provocation test	Research/specialist use	Reproduces symptoms upon allergen exposure; rarely used clinically

The diagnosis of allergic rhinitis is primarily clinical. A patient presenting with the characteristic history of episodic or chronic sneezing, clear watery rhinorrhea, nasal congestion, and pruritus, with identifiable triggers and an atopic background, can be diagnosed on history and physical examination alone. The physical exam findings of pale, boggy (edematous) nasal turbinates with clear secretions and the external signs of chronicity (allergic shiners, Dennie-Morgan lines, transverse nasal crease) reinforce the diagnosis.

When confirmation of the causative allergen is needed, particularly before starting allergen immunotherapy, the skin prick test is the gold standard. It is rapid (results in 15-20 minutes), cost-effective, and has high sensitivity. A positive test produces a wheal-and-flare response. Important caveats: patients must discontinue first-generation antihistamines for 3 to 5 days and second-generation antihistamines for 7 days before testing to avoid false negatives. Patients with severe dermatologic conditions (e.g., widespread eczema or dermatographism) are poor candidates for SPT.

Serum allergen-specific IgE testing (formerly known as RAST, now performed via ImmunoCAP) is the alternative when skin testing is not feasible. This is the appropriate test in patients who cannot stop antihistamines, have diffuse skin disease, or are at elevated risk for anaphylaxis. It is less sensitive than SPT but offers the advantage of no risk for systemic reaction and no interference from medications.

A nasal smear showing eosinophils supports the diagnosis and helps distinguish allergic rhinitis from non-allergic rhinitis (which may show neutrophils instead). However, this finding alone is not confirmatory, as non-allergic rhinitis with eosinophilia syndrome (NARES) also demonstrates nasal eosinophilia.

4. Management and Treatment

Step	Intervention	Notes
All patients	Allergen avoidance and environmental control	Foundation of treatment; reduce dust mite exposure with encasings, HEPA filters, dehumidification
Mild intermittent	Second-generation oral antihistamine PRN	Cetirizine 10 mg/day, loratadine 10 mg/day, or fexofenadine 180 mg/day
Moderate-severe or persistent	Intranasal corticosteroid (first-line)	Fluticasone propionate 1-2 sprays per nostril daily; mometasone 2 sprays per nostril daily
Moderate-severe with inadequate INCS response	INCS + intranasal antihistamine combination	Azelastine/fluticasone (e.g., Dymista) 1 spray per nostril BID
Prominent ocular symptoms	Add oral antihistamine or ocular antihistamine drops	Olopatadine 0.1% 1 drop BID or ketotifen 0.025% 1 drop BID
Severe nasal congestion (short-term only)	Intranasal decongestant (oxymetazoline)	Maximum 3 to 5 days only to prevent rhinitis medicamentosa
Refractory to pharmacotherapy	Allergen immunotherapy (subcutaneous or sublingual)	3 to 5 year course; only for confirmed IgE-mediated disease

Step 1: Allergen Avoidance. All patients should receive counseling on environmental control measures. For dust mite allergy, this includes mattress and pillow encasements, washing bedding in hot water (≥ 60 degrees C) weekly, reducing indoor humidity below 50%, and removing carpets from bedrooms. For pollen allergy, keeping windows closed during high-pollen days, showering after outdoor activity, and monitoring pollen counts are recommended. While evidence for individual measures is modest, the combined approach reduces allergen load meaningfully.

Step 2: Pharmacotherapy. The cornerstone of treatment for moderate-severe or persistent allergic rhinitis is the intranasal corticosteroid (INCS). Per the ARIA 2024-2025 guidelines, INCS is recommended over oral antihistamines as first-line therapy because it addresses all symptoms including congestion, which antihistamines handle poorly. Fluticasone propionate (Flonase) 1-2 sprays (50 mcg/spray) per nostril once daily or mometasone furoate (Nasonex) 2 sprays (50 mcg/spray) per nostril once daily are the most commonly tested agents. Onset of effect takes several days to 2 weeks for full benefit; patients must be counseled that this is not a rescue medication. The proper technique is to aim the spray laterally (toward the ipsilateral ear), not toward the septum, to avoid septal irritation and epistaxis.

For mild intermittent disease, a second-generation oral antihistamine taken as needed is appropriate. The second-generation agents (cetirizine 10 mg daily, loratadine 10 mg daily, fexofenadine 180 mg daily) are preferred because they are non-sedating and have no anticholinergic side effects, unlike first-generation agents (diphenhydramine, chlorpheniramine). First-generation antihistamines cross the blood-brain barrier and cause sedation, impaired cognition, and urinary retention, making them a poor choice for routine use.

When INCS alone provides insufficient relief, the ARIA 2024-2025 guidelines recommend the combination of intranasal corticosteroid plus intranasal antihistamine (azelastine/fluticasone) over either agent alone. This fixed-dose combination provides faster onset (within 30 minutes from the azelastine component) while maintaining the broad anti-inflammatory effect of the steroid.

Leukotriene receptor antagonists (montelukast 10 mg daily) are less effective than INCS and are positioned below oral antihistamines in the treatment hierarchy. However, montelukast has a role in patients with concomitant asthma and allergic rhinitis, where a single agent can address both conditions. The FDA has added a black box warning for montelukast regarding neuropsychiatric events (mood changes, suicidal ideation), making this a high-yield testing point.

Intranasal decongestants (oxymetazoline 0.05%, 2 sprays per nostril BID) provide rapid congestion relief but must be limited to 3 to 5 days maximum. Prolonged use causes rebound congestion known as rhinitis medicamentosa, where the nasal mucosa becomes dependent on the decongestant and congestion worsens upon discontinuation. The mechanism involves downregulation of adrenergic receptors in the nasal vasculature.

Step 3: Allergen Immunotherapy. For patients with confirmed IgE-mediated allergic rhinitis who remain symptomatic despite optimal pharmacotherapy, allergen immunotherapy (either subcutaneous [SCIT] or sublingual [SLIT]) is indicated. This is the only treatment that modifies the natural history of the disease. The course is typically 3 to 5 years in duration. SCIT involves a build-up phase (weekly injections with incrementally increasing doses over 3-6 months) followed by a maintenance phase (monthly injections). SLIT tablets are taken daily at home. Immunotherapy induces immune tolerance by shifting the immune response from Th2-dominant to Th1/Treg-dominant, with production of blocking IgG4 antibodies. The principal risk of SCIT is anaphylaxis, which is why it must be administered in a supervised medical setting with a 30-minute observation period.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Vasomotor (non-allergic) rhinitis	Chronic rhinorrhea and nasal congestion in an adult	No itching, no sneezing paroxysms, triggered by temperature changes/irritants rather than allergens; negative skin prick test; nasal smear shows no eosinophils
Rhinitis medicamentosa	Severe nasal congestion, may coexist with allergic rhinitis	History of prolonged intranasal decongestant use (> 5 days); beefy-red, erythematous turbinates (not pale/boggy); resolves with decongestant withdrawal
Nasal polyposis	Chronic nasal congestion, hyposmia, rhinorrhea	Painless, glistening, gray, pedunculated masses on nasal exam; bilateral; associated with Samter triad (aspirin sensitivity + asthma + nasal polyps); does not have seasonal pattern
Acute viral rhinitis (common cold)	Sneezing, rhinorrhea, congestion	Self-limited (7-10 days); rhinorrhea becomes mucopurulent (yellow-green); no pruritus; no allergic facies; no seasonal recurrence
NARES (non-allergic rhinitis with eosinophilia syndrome)	Nasal eosinophilia, symptoms overlap with allergic rhinitis	Negative skin prick test and negative serum specific IgE despite eosinophils on nasal smear; no identifiable allergen trigger
CSF rhinorrhea	Unilateral clear nasal discharge	Watery discharge but unilateral, worsened by leaning forward or Valsalva; positive for beta-2 transferrin; usually has a history of head trauma or neurosurgery
Foreign body (pediatric)	Nasal congestion and discharge in a child	Unilateral, foul-smelling, purulent or blood-tinged discharge; no bilateral symptoms; no atopic history needed

6. Traps and High-Yield Pearls

The most common way students lose points on allergic rhinitis questions is by selecting an oral antihistamine as first-line treatment for a patient with moderate-severe or persistent disease. The reflex to pick "antihistamine for allergy" is strong, but the correct answer for a patient whose chief complaint includes nasal congestion alongside sneezing and rhinorrhea is the intranasal corticosteroid. Antihistamines handle itching, sneezing, and rhinorrhea but do not adequately address congestion, which is the late-phase eosinophil-driven component.

A second common trap involves rhinitis medicamentosa. When a vignette describes worsening nasal congestion despite using "nasal spray" for several weeks, the test-writer is testing whether you recognize rebound congestion from decongestant overuse. The answer is discontinuation of the decongestant and initiation of INCS, not escalation to another decongestant or oral therapy.

Third, watch for the montelukast distractor. It will appear as an answer choice in an allergic rhinitis vignette, and while it is a real medication used in this condition, it is inferior to both INCS and oral antihistamines as monotherapy. The one scenario where it becomes a reasonable answer is when the patient has coexisting asthma, where a single agent addressing both airway and nasal inflammation is attractive.

Finally, be attentive to the distinction between allergic and non-allergic rhinitis. The test-writer will include or omit pruritus and sneezing deliberately. A middle-aged patient with chronic congestion and rhinorrhea but no itching, no sneezing, no atopic history, and symptoms triggered by cold air or strong odors is vasomotor rhinitis, not allergic rhinitis, and the workup and management differ accordingly.

The core competency being tested is the ability to match the pathophysiologic phase (early vs. late) to the correct pharmacologic intervention and to recognize the clinical and physical exam features that anchor the diagnosis against its closest mimics.

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