Allergic Rhinitis Definition Hypersensitivity of the nasal mucosa due to exposure to allergens Acute and seasonal or chronic and perennial

Allergic Rhinitis What happens in allergic rhinitis? Exposure to allergen IgE production by the body Formation of allergen IgE complex Binding of the complex to mast cells Degranulation of the mast cells and release of inflamatory mediators including histamine. Vasodilation Increase in capillary permability.

Allergic Rhinitis First exposure – Phase of sensitization On re-exposure- Mast cell degranulation Exposure of genetically predisposed individuals to allergens (pollen, animal dander, fur) Activation of T-lymphocytes Stimulates IgE production by B-lymphocytes IgE coat mast cells [on re-exposure mast cell degranulation]

Allergin Rhinitis: Inflammatory cells Mast cells Contain Granules (histamine) Other mediators (leukotrienes and PGs) Lymphocytes T cells Increased mobilisation of inflammatory cells Eosinophils, macrophages, neutrophils Eosinophils Major basic protein, Eosinophilic Cationic Protein (epithelial injury, nasal block)

Allergic Rhinitis: Inflammatory mediators Released by inflammatory cells (mast cells, eosinophils, lymphocytes) Leukotrienes hypersecretion of mucus oedema (Increased vascular permeability) Histamine itching, rhinorrhea (Allergic rhinitis) Cytokines Interleukins (IL) IL-4 (IgE production) IL-3 and IL-5 (eosinophil, mast cell recruitment / activation) Leukotrienes – formerly identified as slow-reacting substance of anaphylaxis (SRS-A), are well known for their bronchoconstricting activity. They are considered more potent than histamine having much longer duration of action than inhaled histamine. Their other inflammatory actions include: Hypersecretion of mucus from goblet cells leading to formation of mucus plugs Increase vascular permeability leading to airway edema Help in migration of leukocytes in bronchial tissues Histamine – it is a potent broncho-constrictor. It also produces vasodilation, increases vasopermeability that increases influx of inflammatory cells from circulation to tissues. Cytokines – they are non-immunoglobulin protein products produced by certain cells like lymphocytes. Of these, various interleukins play an important role in development of asthma. Interleukin-4 produced by helper T-cell (Th2) is necessary for IgE production. Interleukin 3 and 5 promote eosinophil and mast cell differentiation, recruitment and activation in airways, and prolong the survival of the cells in the airways.

Intermittent AR CLASSIFICATION OF ALLERGIC RHINITIS (AR) < 4 days per week or < 4 weeks Mild Intermittent AR Moderate-Severe Intermittent AR Normal Sleep No impairment of daily activities Normal work and school No troublesome symptoms Abnormal Sleep Impairment of daily activities Problem at work and school Troublesome symptoms

Persistent AR CLASSIFICATION OF ALLERGIC RHINITIS (AR) > 4 days per week or > 4 weeks Mild Persistent AR Moderate-Severe Persistent AR Normal Sleep No impairment of daily activities Normal work and school No troublesome symptoms Abnormal Sleep Impairment of daily activities Problem at work and school Troublesome symptoms

Allergic Rhinitis 2 Types: Seasonal (summer, spring, early autumn) tree pollens, grass pollens, mold spores lasts several weeks, disappears and recurs following year at the same time Perennial -inhaled: house dust, wool, feathers, foods, tobacco, hair -ingested: wheat, eggs, milk, nuts  occurs intermittently for years with no pattern or may be constantly present

Allergic Rhinitis Clinical features Nasal obstruction with pruritis, sneezing Clear rhinorrhea (containing increased eosinophils) Itching of eyes with tearing Frontal headache and pressure Mucosa  edematous, pale or violet in color Allergic salute  transverse nasal skin crease from rubbing the nose

Allergic Rhinitis Diagnosis History (don’t forget to ask about atopy & family history) Physical examination: 1. look for redness ,swelling of the mucosa (particularly the turbinates) &mucoid discharge. 2.check for structural anomalies such as septal deviation or nasl polyps. Sensitivity test for specific allergen ( skin prick tests)

Allergic Rhinitis Treatment 1. identification and avoidance of allergen 2.during the acute attach: -antihistamine (systemic or intranasal) -local steroids -decongestant( ephedrine) 3.sodium cromoglycate mast cell stabilizer used as prophyaxis 4. desensitization we keep exposing the body to gradually increased amounts of allergen until the body fails to produce IgE as a result to exposure.

Drug options for Allergic Rhinitis Drug type Itch / sneezing Discharge Blockage Impaired smell Nasal preparations Antihistamines +++ ++ + _ AZELASTINE Anticholinergics Ipratropium Decongestants Xylometazoline Oxymetazoline Mast Cell Stabilizers Sodium cromoglycate Topical Corticosteroids Fluticasone Nometasone 2 sprays/nostril OD

Treatment Options: Allergic Rhinitis Antihistamines Oral: Most common form of Treatment. (Drowsiness / Dryness of mouth / Urinary retention / Blurred vision / appetite +).Cetrizine, Rupatidine Nasal Spray : Azelastine. Potent H1 blocker with immediate effect / Also blocks other mediators (LT, PAF) Corticosteroids Nasal Sprays: Most effective treatment of AR / certain types of perennial rhinitis (Beclomethasone / Budesonide / Fluticasone / Mometasone. Block both EAR / LAR : Reduce swelling & secretions in nasal mucosa (anti-inflammatory) Oral Corticosteroids: Short term

Allergic Rhinitis Complications - chronic sinositis - polyps( swollen edematous nasal mucosal tissue , they can cause complete nasal obstruction) - serous otitis media

Vasomotor Rhinitis - It is a very common type of non- inflammatory, non-allergic rhinitis -Characterized by a combination of symptoms that includes nasal obstruction and rhinorrhea -vasomotor rhinitis is a diagnosis of exclusion reached after taking a careful history, performing a physical examination, and, in select cases, testing the patient with known allergens

Vasomotor Rhinitis Caused by: -temperature change -alcohol, dust, smoke -stress, anxiety, neurosis -endocrine – hypothyroidism, pregnancy, menopause -parasympathomimetic drugs

Vasomotor Rhinitis Clinical features: -Chronic intermittent nasal obstruction -Rhinorhea (thin, watery) -Mucosa and turbinates : swollen, pale between exposure We have 2 types ; eosinophilic & non eosinophilic (according to the number of eosinophils found in the nasal secretion)

Vasomotor Rhinitis TYPES Eosinophilic & Non eosinophilic (according to the number of eosinophils found in the nasal secretion)

Vasomotor Rhinitis Treatment: -Elimination of irritant factor -Parasympathetic blocker -Steroids -Surgery -Symptomatic relief with exercise