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

2. 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.

3. 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]

4. 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)

5. 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.

6. 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

7. 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

8. 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

9. 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

10. 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)

11. 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.

12. 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

13. 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

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

15. 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

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

17. 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)

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

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