Allergic Rhinitis Past Paper PDF

# Allergic Rhinitis ## Outline: - Introduction - Anatomy - Definition - Immunology - Pathophysiology - Diagnosis - Treatments - Hormone rhinitis ## Anatomy & Function - Temperature regulation - Olfaction - Humidification - Filtration and protection ## Allergic Rhinitis - Inflammation of the m...

# Allergic Rhinitis ## Outline: - Introduction - Anatomy - Definition - Immunology - Pathophysiology - Diagnosis - Treatments - Hormone rhinitis ## Anatomy & Function - Temperature regulation - Olfaction - Humidification - Filtration and protection ## Allergic Rhinitis - Inflammation of the mucosal lining of the nose caused by inappropriate hypersensitivity reaction to an aeroallergen - IgE mediated immune response, with mast cell activation and release of cytokines ## Epidemiology of AR - Very prevalent disease - Prevalence of AR in Kenya is 13% - UK population - 10-20% - Affects approximately 1/3 of US citizens. - Occurs in any stage of life with more than 10% of the population affected - AR is more common in children (40%) than adults (10-30%) - Commonest allergic condition in children under 18 years, and the symptoms tend to improve with age The following graph depicts the prevalence of Rhinitis and Wheeze in Kenya: | Prevalence (%) | Year | |---|---| | 6.6 | 1995 | | 14.9 | 2001 | | 12.6 | 2001 | | 38.6 | 2001 | ## Aetiology / Risk factors - Multi-factorial - Both genetic and environmental factors - Prevalence of AR is greatest in: - Higher socioeconomic classes - Non-whites - Polluted areas - Individuals with family history of allergy. - People with positive allergic skin tests - First-born children - Children with high serum IgE levels (>100iu/ml) before 6 years of age ## Immunology - Atopic individuals produce IgE-mast cell TH2 lymphocytic response - Low level exposure to antigen is taken up by an APC (antigen-presenting cell) - Antigen is processed, and the epitope is expressed on the cell surface by MHC II ## Pathophysiology **Early Response:** - IgE-coated mast cells recognize allergens in the mucosal lining, and undergo degranulation - Preformed histamine, heparin, tryptase, kininogenase, and chymase cause initial damage - Newly formed mediators (leukotrienes and prostaglandins) are produced by breakdown of phospholipid cell membrane - These cause vessels to leak leading to watery rhinorrhea, nasal edema/congestion, and sneezing/pruritis **Late Response:** - Mast cells also secrete chemokines which are expressed on endothelial cells - These allow other leukocytes to attach, and migrate into tissues - IL-5 is a potent chemoattractant of eosinophils, T lymphocytes, and macrophages - Over the course of 4 to 8 hours, these cells release their contents, causing further inflammation ## Sensitization and early phase response: A diagram is shown on the slide illustrating sensitization and early phase response. The diagram shows how allergens react with mast cells and triggers the release of inflammatory mediators. <start_of_image> Areas within this diagram are labelled as follows: * **Sensitization Response:** * Allergens * APC * IgE * TH2 cell * Interleukins * IgE-coated mast cells * Plasma cells * B-cell * **Early Phase:** * Allergen * Degranulation * Histamine * Leukotrienes * Prostaglandins * Bradykinins * PAF * Vasodilation * Vascular permeability * Mucus production * Bronchoconstriction ## Allergic Rhinitis: Pathogenesis and Clinical findings A diagram is shown on the slide illustrating allergen sensitization, primary reaction phase, and secondary reaction phase in Allergic Rhinitis. * **Allergy Sensitization: ** * Antigen exposure * APC (macrophages, HLA class II) process antigen into * APC present peptides to Helper T cells * Helper T cells release Interleukins (IL-4 and IL-3) * IL-4 and IL-3 stimulate B- cell transformation to IgE producing Plasma Cells * IgE Abs coat mast cells within nasal mucosa and basophils in the plasma * **Primary Reaction Phase: ** * Antigen exposure * Antigen binds to IgE on mast cells and basophils * Mast cells & basophils release mediators: preformed (histamine, serotonin, protease) & newly-generated (leukotrienes, prostaglandins, TNF-a) * **Secondary Reaction Phase: ** * Presence of mediators * Recruitment of inflammatory cells (neutrophils, eosinophils, macrophages, lymphocytes), bone marrow proliferation of eosinophils * Second phase of mediators released * Mucous gland stimulation * Increased secretion * Sensory nerve stimulation * Vasodilation * Vascular permeability increased * Plasma exudation * Rhinorrhea * Sneezing and itching * Congestion and pressure * Tissue edema ## Allergic Triggers - **Allergens:** Highly soluble proteins or glycol-protein - MW 10,000 – 40,000 - **Dust mites:** Carpeting, upholstered furniture - **Animals:** Furry or feathered - **Pollens:** PE, recess The following text details the concept of how fecal matter from dust mites feeds on squamous skin and leads to an allergy. A picture illustrates this concept. “Concept: fecal material from mites feeding on the squamous skin leads to an allergy” ## Allergic Triggers II - **Cockroaches** - **Molds:** Water damage, leaking roofs, poorly maintained heating/cooling systems. Can be encountered outdoors as well as indoors. - **Foods:** Uncommon for chronic symptoms. ## Environmental triggers at school **Indoors:** - Chalk dust - Insufficient airflow - Second-hand smoke - Glue/paste - Pets - Molds - Dust/dust mites - Cockroaches - Paints - Cleaning agents - New furnishings **Outdoors:** - Pollens (grass, trees, weeds) - Molds - Pesticides ## Diagnosis - History - Duration & time course of symptoms - Possible triggers for symptoms - Response to medications. - Family history of allergic disease - Environmental exposures - Occupational exposures - Effects on quality of life. - Comorbid conditions - Physical exam: - General appearance: Allergic shiners, allergic salute, malaise - Nose: Septal deviation, polyps, drainage, turbinate hypertrophy, hyponasality- rhinolalia clausia. - Mouth: Cobblestoning of oropharynx - Ear: Middle ear pathology - Neck: Lymphadenopathy, thyroid enlargement - Chest: Wheezing - Skin: Eczema ## AR and Comorbid Airway Disease - An image of a diagram illustrates common comorbid airway diseases with Allergic Rhinitis. - Otitis Media with Effusion - Upper Respiratory Infection - Nasal Polyposis - Allergic Rhinitis - Asthma - Sinusitis ## Symptoms - Sneezing - Rhinorrhea - Nasal congestion - Post-nasal drip - Cough - Nasal pruritis - Watery eyes - General fatigue - Diminished quality of life ## Classification of Allergic Rhinitis | Classification | Symptoms | |---|---| | Intermittent | <4 days per week or for less than 4 weeks | | Persistent | >4 days per week and for more than 4 weeks | | Classification | Further details | |---|---| | Mild | Normal sleep, normal daily activities, normal work and school, no troublesome symptoms | | Moderate-Severe | One or more of the following: abnormal sleep, impairment of daily activities, sport, leisure, problems at school or work, troublesome symptoms | ## Physical exam - General appearance: Allergic shiners, allergic salute, malaise - Nose: Septal deviation, polyps, drainage, turbinate hypertrophy, hyponasality- rhinolalia clausia - Mouth: Cobblestoning of oropharynx - Ear: Middle ear pathology - Neck: Lymphadenopathy, thyroid enlargement - Chest: Wheezing - Skin: Eczema - An image shows a close up of a nasal passage illustrating serous nasal discharge with hypertrophic, pale inferior turbinates. - An image depicts the "allergic salute," which is common in children. - An image depicts adenoid facies, which is common in patients with chronic allergic rhinitis. ## DDX - **Non-allergic rhinitis:** Infectious, NARES, vasomotor rhinitis, atrophic rhinitis, drug induced, hormonally induced, exercise, reflex - **Structural/mechanical factors:** Septal deviation, turbinate hypertrophy, adenoid hypertrophy, foreign body, tumor - **Inflammatory/immunologic:** Wegener's, sarcoidosis, midline granuloma, SLE, Sjogren's, CSF rhinorrhea ## Allergy Testing - Nasal smear - Skin testing (An image shows a person undergoing a skin multi-test. An image then shows the whealing response to the allergy test). - In vitro testing ## Treatment - **Environmental control:** Best treatment is prevention - Animal dander - Dust mites - High filtration air filters - Hot water laundry - Special bedding - Pollen - Pollen masks - **Pharmacologic treatment:** - Alpha-adrenergic agonists: Pseudoephedrine, oxymetazoline. Effective in reducing mucosal edema, alpha 1 & 2 adrenergic-vasoconstriction, Wide variation of patient tolerance due to insomnia and irritability. Rhinitis medicamentosa - Inhaled cromolyn: Inhibits the degranulation of sensitized mast cells. Inhibits both the early and late phase. Mainly prophylactic. OTC- 4% nasal spray four times daily. Very safe. - Antihistamines: Currently the primary drug for the treatment of nasal allergy. Compete with histamine for the H1 receptor. Most effective when taken prophylactically. Anticholinergic, antiserotonergic, and anti alpha adrenergic. Lipid soluble and cross the Blood Brain Barrier. Most effective at reducing symptoms of sneezing, nasal itching, and rhinorrhea. - Leukotriene inhibitors: Act similar to antihistamines by competitive inhibition of the leukotriene receptor. Montelukast, zirfilukast. Very successful in asthma. - Inhaled nasal corticosteroids: Primarily block the late phase reaction. Only a small fraction is absorbed locally. Side effects: Atrophy/ nasal septal perforation. Epistaxis 5-8%. Nasal drying. - Systemic and Intraturbinal Corticosteroid injections: Budesonide, Mometasone, fluticasone. Increased potency. Reduced systemic availability and activity. Quicker onset of action. More effective than oral antihistamines at relieving all nasal symptoms as well as improving the total nasal symptom score. May be appropriate for replacing antihistamines as first line therapy for management of nasal allergy. - Systemic corticosteroids: The most potent agents for relieving the symptoms of allergic rhinitis. Because of the side effects, they are reserved for severe or chronic symptoms ## Current Treatment Guidelines: ARIA A table is shown depicting the current treatment guidelines for Allergic Rhinitis, based on the ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines: | Classificaiton | Treatment | |---|---| | Mild Intermittent | Local chromone (including ocular) | | Moderate-Severe Intermittent | Intranasal steroid | | Mild Persistent | Allergen avoidance | | Moderate-Severe Persistent | Intranasal (<10 days) or oral decongestant, Oral or local nonsedating antihistamine, Immunotherapy | ## Immunotherapy - Medical procedure that uses controlled exposure to known allergens to reduce the severity of allergic disease. - Immunologic tolerance: decline in allergen-specific responsiveness - Increases in allergen-specific IgG blocking antibody - When allergen is injected IgG4 antibody specific for the allergen is produced - IgG4 block the synthesis of IgE production by neutralizing the antigen - Elevated IgE levels decline. - IgG4 antibodies preferentially produced to IgE by a separate set of B & T cells. - Ag-specific T cells suppress plasma cell production of IgE. - IgG4 intercept and neutralize allergen before it binds to cell-surface IgE ## Types of Immunotherapy - Injectable vaccine – mainstay of therapy in the US - Sublingual - used widely in Europe. Wilson et al (2005) performed Cochrane database meta-analysis 22 RCT, found therapy works, but difficult to compare with injection immunotherapy. Grade B. - Intranasal - currently under investigation for children and adults with allergic rhinitis. - Subcut-Only approved route of administration in the United States. Normally involves a weekly subcutaneous injection of an extract of the allergen, in solution, in increasing doses until a standard maintenance dose is reached. ## Surgery - Minor role - Septoplasty - Partial turbinate resections - Rhinosinusitis - Polyps ## Hormonal Rhinitis An image of a pregnant silhouette is shown. ## Pregnancy & Rhinitis - No predictable pattern - Rising progesterone and estrogen levels during pregnancy may increase glandular secretion & vasodilation, increased blood volume – pooling. - Estrogen is also believed to increase hyaluronic acid in nasal mucosa. - Increased cortisol – improved symptoms ## Rx in Pg - Chlorpheniramine - Local cromons - 2nd gen antihistamines after 1st trimester - Immunotherapy- continue but don’t start in pregnancy.