Allergic Rhinitis PDF, Our Lady of Fatima University

Our Lady of Fatima University Allergic Rhinitis College of Pharmacy PHCP312 Learning Objectives: At the end of the discussion, the student must be able: To explain the pathophysiology of the Allergic Rhinitis To identi...

Our Lady of Fatima University Allergic Rhinitis College of Pharmacy PHCP312 Learning Objectives: At the end of the discussion, the student must be able: To explain the pathophysiology of the Allergic Rhinitis To identify the factors that may induce and potentiate the disease To discuss the clinical presentation as well the diagnosis and laboratory evaluation. To evaluate the therapeutic outcome. Outline Introduction Pathophysiology Clinical Presentation Treatment algorithm and Pharmacologic Therapy Evaluation of Outcomes Hypersensitivity Inappropriate or exaggerated response to an antigen or an allergen ☐ Antigen: ☐ Any substance that induces the immune system to produce antibodies against it ☐ Types: ☐ Exogenous: Antigens that enters the body, trapped in antigen presenting cells ( Macrophages/ Dendritic cells) ☐ Micro ogranisms, allergens ☐ Endogenous: Body’s own cell or sub fragments ☐ Blood group antigen, histocompatibility leucocyte antigen ☐ Auto antigen: normal proteins or complexes that is recognized by the immune system of someone with an autoimmune condition ☐ Thyroglobulin 4 Types of Hypersensitivity Reaction (ACID) Type 1: Allergic reaction ( immediate hypersensitivity) ☐ IgE mediated release of histamine, mast cells and basophils ☐ Reaction within 1 hour ☐ Ex: Bee sting, latex allergy, medications ( penicillin) urticaria, anaphylaxis, atopy ☐ Atopy: refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema) ☐ Commonly associated with heightened response of IgE 4 Types of Hypersensitivity Reaction (ACID) Type 2: Cytotoxic reaction ☐ Involves IgG and IgM bound cell surface antigens ☐ Hours to days ☐ Ex: Hemolytic reactions with medications, graft rejections 4 Types of Hypersensitivity Reaction (ACID) Type 3: Immune complex reaction ☐ Involves circulating IgG and IgM immune complex that deposits in post capillary venules ☐ 1-3 weeks ☐ Example: SLE, Serum sickness 4 Types of Hypersensitivity Reaction (ACID) Type 4: Delayed hypersensitivity ☐ Cell mediated immunity ☐ Mediated by T-cells rather than antibodies ☐ Days- weeks ☐ Example: Mantoux test (PPD) ☐ Size of induration :10-15mm ☐ Ex: nickel allergy, SJS, poison ivy ☐ Poison ivy due to Urushiol Allergic Rhinitis Allergic rhinitis involves inflammation of nasal mucous membranes in sensitized individuals when inhaled allergenic particles contact mucous membranes and elicit a response mediated by immunoglobulin E (IgE). There are two types: Seasonal Persistent (formerly called “perennial”) Pathophysiology Airborne allergens enter the nose during inhalation and are processed by lymphocytes, which produce antigen-specific IgE, sensitizing genetically predisposed hosts to those agents. On nasal reexposure, IgE bound to mast cells interacts with airborne allergens, triggering release of inflammatory mediators. An immediate reaction occurs within seconds to minutes, resulting in rapid release of preformed and newly generated mediators from the arachidonic acid cascade.  Mediators of immediate hypersensitivity: Histamine, leukotrienes, prostaglandin, tryptase, and kinins. These mediators cause: Vasodilation, increased vascular permeability, and production of nasal secretions. Histamine produces rhinorrhea, itching, sneezing, and nasal obstruction.  A late-phase reaction may occur 4 to 8 hours after initial allergen exposure due to cytokine release from mast cells and thymus-derived helper lymphocytes. This inflammatory response causes persistent chronic symptoms, including nasal congestion. Clinical Presentation Seasonal (hay fever) allergic rhinitis occurs in response to specific allergens (pollen from trees, grasses, and weeds) present at predictable times of the year (spring and/or fall) and typically causes more acute symptoms. Persistent allergic rhinitis occurs year-round in response to nonseasonal allergens (eg, dust mites, animal dander, and molds) and usually causes more subtle, chronic symptoms. Many patients have a combination of both types, with symptoms year-round and seasonal exacerbations. Based on frequency Intermittent: ☐ Response lasting 4 weeks/ year Mild: ☐ Symptoms that do not interfere with quality of life Moderate to severe ☐ Symptoms that interfere with quality of life such as sleep disturbance and work performance  Symptoms include clear rhinorrhea, sneezing, nasal congestion, postnasal drip, allergic conjunctivitis, and pruritic eyes, ears, or nose. In children, physical examination may reveal dark circles under the eyes (allergic shiners), a transverse nasal crease caused by repeated rubbing of the nose, adenoidal breathing, edematous nasal turbinates coated with clear secretions, tearing, and periorbital swelling. Patients may complain of loss of smell or taste, with sinusitis or polyps the underlying cause in many cases. Postnasal drip with cough or hoarseness can be bothersome. Diagnosis Medical history Allergy testing ☐ Careful description of ☐ Determines whether rhinitis is symptoms caused by immune response to ☐ Environmental factors and allergens. exposures ☐ Immediate-type hypersensitivity ☐ Results of previous therapy skin tests are commonly used. ☐ Use of medications ☐ Percutaneous testing is safer and more generally accepted than ☐ Previous nasal injury or intradermal testing, which is surgery usually reserved for patients ☐ Family history requiring confirmation. ☐ The radioallergosorbent test (RAST) can detect IgE antibodies in the blood that are specific for a given antigen, but it is less sensitive than percutaneous tests. Pharmacologic Therapy Histamine H1-receptor antagonists bind to H1 receptors without activating them, preventing histamine binding and action. They are effective in preventing the histamine response but not in reversing its effects after they have occurred. Antihistamines are more effective when taken 1 to 2 hours before anticipated exposure to the offending allergen. Decongestants ☐ sympathomimetic agents that act on adrenergic receptors in nasal mucosa to produce vasoconstriction, shrink swollen mucosa, and improve ventilation. ☐ Rhinitis medicamentosa (rebound vasodilation with congestion) may occur with prolonged use of topical agents (>3–5 days). ☐ Phenylephrine has replaced pseudoephedrine in many nonprescription antihistamine–decongestant combination products because of legal restrictions on pseudoephedrine sales Nasal Corticosteroids ☐ Intranasal corticosteroids relieve sneezing, rhinorrhea, pruritus, and nasal congestion with minimal side effects. ☐ They reduce inflammation by blocking mediator release, suppressing neutrophil chemotaxis, causing mild vasoconstriction, and inhibiting mast cell–mediated, late-phase reactions. ☐ Example: Beclomethasone, Budesonide, Flunisolide, Fluticasone, mometasone, Triamcinolone Cromolyn Sodium ☐ a mast cell stabilizer, is available as a nonprescription nasal spray for symptomatic prevention and treatment of allergic rhinitis. ☐ It prevents antigen-triggered mast cell degranulation and release of mediators, including histamine. ☐ The most common side effect is local irritation (sneezing and nasal stinging). ☐ For seasonal rhinitis, ☐ treatment should be initiated just before the start of the offending allergen’s season and continue throughout the season. ☐ For persistent rhinitis, ☐ effects may not be seen for 2 to 4 weeks; antihistamines or decongestants may be needed during this initial phase of therapy Ipratropium bromide an anticholinergic agent that may be useful in persistent allergic rhinitis. It exhibits antisecretory properties when applied locally and provides symptomatic relief of rhinorrhea. Montelukast ☐ a leukotriene receptor antagonist approved for treatment of persistent allergic rhinitis in children as young as 6 months and for seasonal allergic rhinitis in children as young as 2 years. It is effective alone or in combination with an antihistamine. ☐ Montelukast is no more effective than antihistamines and less effective than intranasal corticosteroids; therefore, it is considered third-line therapy after those agents. Immunotherapy The process of administering doses of antigens responsible for eliciting allergic symptoms into a patient with the intent of inducing tolerance to the allergen when natural exposure occurs. For subcutaneous immunotherapy, very dilute solutions are given initially once or twice weekly. Sublingual immunotherapy is available for ragweed and certain grass allergies  Adverse reactions with subcutaneous immunotherapy include mild local adverse reactions include induration and swelling at the injection site. More severe reactions (generalized urticaria, bronchospasm, laryngospasm, vascular collapse, and death from anaphylaxis) occur rarely. Severe reactions are treated with epinephrine, antihistamines, and systemic corticosteroids. The most common reactions with sublingual immunotherapy are pruritus of the mouth, ears, and tongue; throat irritation; and mouth edema. Non Pharmacologic Treatment ☐ Avoiding offending allergens ☐ Important but difficult to accomplish, especially for perennial allergens. ☐ Mold growth can be reduced by keeping household humidity less than 50% and removing obvious growth with bleach or disinfectant. ☐ Removing pets from the home, if feasible. ☐ Reducing exposure to dust mites ☐ Encasing bedding with impermeable covers and washing bed linens in hot water has little benefit, except perhaps in children. ☐ Prevent poor air quality in homes ☐ Avoiding wall-to-wall carpeting, ☐ Using moisture control to prevent mold accumulation, and ☐ Controlling sources of pollution such as cigarette smoke. ☐ On seasonal allergic rhinitis ☐ Keep windows closed and minimize time spent outdoors during pollen seasons. ☐ Filter masks can be worn while gardening or mowing the lawn. Evaluation of Outcomes 1. Monitor patients regularly for reduction in severity of identified target symptoms and presence of side effects. 2. Ask patients about their satisfaction with the management of their allergic rhinitis. 3. Management should result in minimal disruption to their normal lifestyle. 4. The Medical Outcomes Study 36-Item Short Form Health Survey and the Rhinoconjunctivitis Quality of Life Questionnaire measure symptom improvement and parameters such as sleep quality, nonallergic symptoms (eg, fatigue and poor concentration), emotions, and participation in a variety of activities. References: Pharmacotherapy Handbook 10th edition by Joseph Dipiro Basic and Clinical Pharmacology 14th Edition by Bertram Katzung Additional Resources: 1. Allergic Rhinitis from Osmosis 2. Rhinitis Medicamentosa