Allergic Rhinitis IP3 Rat3 PDF

Answers to Objectives 1-20 1. Define rhinitis, allergic rhinitis, and allergic conjunctivitis. ​ ​ Rhinitis: Inflammation of the nasal mucous membrane with symptoms like nasal congestion, rhinorrhea, sneezing, and itching. ​ ​ Allergic Rhinitis: An IgE-mediated inflammatory response of t...

Answers to Objectives 1-20 1. Define rhinitis, allergic rhinitis, and allergic conjunctivitis. ​ ​ Rhinitis: Inflammation of the nasal mucous membrane with symptoms like nasal congestion, rhinorrhea, sneezing, and itching. ​ ​ Allergic Rhinitis: An IgE-mediated inflammatory response of the nasal mucous membranes after exposure to inhaled allergens. ​ ​ Allergic Conjunctivitis: Inflammation of the conjunctiva caused by an IgE-mediated response, associated with itching, redness, and tearing. 2. Differentiate the definitions of perennial allergic rhinitis, seasonal allergic rhinitis, and episodic allergic rhinitis. ​ ​ Seasonal Allergic Rhinitis: Occurs in response to allergens present at specific times of the year (e.g., tree, grass, and weed pollens). ​ ​ Perennial Allergic Rhinitis: Occurs year-round due to constant exposure to allergens like mold spores, house dust mites, animal dander, and cockroaches. ​ ​ Episodic Allergic Rhinitis: Occurs after sporadic exposures to allergens not commonly encountered in the patient’s environment. 3. Differentiate the allergens causing perennial allergic rhinitis and seasonal allergic rhinitis. ​ ​ Seasonal Allergic Rhinitis: Caused by tree pollens (spring), grass pollens (late spring to early summer), and weed pollens (late summer to early fall). ​ ​ Perennial Allergic Rhinitis: Caused by mold spores, house dust mite fecal proteins, animal dander, and cockroaches. 4. Predict the allergens causing symptoms in a patient when given a patient who experiences worsening of symptoms in a given season. ​ ​ Spring: Tree pollens ​ ​ Late Spring to Early Summer: Grass pollens ​ ​ Late Summer to Early Fall: Weed pollens. 5. List the risk factors for allergic rhinitis. ​ ​ Family history of atopy ​ ​ Higher socioeconomic status ​ ​ Higher serum IgE levels (>100 IU/mL) before age six ​ ​ Positive allergy skin prick test. 6. List the most common causes of drug-induced rhinitis. ​ ​ ACE inhibitors ​ ​ Aspirin and NSAIDs  ​ ​ α-receptor antagonists ​ ​ Clonidine ​ ​ Guanfacine ​ ​ Phosphodiesterase-5 selective inhibitors. 7. Describe the structure and function of the nasal cavity. The nasal cavity provides an airway for respiration, moistens and warms entering air, filters and cleans inspired air, serves as a resonating chamber for speech, and houses olfactory receptors. It is lined by a mucous membrane with goblet cells and serous glands that trap and destroy bacteria. 8. Explain the structure and function of the mucous membrane. The mucous membrane consists of an epithelium supported by connective tissue, coated with mucus secreted by goblet cells and mucous glands. It traps dust, bacteria, and debris, while serous fluid containing lysozyme destroys bacteria. 9. Illustrate the function of nasal turbinates and their impact on airflow through the nasal cavity. Nasal turbinates, also called nasal conchae, are mucosa-covered projections that increase surface area. They swell with blood flow, reducing airflow and causing nasal congestion. 10. Describe the structure and function of conjunctiva. The conjunctiva is a thin, transparent mucous membrane that lines the eyelids and covers the visible part of the eye, secreting oils and mucus to lubricate the eye. 11. Define hypersensitivity reaction. A hypersensitivity reaction is an injurious or pathologic immune response caused by an excessive or aberrant immune reaction. 12. Define the four types of hypersensitivity reactions, and provide an example for each. ​ 1.​ Type I (Immediate Hypersensitivity): IgE-mediated (e.g., allergic rhinitis, food allergies) ​ 2.​ Type II (Antibody-Mediated): Autoantibodies cause tissue injury (e.g., Graves’ disease) ​ 3.​ Type III (Immune Complex-Mediated): Immune complexes cause inflammation (e.g., systemic lupus erythematosus) ​ 4.​ Type IV (T cell-Mediated): T cells mediate autoimmune reactions (e.g., type 1 diabetes mellitus). 13. Define allergen. An allergen is a protein that elicits an allergic response. 14. Define sensitization and describe the process of sensitization. Sensitization is the process by which an individual becomes sensitive to an allergen. APCs present the allergen to CD4 T cells, which activate B cells to produce IgE. The IgE binds to mast cells and basophils, making them sensitive to future allergen exposure. 15. Explain the roles of mast cells, basophils, and eosinophils in allergic rhinitis. ​ ​ Mast Cells: Release histamine and other mediators during allergic reactions ​ ​ Basophils: Similar to mast cells, they release histamine upon activation  ​ ​ Eosinophils: Release toxic proteins that contribute to tissue damage and inflammation. 16. Describe the two phases of allergic rhinitis and explain what immunological processes are involved in each. ​ ​ Early Phase: Occurs within minutes; involves mast cell degranulation and release of histamine, prostaglandins, and leukotrienes. ​ ​ Late Phase: Occurs 4-8 hours later; involves recruitment of eosinophils and TH2 cells, causing prolonged inflammation. 17. Explain the biological mechanism for the following symptoms: ​ ​ Rhinorrhea: Parasympathetic stimulation of mucus secretion ​ ​ Nasal Itching and Sneezing: Histamine activation of sensory nerves ​ ​ Nasal Congestion: Vasodilation and increased vascular permeability ​ ​ Allergic Conjunctivitis: Allergen-induced vasodilation and edema in the conjunctiva. 18. Define the role of TH2 cells in allergic rhinitis. TH2 cells secrete cytokines like IL-4 and IL-13, which promote IgE production and eosinophil recruitment. 19. Describe the role of histamine in allergic rhinitis and explain its mechanism of action. Histamine binds to H1 receptors, causing vasodilation, increased vascular permeability, smooth muscle contraction, and stimulation of sensory nerves, leading to symptoms like sneezing, itching, and nasal congestion. 20. List the symptoms of allergic rhinitis and review the findings on physical exam for a patient with allergic rhinitis. ​ ​ Symptoms: Clear rhinorrhea, sneezing, nasal congestion, pruritic ears/nose/palate, allergic conjunctivitis. ​ ​ Physical Exam Findings: Transverse nasal crease, allergic shiners, pale nasal mucosa. Let me know if you need further objectives answered! I’ll now extract and answer objectives 21-48 from the document. Please hold on. Answers to Objectives 21-48 21. List the complications of allergic rhinitis. ​ ​ Inability to sleep ​ ​ Fatigue ​ ​ Poor work or school efficiency ​ ​ Postnasal drip with cough ​ ​ Loss of smell or taste ​ ​ High-arched, V-shaped palate ​ ​ Permanent transverse crease across the nose ​ ​ Dark circles under the eyes  ​ ​ Asthma ​ ​ Recurrent and chronic sinusitis ​ ​ Epistaxis (nosebleed) ​ ​ Nasal polyps ​ ​ Sleep apnea. 22. Differentiate the available allergen tests. ​ 1.​ Epicutaneous Skin Test (Scratch/Prick Test): ​ ​ Fast, least expensive, positive within 15-30 minutes. ​ 2.​ Intradermal Skin Test: ​ ​ Injects diluted allergen, used if epicutaneous tests are negative. ​ 3.​ Radioallergosorbent Test (RAST): ​ ​ In vitro, more expensive, less sensitive than skin tests. 23. Describe the nonpharmacotherapy patient counseling points for patients with allergic rhinitis. ​ ​ Identify and avoid triggers when practical. ​ ​ Reduce mold growth by keeping household humidity below 50%. ​ ​ Use impermeable covers for mattresses and pillows. ​ ​ Wash bed linens in hot water. ​ ​ Use washable rugs instead of carpeting. ​ ​ Use HEPA filters to remove allergens. ​ ​ Wear masks during outdoor activities during pollen season. ​ ​ Use saline irrigation for nasal clearance. 24. Explain the rationale for intranasal drug delivery including advantages of intranasal drug delivery for management of allergic rhinitis. ​ ​ Delivers medication directly to the site of inflammation (nasal tissue). ​ ​ Minimizes systemic drug exposure, reducing adverse effects. 25. List the patient counseling points for intranasal drug delivery. ​ 1.​ Clear nasal passages before administration. ​ 2.​ Avoid blowing the nose for 10 minutes after administration. ​ 3.​ Direct the spray away from the nasal septum. ​ 4.​ Do not use in patients with recent nasal surgery or trauma.  ​ 5.​ Local irritation may occur initially. 26. Match drugs to their pharmacologic classes. ​ ​ First Generation Antihistamines: Diphenhydramine, Chlorpheniramine ​ ​ Second Generation Antihistamines: Loratadine, Cetirizine ​ ​ Intranasal Antihistamines: Azelastine ​ ​ Intranasal Corticosteroids: Fluticasone, Mometasone ​ ​ Mast Cell Stabilizer: Cromolyn ​ ​ Sympathomimetic Decongestants: Pseudoephedrine, Phenylephrine ​ ​ Leukotriene Receptor Antagonist: Montelukast. 27. Predict the pharmacologic response of blockade of H1 receptors in the central and peripheral nervous systems. ​ ​ Peripheral: Reduces allergic symptoms like sneezing, rhinorrhea, and itching. ​ ​ Central: Causes sedation and drowsiness. 28. Describe the difference between first and second generation antihistamines with regard to drug distribution and autonomic receptor selectivity. ​ ​ First Generation: Cross the blood-brain barrier, cause sedation, block muscarinic receptors leading to anticholinergic effects. ​ ​ Second Generation: Do not cross the blood-brain barrier significantly, less sedative, minimal anticholinergic effects. 29. Predict the adverse effects of medications used to treat allergic rhinitis and differentiate between the adverse effect profiles of first and second generation oral antihistamines. ​ ​ First Generation: Sedation, drowsiness, anticholinergic effects (dry mouth, urinary retention). ​ ​ Second Generation: Less sedation, minimal anticholinergic effects. 30. Differentiate first generation antihistamines by chemical class. ​ ​ Ethanolamine Ether: Diphenhydramine ​ ​ Alkyl Amine: Chlorpheniramine ​ ​ Phenothiazine: Promethazine. 31. Describe the chemical relationship between loratadine and desloratadine. Desloratadine is the active metabolite of loratadine, formed by CYP3A4 metabolism. 32. Rank first generation antihistamines by relative sedative effects. ​ ​ Most sedating: Promethazine, Diphenhydramine ​ ​ Least sedating: Brompheniramine, Chlorpheniramine. 33. Predict the effect of peripheral α-adrenergic receptor activation on tissues controlled by the autonomic nervous system.  ​ ​ Causes vasoconstriction, reducing blood flow and congestion. 34. Explain how α-1 adrenergic agonists are effective for relieving congestion. ​ ​ Bind to α-1 receptors in vascular smooth muscle, causing vasoconstriction and reduced nasal swelling. 35. Identify neurotransmitters that pseudoephedrine and phenylephrine mimic and explain why this is an effective drug design strategy. ​ ​ Mimic norepinephrine and epinephrine, selectively activating α-1 receptors to reduce nasal congestion. 36. Define rhinitis medicamentosa and conjunctivitis medicamentosa, explain their mechanisms, and describe patient counseling points. ​ ​ Rhinitis Medicamentosa: Rebound congestion from prolonged use of intranasal decongestants. ​ ​ Conjunctivitis Medicamentosa: Rebound hyperemia from prolonged use of ophthalmic vasoconstrictors. ​ ​ Counseling: Limit use to 3 days for intranasal decongestants and 10 days for ophthalmic vasoconstrictors. 37. Describe the general mechanism by which all corticosteroids work. Corticosteroids block immune mediator release, reduce neutrophil chemotaxis, decrease edema, and inhibit mast cell-mediated reactions. 38. Describe the effect of corticosteroids on inflammatory and immunologic processes common to allergic rhinitis. ​ ​ Reduce inflammation by inhibiting cytokine production and immune cell recruitment. 39. Explain the difference in risk for HPA axis suppression between intranasal, ophthalmic, and systemic corticosteroids. ​ ​ Systemic: High risk of HPA axis suppression. ​ ​ Intranasal and Ophthalmic: Minimal risk due to low systemic absorption. 40. Explain why pseudoephedrine is more effective than phenylephrine when taken as an oral dosage form. Pseudoephedrine undergoes less first-pass metabolism, resulting in higher bioavailability. 41. Explain the mechanisms exhibited by intranasal antihistamines and how these differ from oral antihistamines. ​ ​ Intranasal antihistamines provide localized action and additional mast cell stabilizing effects, while oral antihistamines act systemically. 42. Describe immunotherapy for the management of allergic rhinitis, including adverse effects and good/poor candidates. ​ ​ Adverse Effects: Local reactions, anaphylaxis ​ ​ Good Candidates: Severe symptoms unresponsive to other treatments ​ ​ Poor Candidates: Uncontrolled asthma, cardiovascular disease. 43. Differentiate subcutaneous immunotherapy and sublingual immunotherapy.  ​ ​ Subcutaneous: More allergens covered, longer-lasting effects. ​ ​ Sublingual: No injections, can be administered at home. 44. Identify the metabolism profile of a drug that may have a pharmacokinetic interaction with antihistamines. Second generation antihistamines are metabolized by CYP3A4, and inhibitors of this enzyme may increase their levels. 45. Identify the general type of drug that may have a pharmacodynamic interaction with antihistamines. CNS depressants like ethanol and benzodiazepines can interact with antihistamines, increasing sedation. 46. List complementary medications considered possibly effective and safe for allergic rhinitis and describe their proposed mechanism of action. ​ ​ Butterbur: Decreases histamine and leukotriene levels. ​ ​ Tinospora cordifolia: Reduces mast cell histamine release. 47. Select the most appropriate medication for a patient case of allergic rhinitis. Selection depends on symptom severity, comorbidities, and patient preference. Intranasal corticosteroids are often first-line. 48. Identify the drugs of choice for the management of allergic rhinitis during pregnancy. ​ ​ Second-generation antihistamines (loratadine, cetirizine) ​ ​ Intranasal corticosteroids (budesonide) ​ ​ Intranasal cromolyn.