Respiratory Module #5 PDF

Summary

This document is a lecture presentation on respiratory topics, including Upper Respiratory Tract Infections (URIs), Common Cold, Causes, Goals of Drug Therapy, Decongestants, Expectorants, Antitussives, Antiinflammatories, and more. The presentation was delivered at Downstate Health Sciences University.

Full Transcript

Respiratory NRMS 5110 Advanced Pharmacology Jessica Dong, DNP, FNP-BC Upper Respiratory Tract Infections (URIs) Common Cold Aka acute infectious rhinitis, nasopharyngitis, rhinopharyngitis, or acute coryza Signs and symptoms Nasal congestion and discharge Sneezing; postnasal drip Fullnes...

Respiratory NRMS 5110 Advanced Pharmacology Jessica Dong, DNP, FNP-BC Upper Respiratory Tract Infections (URIs) Common Cold Aka acute infectious rhinitis, nasopharyngitis, rhinopharyngitis, or acute coryza Signs and symptoms Nasal congestion and discharge Sneezing; postnasal drip Fullness and tenderness over the sinuses Fever, headache Malaise, myalgia Sore throat, coughing Full feeling around the eyes and ears Common Cold: Causes Human rhinovirus (most common) Coronavirus Respiratory syncytial virus Influenza virus Human parainfluenza virus Human metapneumovirus Adenovirus Goals of Drug Therapy Relief of symptoms Reduction of the risk for complications Prevention of spread to others Decongestants Somewhat effective for the short-term relief of cold symptoms Topical decongestants should be used for 3 days; may cause rebound congestion Topical decongestants Nasal spray and pump mist preparations  Oxymetazoline hydrochloride (Afrin)  Phenylephrine hydrochloride (Afrin Children’s, Little Remedies, Neo- Synephrine) Oral decongestants  Pseudoephedrine (Sudafed)  Phenylephrine (Sudafed PE) Decongestants Mechanism of Action Sympathomimetic agents; stimulate alpha- and beta-adrenergic receptors, cause vasoconstriction in the respiratory tract mucosa to improve ventilation Contraindications Patients with narrow-angle glaucoma, severe uncontrolled hypertension, and coronary artery disease Patients who have taken monoamine oxidase (MAO) inhibitors within 14 days Caution in patients with hypertension, cardiovascular disease, renal impairment, hyperthyroidism, diabetes, prostatic hypertrophy, and urinary incontinence Adverse Events Increased blood pressure and heart rate, palpitations Headaches, dizziness Gastrointestinal (GI) upset Tremor, insomnia Expectorants  Guaifenesin (Antitussin, Mucinex, Robitussin) Available in both liquid and tablet oral preparations Use of guaifenesin should generally not last beyond 1 week Mechanism of Action Increase the output of respiratory tract fluid by decreasing the adhesiveness and surface tension of the respiratory tract, facilitate the removal of viscous mucous Adverse Events Drowsiness, headache, dizziness, GI upset Antitussives  Dextromethorphan (Delsym)  Benzonatate (Tessalon Perles) Available in oral preparations (liquids, gels, capsules, lozenges, sublingual strips) Minimal benefit with the common cold; may reduce cough frequency and help achieve sleep Mechanism of Action Cough suppressants: diminish the cough reflex by direct inhibition of the cough center in the medulla Contraindications Patients who have have taken MAO inhibitors within 2 weeks Adverse Events Dizziness, nausea, drowsiness Antiinflammatories and Analgesics Cyclooxygenase inhibitors: such as nonsteroidal antiinflammatory drugs (NSAIDs)  Naproxen (Naprosyn, Aleve)  Available as oral tablet or suspension  This is the NSAID of choice in the American College of Clinical Pharmacy guidelines because it does not impact viral shedding Mechanism of Action Inhibit prostaglandin secretions to reduce headache, malaise, myalgias, cough, and even sneezing Antiinflammatories and Analgesics Contraindications Caution in patients with active peptic ulcers or GI bleeds, bleeding disorders, asthma, severe hepatic impairment, severe renal impairment (CrCl2 days/week, but Daily Throughout the day not daily Nighttime ≤2 times/month 3–4 times/month >Once a week, but Often 7 times/week awakenings not nightly SABA used to control ≤2 days/week >2 days/week, but Daily Several times a day symptoms (but not to not daily, and not prevent exercise- more than once a day induced bronchospasm) Effect on normal None Minor limitation Some limitation Severe limitation activity Lung function tests Normal FEV1 between FEV1 >80% of FEV1 >60% but predicted; 5% FEV1/FVC normal Asthma Drug Therapy All patients with an asthma diagnosis should receive an ICS-containing controller drug, either as needed for mild asthma or daily for more severe asthma to reduce the risk of asthma-related exacerbation, hospitalization, and death. Stepping-up controller drugs are recommended for uncontrolled asthma despite appropriate inhaler technique and good drug adherence. Stepping-down controller drugs are recommended for persons with good asthma control for about 3 months. Step 1 As needed low-dose ICS- formoterol Step 2 As needed low-dose ICS- formoterol or Daily low-dose ICS  plus as needed low-dose ICS-formoterol Step 3 Low-dose ICS-LABA  plus as needed low-dose ICS-formoterol Step 4 Medium-dose ICS-LABA  plus as needed low-dose ICS-formoterol Step 5 High-dose ICS-LABA Add on therapies: tiotropium, anti- IgE, anti-LK-5/5R, anti-IL-4R Refer for phenotype assessment  plus as needed low-dose ICS-formoterol Classification of COPD Gold A As needed SABA or SAMA  plus patient education and vaccination, smoking cessation Gold B Daily LABA or LAMA  plus as needed SABA or SAMA, patient education and vaccination, smoking cessation, pulmonary rehabilitation, oxygen Gold C Daily LABA or LAMA  plus as needed SABA or SAMA, patient education and vaccination, smoking cessation, pulmonary rehabilitation, theophylline, oxygen Gold D Daily LABA/LAMA combo  plus as needed SABA or SAMA, patient education and vaccination, smoking cessation, pulmonary rehabilitation, theophylline, PDE-4 inhibitor, macrolide antibiotic, oxygen, surgical interventions, palliative care Allergies and Allergic Reactions Allergy: an exaggerated immune response resulting from an antibody– antigen reaction (causing inflammation and tissue damage)  Antibodies (aka immunoglobulins): bind to foreign substances and remove it from the circulation  Invasion or contact with a foreign substance results in the production and secretion of antibodies  A foreign substance is an antibody generator—known as an antigen (aka allergen)  Allergens can be food based, chemical, or environmental  The exaggerated response to an antigen—is referred to as a hypersensitivity Anergy: the unexpected failure of the immune system to respond to the challenge of a foreign substance (antigen or allergen) Classification of Allergic Reactions Coombs and Gell Classification Type I hypersensitivity reactions: (immediate reactions; IgE mediated) Type II hypersensitivity reactions: (cytotoxic reactions; IgG/IgM) Type III hypersensitivity reactions: (immune complex reactions; IgG/IgM) Type IV hypersensitivity reactions: (delayed-type reactions; T-cell mediated) Type I Hypersensitivity Reactions Type I hypersensitivity reactions: (immediate reactions; IgE mediated) Involve the interaction between an antigen and a specific immunoglobulin (Ig) E antibody These antibodies are bound to mast cells and basophils When an antigen binds to these antibodies, the cell releases histamine, leukotrienes, and prostaglandins  vasodilation and increase capillary permeability, allowing eosinophils and other inflammatory cells to infiltrate tissues The first contact results in the formation of the antibody. The subsequent contact with the same antigen results in the antibody– antigen reaction, resulting in this type 1 hypersensitivity reaction. The antibody–antigen reaction triggers the immune response, which results in allergic symptoms (can affect the airways, eyes, skin, or entire body) Examples: anaphylaxis, asthma, allergic rhinitis Type II Hypersensitivity Reactions Type II hypersensitivity reactions: (cytotoxic reactions; IgG/IgM) Occur when antibodies (IgG/IgM) react with an antigenic component of a cell The antibody–antigen reaction activates killer T cells or macrophages against antigens on the cell This leads to direct cytotoxic action or complement-mediated lysis Examples: transfusion reactions, hemolytic anemias Type III Hypersensitivity Reactions Type III hypersensitivity reactions: (immune complex reactions; IgG/IgM) Result from immune complexes that activate the complement system Immune complexes of antibody and antigen are deposited in the tissue The complement system is activated, and polymorphonuclear leukocytes are attracted to the site of the complex, causing local tissue damage Examples: autoimmune disease, systemic lupus erythematosus (SLE) Type IV Hypersensitivity Reactions Type IV hypersensitivity reactions: (delayed-type reactions; T-cell mediated) These cell-mediated reactions are the result of sensitized T lymphocytes coming into contact with a specific antigen Antigen-sensitized T cells release inflammatory substances after a second contact with the same antigen The delayed reaction typically takes 2 to 3 days or up to a week Examples: tuberculin skin test, contact dermatitis (poison ivy), allergic dermatitis Anaphylaxis and Anaphylactoid Reactions Anaphylaxis is a type I hypersensitivity reaction involving IgE- mediated release of histamine, leukotrienes, and other mediators from already sensitized mast cells and basophils.  Release of these mediators results in symptoms of angioedema, flushing, pruritus, urticaria, nausea, vomiting, and wheezing  Onset of the reaction is quick, generally within 1 to 30 minutes Anaphylactoid reactions are non-IgE mediated, and the agent causes a direct release of histamine and other inflammatory toxins  Similar in appearance to anaphylaxis but may occur after the first injection of certain drugs and contrast media.  Example of anaphylactoid reaction: “red man syndrome” with vancomycin Treatment of anaphylactic symptoms: IM epinephrine (1 mg/mL preparation)  0.2-0.5 mL in adults; 0.3 mL maximum for children  May be repeated every 5 to 15 minutes as necessary Allergic Rhinitis Allergic rhinitis is an airway allergy. Can be seasonal or perennial.  Seasonal allergies (hay fever)  Perennial allergies Causes: pollen (grass, trees, weeds), dust mites, mold spores, enzymes (in detergents), and insect body parts Allergic Rhinitis Signs and symptoms Ocular pruritus (itching of the eyes) Swelling and watery discharge from the eyes Conjunctival inflammation (inflammation of the membrane lining the eyelids) Allergic shiners (dark circles under the eyes) Rhinorrhea Nasal congestion Nasal pruritus Pale, swollen nasal mucous membranes Irritability, lethargy, fatigue Allergic Rhinitis Treated through avoidance of the allergen, pharmacologic agents, and immunotherapy Avoidance of the allergen (reduced exposure of allergen)  use of air conditioners, dehumidifiers, air purifiers, encasing mattresses, washing bedding in very hot water, removing carpeting and upholstered furniture, and removing pets from the home if allergic Allergic Rhinitis Pharmacologic agents: antihistamines, nasal decongestants, and intranasal corticosteroids  Nonsedating antihistamines  Cetirizine (Zyrtec)  Fexofenadine (Allegra)  Loratadine (Claritin)  Nasal decongestants  Oxymetazoline (Afrin)  Phenylephrine (Neo-Synephrine)  Pseudoephedrine  Intranasal Corticosteroids  Ciclesonide (Omnaris)  Fluticasone furoate (Flonase Sensimist)  Fluticasone propionate (Flonase Allergy Relief)  Mometasone (Nasonex 24HR Allergy) Allergic Rhinitis Immunotherapy (aka desensitization, hyposensitization, or allergy shots)  Repeated subcutaneous injections of gradually increasing concentrations of the allergens responsible for the patient’s allergy symptoms, patients must have documented IgE antibodies to these allergens  Clinical benefit related to administration of high doses of allergens weekly or every other week.  The duration of treatment is typically 3 to 5 years, but if there is no improvement after first year, immunotherapy is discontinued References Poole, Virginia. (2022). Pharmacotherapeutics for Advanced Practice: A Practical Approach (5th ed.). Wolters Kluwer Health.

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