Lecture 20 - Asthma and COPD

‭Asthma‬ ‭Pathophysiology‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭●‬ ‭●‬ ‭ llergen starts inflammatory process‬ A ‭Binds to mast cells and IgE antibodies‬ ‭Mediators can cause immediate bronchospasm and immune response simultaneously‬ ‭Promote infiltration and inflammatory response‬ ‭Inflammatory cells release their own mediators, causing smooth muscle hypertrophy‬ ‭Leads to bronchial hyperreactivity (more reactivity, more bronchospasm)‬ ‭S/S‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭●‬ ‭ ense of breathlessness‬ S ‭Chest tightening‬ ‭Wheezing‬ ‭Dyspnea‬ ‭Cough‬ ‭Treatment Goals‬ ‭‬ H ● ‭ ighly treatable‬ ‭●‬ ‭Reducing impairment: Decrease S/S to maintain normal pulmonary function‬ ‭●‬ ‭Reducing risk: Focus on preventing recurrent exacerbations‬ ‭Non-Pharmacological Management of Chronic Asthma‬ ‭‬ R ● ‭ educe exposure to allergens and triggers‬ ‭●‬ ‭Sources of allergens: House dust mites, pets, cockroaches, mold‬ ‭●‬ ‭Factors that can exacerbate asthma: Tobacco smoke, wood smoke, household sprays‬ ‭Chronic Obstructive Pulmonary Disease (COPD)‬ ‭Pathophysiology‬ ‭ ‬ I‭ rreversible, progressive disorder that results from smoking and exposure to air pollution‬ ● ‭●‬ ‭Two pathologic processes; one can be more significant than the other‬ ‭Chronic Bronchitis‬ ‭‬ C ● ‭ hronic cough and excessive sputum production‬ ‭●‬ ‭Results from hypertrophy of mucous-secreting glands in the epithelium of larger airways‬ ‭●‬ ‭Causes mucus-plugging and inflammation‬ ‭Emphysema‬ ‭‬ E ● ‭ nlargement of the air space within the bronchioles and alveoli‬ ‭●‬ ‭Caused by deterioration of the walls of these air spaces‬ ‭●‬ ‭Results in less surface area for gas exchange‬ ‭S/S‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭●‬ ‭ hronic cough‬ C ‭Excessive sputum production‬ ‭Wheezing‬ ‭Dyspnea‬ ‭Poor exercise tolerance‬ ‭Treatment Goals‬ ‭‬ R ● ‭ educe symptoms: Improve the patient’s health status and exercise tolerance‬ ‭●‬ ‭Reduce risks and mortality: Prevent progression of COPD and manage exacerbations‬ ‭Pharmacologic Treatment of Reactive Airway Disease‬ ‭Goals of Drug Therapy‬ ‭‬ D ● ‭ ecrease inflammation‬ ‭●‬ ‭Relieve symptoms‬ ‭Two Main Pharmacologic Classes‬ ‭‬ A ● ‭ nti-inflammatory agents: Glucocorticoids‬ ‭●‬ ‭Bronchodilators: Beta-2 agonists‬ ‭Administration of Drugs via Inhalation‬ ‭Advantages‬ ‭‬ T ● ‭ herapeutic effects are enhanced‬ ‭●‬ ‭Systemic effects are minimized‬ ‭●‬ ‭Relief of acute attacks is rapid (by bronchodilators)‬ ‭Devices for Delivery‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭ etered-dose inhalers (MDIs)‬ M ‭Respimats‬ ‭Dry-powder inhalers (DPIs)‬ ‭Nebulizers‬ ‭Anti-Inflammatory Drugs: Glucocorticoids‬ ‭Mechanism of Action‬ ‭●‬ D ‭ ecrease synthesis and release of inflammatory mediators (leukotrienes, histamine,‬ ‭prostaglandins)‬ ‭●‬ ‭Reduce infiltration and activity of inflammatory cells (eosinophils, leukocytes)‬ ‭Inhaled Glucocorticoids‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭ rototype: Beclomethasone (Qvar)‬ P ‭First-line therapy for managing inflammatory component of asthma and COPD‬ ‭Generally used daily‬ ‭Effective and safer than systemic glucocorticoids‬ ‭Adverse Effects‬ ‭●‬ ‭Oropharyngeal candidiasis and/or dysphonia‬ ‭○‬ ‭Rinse and gargle after use‬ ‭○‬ ‭Use a spacer‬ ‭●‬ ‭Adrenal suppression‬ ‭●‬ ‭Bone loss‬ ‭●‬ ‭Slows growth in children/adolescents but does not decrease overal adult height‬ ‭Nursing Implications/Patient Education‬ ‭‬ F ● ‭ or long-term suppression of inflammation; not PRN‬ ‭●‬ ‭Teach how to properly use device (MDI, DPI, nebulizer)‬ ‭●‬ ‭Minimize adverse effects by:‬ ‭○‬ ‭Rinsing and gargling after use‬ ‭○‬ ‭Risk of adrenal suppression‬ ‭●‬ ‭Minimize risk of bone loss by:‬ ‭○‬ ‭Vitamin D/calcium intake‬ ‭○‬ ‭Weight-bearing exercise‬ ‭Oral Glucocorticoids‬ ‭●‬ ‭Prototype: Prednisone/prednisolone‬ ‭Therapeutic Use‬ ‭‬ M ● ‭ oderate-severe persistent asthma‬ ‭●‬ ‭Management of acute exacerbations of asthma or COPD‬ ‭●‬ ‭Treatment should be as brief as possible‬ ‭Adverse Effects‬ ‭Short-Term Therapy‬ ‭●‬ ‭Less than 10 days‬ ‭●‬ ‭GERD‬ ‭●‬ ‭Increased appetite‬ ‭Long-Term Therapy‬ ‭●‬ ‭More than 10 days‬ ‭●‬ ‭Most concerning: Adrenal suppression‬ ‭○‬ ‭Decreases the ability of the adrenal cortex to produce endogenous glucocorticoids‬ ‭○‬ ‭Can be life-threatening in times of physiologic stress/trauma‬ ‭○‬ ‭Discontinuation of treatment or switching to an inhaled glucocorticoids requires‬ ‭titration of oral dose‬ ‭●‬ ‭Most common: Osteoporosis‬ ‭○‬ ‭Suppresses calcium absorption and inhibits bone formation‬ ‭●‬ ‭Hyperglycemia‬ ‭●‬ ‭Peptic ulcer disease‬ ‭●‬ ‭Growth suppression in young patients‬ ‭Nursing Implications/Patient Education‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭●‬ ‭ hort-term use‬ S ‭Risk of adrenal suppression‬ ‭No abrupt discontinuation‬ ‭Additional glucocorticoids may be needed in times of stress/trauma‬ ‭Minimize risk of bone loss by:‬ ‭○‬ ‭Vitamin D/calcium intake‬ ‭○‬ ‭Baseline bone density‬ ‭Other Anti-Inflammatory Agents‬ ‭Leukotriene Modifiers‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭●‬ ‭ rototype: Montelukast (Singulair)‬ P ‭Second-line agents‬ ‭Suppress effects of leukotrienes‬ ‭Generally well tolerated‬ ‭Daily oral administration‬ ‭Mechanism of Action‬ ‭‬ B ● ‭ locks receptor activation by the body’s leukotrienes‬ ‭●‬ ‭Suppresses inflammatory response and smooth muscle constriction‬ ‭Therapeutic Indication‬ ‭‬ T ● ‭ reatment and prophylaxis of asthma and COPD‬ ‭●‬ ‭Exercise-induced bronchospasm‬ ‭●‬ ‭Allergic rhinitis‬ ‭Adverse Effects‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭ eported in post-marketing‬ R ‭Depression‬ ‭Mood changes‬ ‭Suicidality (rare)‬ ‭Mast Cell Stabilizers‬ ‭●‬ ‭Prototype: Cromolyn sodium (Cromolyn)‬ ‭Mechanism of Action‬ ‭‬ S ● ‭ tabilizes cytoplasmic membrane of mast cells‬ ‭●‬ ‭Prevents release of histamine and other mediators to suppress inflammation‬ ‭Therapeutic Use‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭ rophylaxis‬ P ‭Second-line choice for mild-moderate chronic asthma‬ ‭Exercise-induced bronchospasm‬ ‭Allergic rhinitis‬ ‭Route‬ ‭●‬ ‭Inhalation, nebulizer‬ ‭Adverse Effects‬ ‭‬ S ● ‭ afest of all anti-asthma medications, but not as effective as glucocorticoids‬ ‭●‬ ‭Cough, bronchospasm‬ ‭Patient Education‬ ‭‬ ● ‭●‬ ‭●‬ ‭●‬ ‭ rug is for acute and long-term prophylaxis of asthma‬ D ‭How to use a nebulizer‬ ‭May take several weeks for therapeutic effect to develop for long-term prophylaxis‬ ‭Administer 15 minutes prior to exercise‬ ‭Bronchodilators‬ ‭‬ P ● ‭ rovide symptomatic relief but do not alter the underlying disease process (inflammation)‬ ‭●‬ ‭Conjunctive therapy with a glucocorticoid for long-term suppression of inflammation‬ ‭Beta-2 Adrenergic Agonists‬ ‭‬ S ● ‭ hort-acting beta-2 agonists‬ ‭●‬ ‭Long-acting beta-2 agonists‬ ‭●‬ ‭Oral/systemic agents‬ ‭Mechanism of Action‬ ‭●‬ ‭Activation of beta-2 receptors in pulmonary smooth muscle to promote bronchodilation‬ ‭○‬ ‭Usually activated by endogenous catecholamines‬ ‭Beta-2 Receptor Locations‬ ‭●‬ ‭Lungs‬ ‭●‬ ‭Heart‬ ‭●‬ ‭Smooth muscle vasculature‬ ‭●‬ ‭Uterus‬ ‭●‬ ‭Liver‬ ‭●‬ ‭Kidneys‬ ‭Short-Acting Beta-2 Agonists (SABAs)‬ ‭‬ P ● ‭ rototype: Albuterol (Proventil)‬ ‭●‬ ‭Rescue inhalers designed for PRN use‬ ‭●‬ ‭Effects are immediate and last 30-60 minutes‬ ‭Mechanism of Action‬ ‭●‬ ‭Mimics catecholamines to active beta-2 receptors in the smooth muscle of the lung‬ ‭●‬ ‭Promote bronchodilation‬ ‭Indications/Administration‬ ‭●‬ ‭Acute/ongoing attack: Nebulizer administration most effective‬ ‭●‬ ‭Exercise-induced asthma: Prior to exercise to prevent an attack‬ ‭Adverse Effects‬ ‭●‬ ‭Minimal, but generally systemic: Tachycardia, angina, tremors‬ ‭●‬ ‭Use in excess: Tachycardia, angina, seizures, cardiac arrest (leading to death)‬ ‭Nursing Implications‬ ‭●‬ ‭If a patient is using a SABA more than twice weekly, asthma is not well managed‬ ‭Long-Acting Beta-2 Agonists (LABAs)‬ ‭‬ P ● ‭ rototype: Salmeterol (Serevent)‬ ‭●‬ ‭Prolonged effect over 12 hours‬ ‭Use in Asthma and COPD‬ ‭●‬ ‭Long-term control in patients who experience frequent attacks‬ ‭●‬ ‭Dosing is on a fixed schedule‬ ‭●‬ ‭Preferred treatment in stable COPD‬ ‭●‬ ‭When used to treat asthma, must always be combined with a glucocorticoid‬ ‭○‬ ‭Monotherapy is contraindicated in asthma patients‬ ‭Adverse Effects‬ ‭●‬ ‭Increased risk of severe attack/death in both inhaled and oral preparations‬ ‭Inhaled Preparations‬ ‭●‬ ‭Can have systemic effects if used excessively‬ ‭●‬ ‭Tachycardia, angina, tremors‬ ‭Oral Preparations‬ ‭●‬ ‭Terbutaline, albuterol‬ ‭●‬ ‭Non-selectivity can cause activation of both beta-1 and beta-2 receptors‬ ‭●‬ ‭Beta-1 effects: Angina, tachydysrhythmias‬ ‭●‬ ‭Beta-2 effects: Tremors, uterine relaxation‬ ‭Patient Education‬ ‭●‬ ‭How to use device‬ ‭○‬ ‭Hand/breath coordination issue‬ ‭○‬ ‭1 minute between dose administration‬ ‭●‬ ‭LABAs are not for aborting attacks‬ ‭●‬ ‭Report symptoms of tachydysrhythmias and/or angina pain‬ ‭Methylxanthines‬ ‭‬ P ● ‭ rototypes: Theophylline, caffeine‬ ‭●‬ ‭Prolonged effect compared to beta-2 agonists‬ ‭Mechanism of Action‬ ‭●‬ ‭Produces bronchodilation by relaxing smooth muscle of the bronchi‬