Asthma - Pharmacotherapy Guide PDF

Asthma Objectives 1.Describe the subjective and objective assessments used to characterize a clinical presentation of asthma. 2.Explain the Th1 and Th2 imbalance and its relationship to asthma. 3.List the factors that initiate, intensify, and modulate the inflammatory responses in the airways. 4....

Asthma Objectives 1.Describe the subjective and objective assessments used to characterize a clinical presentation of asthma. 2.Explain the Th1 and Th2 imbalance and its relationship to asthma. 3.List the factors that initiate, intensify, and modulate the inflammatory responses in the airways. 4.Describe factors that contribute to asthma severity. 5.Identify the advantages and disadvantages of the various pulmonary drug delivery devices. 6.Differentiate the role of the short-acting β2-agonists, anticholinergics, and systemic corticosteroids for management of acute severe asthma. 7.Differentiate the role long-acting and short-acting β2-agonists serve in the treatment of asthma. 8.Contrast the bronchodilator mechanisms of anticholinergics and β2-agonists. Objectives 9. Describe actions related to inhaled corticosteroids that are beneficial in the treatment of asthma. 10. Recommend nonpharmacologic therapy beneficial in the management of asthma. 11. Define components that determine the severity of impairment related to asthma. 12. Recommend a treatment plan based on current asthma symptoms. 13. Evaluate overall asthma control based on current asthma symptoms. 14. Discuss the role of biologic therapy in asthma. Introduction Global Initiative for Asthma (GINA) – updated yearly in summer Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness, and cough that vary over time and in intensity, together with variable expiratory airflow limitation. National Institutes of Health, National Asthma Education and Prevention Program (NAEPP) Expert Panel Report 3 (EPR3) …variable airflow obstruction is often reversible either spontaneously or with treatment, although reversibility may not be complete in some patients with asthma. Epidemiology 8.4% of US population affected Increasing prevalence – was 7.3% in 2001 Socioeconomic disparities Pediatric disease that may persist or resolve by adulthood Boys are more affected at younger age Women are more affected at adult age Despite the relatively low number of asthma deaths (0.19 per 1,000 persons with asthma), 80% to 90% are preventable. Etiology Epidemiologic studies strongly support the concept of a genetic predisposition (e.g., interleukin genes) plus environmental interaction (i.e., atopy) to the development of asthma. Environmental risk factors for the development of asthma include socioeconomic status, family size, exposure to secondhand tobacco smoke in infancy, and in utero, allergen exposure, ambient air pollution, urbanization, viral respiratory infections including respiratory syncytial virus (RSV) and rhinovirus, and decreased exposure to common childhood infectious agents. Altered immune response development Th2 > Th1 Factors that are associated with protecting against, or risk for, developing asthma. These various factors have relative degrees of importance from patient to patient. FLVR, Faecalibacterium, Lachnospira, Veillonella, and Rothia spp; HAV, hepatitis A; RV, rhinovirus; RSV, respiratory syncytial virus. (Reprinted, with permission, from van Tilburg Bernardes E, Arrieta MC. Hygiene hypothesis in asthma development: Is hygiene to blame? Arch Med Res. 2017;48:717–726.) Citation: Chapter 43 Asthma, DiPiro JT, Yee GC, Posey L, Haines ST, Nolin TD, Ellingrod V. Pharmacotherapy: A Pathophysiologic Approach, 11e; 2020. Available at: https://accesspharmacy.mhmedical.com/content.aspx?bookid=2577&sectionid=228901475 Accessed: February 15, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved  Pathophysiology Acute and chronic inflammation Activation of cells bearing allergen-specific immunoglobulin E (IgE) initiates the early phase reaction Rapid activation of airway mast cells and macrophages leading to the rapid release of pro-inflammatory mediators such as histamine, eicosanoids, and reactive O2 species that induce contraction of airway smooth muscle, mucus secretion, and edema Inflammatory mediators induce microvascular leakage with exudation of plasma in the airways promoting airway obstruction Induces a thickened, engorged, and edematous airway Reduce mucus clearance Promote the formation of exudative plugs mixed with mucus and inflammatory & epithelial cells Late-phase inflammatory reaction occurs 6 to 9 hours after allergen provocation and involves the recruitment and activation of eosinophils, CD4+ thymically derived lymphocytes (T cells), basophils, neutrophils, and macrophages Activation of T cells after allergen challenge leads to the release of Th 2- related cytokines that may modulate the late-phase response Pathophysiology Epithelial cells Participate in mucociliary clearance and removal of noxious agents; but also enhance inflammation In asthma, especially fatal asthma, extensive epithelial shedding occurs Eosinophils Release pro-inflammatory mediators, cytotoxic mediators, and cytokines Lymphocytes Th2 cells produce cytokines (IL-4, 5, and 13) that mediate allergic inflammation and inhibit production of Th1 cytokines Pathophysiology Neonates The T-cell population in the cord blood of newborn infants is skewed toward a Th 2 phenotype Imbalance may be corrected by exposure to pathogens (e.g., daycare attendance in first six months of life or having an older sibling) Imbalance may persist with frequent use of antibiotics or urban environment exposures Th1 and Th2 endotypes Th2 high asthma Interleukin activation  inflammatory cell activation and secretion of IgE Th2 low asthma Neutrophilic asthma or mixed, pauci-granulocytic asthma and is less well understood Patients are typically less responsive to corticosteroids, have fewer allergic symptoms, and are diagnosed later in life Pathophysiology Mast cells Once binding of allergen to cell-bound IgE occurs, mediators such as histamine; eosinophil and neutrophil chemotactic factors; LTs C4, D4, and E4; prostaglandins; platelet-activating factor (PAF); and others are released from mast cells Sensitized mast cells are also activated by osmotic stimuli to account for exercise-induced bronchospasm (EIB) Pathophysiology Alveolar macrophages Engulfing and digesting bacteria and other foreign materials Release pro-inflammatory and anti-inflammatory mediators Neutrophils Instrumental in the inflammation arising from occupational exposures such as particulate matter, ozone, and diesel exhaust Mechanism not clear; does release inflammation mediators Fibroblasts Inflammatory cells activated by interleukins Myofibroblasts Increased in numbers beneath the reticular basement membrane Pathophysiology Inflammatory mediators Histamine Induces smooth muscle constriction and bronchospasm and is thought to play a role in mucosal edema and mucus secretion Platelet activating factor (PAF) Bronchospasms, edema, chemotaxis of eosinophils Pathophysiology Inflammatory mediators Arachidonic acid and its metabolites – steroids block PLA Prostaglandins Promote bronchoconstriction, edema, vasodilation and inflammation Thromboxane A2 Bronchoconstriction and inflammation Product of prostaglandin metabolism by thromboxane synthase Leukotrienes – montelukast and monoclonal antibodies block leukotrienes LTs D4 and E4 share a common receptor (LTD4 receptor) that, when stimulated, produces bronchospasm, mucus secretion, microvascular permeability, and airway edema, whereas LTB4 is involved with granulocyte chemotaxis Corticosteroids Glucocorticoids – immune system response Mineralocorticoids – blood pressure response / electrolytes (retain sodium and eliminate potassium) Pathophysiology Adhesin molecules Glycoproteins that facilitate infiltration and migration of inflammatory cells to the site of inflammation Promotes activation of cells and cell–cell communication, and promoting cellular migration and infiltration Mucus production Produced by bronchial epithelial glands and goblet cells Expectorated mucus from patients with asthma tends to have a high viscosity Airway smooth muscles Hypertrophy and hyperplasia are secondary processes caused by chronic inflammation Pathophysiology Neurogenic inflammation Stimulation of these irritant receptors (nonmyelinated C fibers of the afferent system) by mechanical stimulation, chemical and particulate irritants, and pharmacologic agents such as histamine produces reflex bronchoconstriction Induces release of substance P and neurokinin A Amplifies inflammation in asthma by releasing nitric oxide Vasoactive intestinal peptide (VIP) Inhibitory neurotransmitter Inflammatory cells in asthma can release peptidases that can degrade VIP, producing exaggerated reflex cholinergic bronchoconstriction Nitric oxide (NO) Neurotransmitter Produces smooth muscle relaxation in the vasculature and bronchials Appears to amplify the inflammatory process Pathophysiology Airway remodeling Asthma represents a chronic inflammatory process of the airways followed by healing that in some may result in altered structure referred to as remodeling Repair involves replacement of injured tissue by parenchymal cells of the same type and replacement by connective tissue and its maturation into scar tissue Remodeling presents as extracellular matrix fibrosis, an increase in smooth muscle and mucous gland mass, and angiogenesis Pathophysiology Drugs and asthma Estrogen replacement during menopause may exacerbate asthma Outcome absent when estrogen is given in combination with progesterone Mechanism not understood; estrogen decreases may exacerbate asthma during PMS Aspirin Cyclooxygenase-1 (COX-1) inhibition Inhaled corticosteroids (ICSs) are the primary preventive treatment Nonselective β-blocking agents (e.g., propranolol) These drugs do not precipitate bronchospasm but prevent its reversal Clinical Presentation Chronic asthma Acute severe asthma Exercise-induced bronchospasm Nocturnal asthma Clinical Presentation Exercise-induced bronchospasm Drop in FEV1 of 10% or greater from baseline (pre-exercise value) Return of baseline function within ≈ 30 minutes Nocturnal asthma Experts consider nocturnal symptoms to be a sign of inadequately treated persistent asthma May be worsened by GERD, sleep apnea or sinusitis Treatment – Chronic Asthma Goals of asthma management are: 1 – to achieve good control of symptoms and maintain normal activity levels 2 – to minimize future risk of exacerbations, fixed airflow limitation, and side effects All patients (6 years and older) need to have quick-relief medication in the form of short-acting inhaled β2-agonists (w/ or without ICS) or MART available for acute symptoms ICSs are considered the preferred long-term control therapy for persistent asthma in all patients due to their potency and consistent effectiveness Treatment – Chronic Asthma For those patients inadequately controlled on low-dose ICSs either an increased dose of the ICS or the combination of ICS and LABA is recommended Additional drugs / therapies include: montelukast, theophylline, tiotropium, bronchial thermoplasty, allergen immunotherapy given as subcutaneous injections or as sublingual allergen immunotherapy Assess patient every three months during therapy increases and decreases Stepping down ICS doses by 25% to 50% at 3 month intervals is considered feasible and safe for most patients Treatment – Chronic Asthma Children < 6 years old The primary differences in management are that no controller treatment is necessarily indicated for Step 1 and the recommended treatment in Step 3 is doubling the dose of ICS rather than adding LABA as is recommended for older children and adults Preferred method of delivery is by MDI with a valved spacer and facemask, if needed 5 to 10 breaths after actuation are required to inhale the complete dose ICS use, even with low doses, causes reductions in growth velocity in children Most of the available ICS have been studied in young children but not all have marketing approval from the FDA in this age group Treatment – Chronic Asthma Elderly Owing to the increased risk of osteoporosis and cataracts in the elderly, patients requiring high doses of ICSs should have routine height measurements, bone mineral density determinations, and ophthalmic examinations ICS use may contribute to skin bruising Pregnancy & lactation Low-dose ICSs recommended as preferred treatment for mild persistent asthma with the addition of a LABA if not adequately controlled Avoid stepping down therapy during gestation Budesonide and albuterol are preferred drugs Patients who are well-controlled on a particular ICS should remain on current treatment During delivery, fentanyl, rather than morphine, should be used for pain control Morphine may induce more histamine release compared to fentanyl This is one type of self- management action plan. We will review the action plan that we will test on at the end of this lecture. Self-management of worsening asthma in adults and adolescents with a written asthma action plan. (Recreated from and with permission from Global Initiative for Asthma. Global strategy for asthma management and prevention, 2018. Available from: www.ginasthma.org.) Citation: Chapter 43 Asthma, DiPiro JT, Yee GC, Posey L, Haines ST, Nolin TD, Ellingrod V. Pharmacotherapy: A Pathophysiologic Approach, 11e; 2020. Available at: https://accesspharmacy.mhmedical.com/content.aspx?bookid=2577&sectionid=228901475 Accessed: February 15, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved Treatment – Acute Asthma The primary goal is prevention of life-threatening asthma by early recognition of signs of deterioration and early intervention. The asthma-related risk factors for death include: a history of near-fatal asthma requiring intubation and mechanical ventilation; hospitalization or emergency care in the past year; current or recent use of oral corticosteroids; no current use of ICSs; overuse of short-acting inhaled β2-agonist therapy (more than one canister per month); history of psychiatric disease or psychosocial problems; poor medication adherence; lack of a written asthma action plan; and food allergy. Treatment – Acute Asthma The primary therapy of acute exacerbations is pharmacologic, which includes short- acting inhaled β2-agonists and, depending on the severity, systemic corticosteroids, inhaled ipratropium, intravenous magnesium sulfate, and O 2. Treatments are typically administered concurrently to facilitate rapid improvement. Lung function testing by peak expiratory flow (PEF) or FEV1 should be measured before treatment if possible and thereafter at 1 hour after start of treatment and then periodically until response is achieved or no further improvement is evident. Oxygen saturation is also monitored closely preferably by pulse oximetry and is a key parameter in young children who may not be able to perform lung function. Oxygen therapy is initiated to achieve an arterial oxygen saturation of 93% to 95% (0.93- 0.95) in adolescents and adults and 94% to 98% (0.94-0.98) in school-aged children and pregnant women or those with cardiac disease. May also consider Heliox (70:30 – helium to oxygen) Reduces resistance to flow and increases ventilation by converting turbulent flow to more efficient laminar flow Treatment – Acute Asthma Lab Values CORTICOSTEROIDS Β2-AGONISTS Leukocytosis Decreases in potassium, magnesium, No left shift and phosphate Concern for patient with CVD or ↑ glucose and lactic acid concomitant diuretics ↑ glucose and lactic acid Treatment – Acute Asthma Hospitalization? – Defer to Dr. Mac on this one Indicators may include an initial FEV1 less than 25% predicted or PEF that is less than 40% of their personal best, and post-treatment FEV1 or PEF that is 40% to 60% Discharge planning after an ED visit or hospitalization includes arrangement for follow-up care within 1 week as well as review of strategies to improve asthma management Treatment – Acute Asthma Children < 6 years old Require the use of a face mask as opposed to a mouthpiece for delivery of aerosolized medication  We will use the objective measures for mild, moderate and severe in this algorithm to determine course of care for our exams. Severe gets IV option for steroids + optional IV magnesium + optional ICS + everything else mild / moderate cases receive. Look at the differences between RR, pulse, O2 and PEF Management of asthma exacerbations in acute care facility, for example, emergency department. Citation: Chapter 43 Asthma, DiPiro JT, Yee GC, Posey L, Haines ST, Nolin TD, Ellingrod V. Pharmacotherapy: A Pathophysiologic Approach, 11e; 2020. Available at: https://accesspharmacy.mhmedical.com/content.aspx?bookid=2577&sectionid=228901475 Accessed: February 15, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved Same drugs that you use for asthma attacks – but higher doses What is a prednisone equivalent?  13-year-old patient is prescribed prednisone 50 mg PO qday x 5 days, but the mom says What is an equivalent he will not take a tablet. dose of dexamethasone for a What is an equivalent prescription of dose of prednisolone in prednisone 60 mg mL? Commercial qday x 5 days? formulation of prednisolone is 15 mg / 5 mL. Copyrights apply Drug Therapy  Drug Delivery Metered-dose inhalers (MDIs) Hydrofluoroalkane (HFA) propellants These do not deplete the ozone like chlorofluorocarbon (CFC) Dry powder inhalers (DPIs) Breath actuated Patients should be cautioned not to exhale into DPIs because this causes loss of dose and moistens the dry powder, causing aggregation into larger particles Most children younger than 4 years of age cannot generate a sufficient inspiratory flow to use DPIs Jet nebulizers Produce an aerosol from a liquid solution or suspension placed in a cup; tube connected to a stream of compressed air or O2 flows up through the bottom and draws the liquid up an adjacent open- ended tube creating a droplet cloud Ultrasonic nebulizer Produce an aerosol by vibrating liquid lying above a transducer at speeds of about 1 mHz β2-agonists MOA Bronchodilators Inhibition of release of immediate hypersensitivity mediators from mast cells Side effects Tremor, tachycardia, hypokalemia, headache, nervousness, throat irritation, upper respiratory tract infections (URTIs) Tolerance Can occur with chronic administration and seems to plateau after about 1 week of regular therapy but response recovers rapidly after only 3 days of nonuse ICS lessens severity of tolerance Which neurotransmitters act on beta receptors? How many types of beta receptors in humans?  β2-agonists Short-acting (SABA) – dosed every four to six hours Albuterol (Ventolin, ProAir, Proventil) –Rx Levalbuterol (Xopenex) – Rx Epinephrine (Primatene Mist) – OTC Temporary relief of mild symptoms of intermittent asthma in patients 12 years and older and if improvement is not seen within 20 minutes, it becomes worse, or more than 8 inhalations in a 24-hour period, or there are more than two episodes in a week, the patient should see a physician immediately Long-acting (LABA) – dosed twice daily Salmeterol (Serevent) Formoterol (Foradil, Performist) BLACK BOX WARNING - Not to be used as monotherapy for long term control Increased risk of asthma-related death Controller / reliever LABAs are preferred concomitant therapy with ICSs in children 12 years and older and adults for steps 1-5 and children 6 to 11 years of age for steps 3-5 Ultra-LABA – dosed once daily Vilanterol Combination with fluticasone Once-daily dosing for asthma in adults aged 18 and older β2-agonists Nebulized albuterol for severe acute asthma In adults, administration as either continuous or intermittent (every 20 minutes for three doses) over 1 hour results in equivalent improvement In the subset of more severely obstructed patients, continuous nebulization provides greater improvement Continuous nebulization is recommended for patients having an unsatisfactory response (achieving less than 50% of normal FEV1 or PEF) following the initial three doses (every 20 minutes) of aerosolized β2-agonists and potentially for patients presenting initially with PEF or FEV1 values of less than 30% of predicted normal Both children and adults receiving continuously nebulized β2-agonists have demonstrated decreased heart rate as their lung function improves An elevated heart rate is not an indication to use lower doses or to avoid using inhaled β2-agonists Corticosteroids MOA Reduce synthesis and release of pro-inflammatory cytokines Reduce inflammatory cell activation Possible effect on beta receptors: May increase the number of receptors May improve receptor responsiveness to adrenergic stimulation Inhaled Corticosteroids Generic Name Formulation Available Brand Name Beclomethasone Inhaler QVAR RediHaler Budesonide Nebulizer solution Pulmicort (nebulizer solution) Inhaler Pulmicort Flexhaler (inhaler) Combination products also available. Ciclesonide Inhaler Alvesco Flunisolide Inhaler Aerospan Fluticasone Inhaler Flovent HFA, Diskus, Combination products also Armon Air RespiClick, available. Arnuity Ellipta Mometasone Inhaler Asmanex Combination products also available. Systemic Corticosteroids Systemic corticosteroids are indicated in all patients with acute severe asthma exacerbations not responding completely to initial inhaled β2-agonist administration (every 20 minutes for three doses) and should be administered within 1 hour of presentation Adults are effectively treated with a 5- to 7-day course of therapy but children typically require only 3 to 5 days It is recommended that a full dose of the corticosteroid be continued until the patient's PEF reaches 70% of predicted normal or personal best Dexamethasone (Decadron), methylprednisolone (Medrol Dosepak), prednisolone (Prelone), prednisone (Deltone) or hydrocortisone Corticosteroids – Adverse Effects Short-Term Systemic Long-Term Systemic Local Effects via ICS Effects Effects Cough Changes in mood Adrenal axis Dysphonia Fluid retention suppression Oropharyngeal Hyperglycemia Growth suppression candidiasis Hypertension Immunosuppression Increased appetite Osteoporosis Weight gain Anticholinergics MOA Competitive inhibitors of muscarinic receptors Blockade of M2 receptors allows further release of presynaptic acetylcholine, and may antagonize the bronchodilatory effect – a possible basis of paradoxical bronchoconstriction Long-term use of ipratropium has been shown to significantly decrease sputum volume – more important for COPD Albuterol is more effective compared to ipratropium Side effects Abnormal taste, xerostomia, bronchitis, HA, flushing, blurred vision, tachycardia, palpitations, dizziness Anticholinergics Short-acting Ipratropium (Atrovent) DuoNeb (albuterol / ipratropium nebulizer solution) Both albuterol and ipratropium are available as monotherapy nebulizer solution Long-acting Tiotropium (Spirva Respimat) Do not use Spiriva Handihaler for asthma Leukotriene Modifiers MOA Reduction of production or action of leukotrienes in inflammation and allergy; reduces airway edema and smooth muscle contraction Side effects HA, GI upset, psychiatric effects INCREDIBLY Rare: idiosyncratic syndrome similar to the Churg–Strauss syndrome, with marked circulating eosinophilia, heart failure, and associated eosinophilic vasculitis, has been reported in a small number of patients Leukotriene Modifiers Montelukast (Singulair) LTRA - leukotriene receptor antagonist Approved for EIB asthma The FDA approval for montelukast in children younger than age 6 was based on safety and pharmacokinetic studies establishing doses but not on efficacy, although improvement in symptoms and as-needed bronchodilators was noted Zafirlukast (Accolate) LTRA Rare hepatotoxicity Zileuton (Zyflo) 5-Lipoxygenase inhibitor - enzyme that catalyzes the formation of leukotrienes from arachidonic acid Use limited due to the potential for elevated liver enzymes (especially in the first 3 months of therapy), and the potential inhibition of drugs metabolized by the CYP3A4 isoenzymes Biologics Omalizumab (Xolair) Recombinant anti-IgE antibody → decreases inflammatory mediator release Inhibits the binding of IgE on the surface of mast cells Moderate or severe allergic asthma not controlled with ICS Adverse effects: Anaphylaxis (rare) – Blackbox warning Has occurred up to 12 months post 1st dose Injection site reactions – including flu-like symptoms (e.g., myalgias) and pain at site of injection Increased risk of infections Including fungal and helminth Biologics Omalizumab (Xolair) Dosing based on weight and IgE levels Lowest dose Pretreatment serum IgE ≥30 to 100 units/mL: 30 to 90 kg: 150 mg every 4 weeks >90 to 150 kg: 300 mg every 4 weeks Highest dose Pretreatment serum IgE >600 to 700 units/mL: 30 to 60 kg: 375 mg every 2 weeks >60 kg: Use not recommended Several other doses available with similar 2 to 4 week interval Biologics Dupilumab (Dupixent) Interluekin-4 antagonist→ decreases inflammatory mediator release Moderate or severe allergic asthma not controlled with maintenance therapy Adverse effects: Anaphylaxis – does not have a Blackbox warning Injection site reactions – including flu-like symptoms and injection site pain Increased risk of infections Herpes Helminths Biologics Recombinant Interleukin-5 Antagonists Severe asthma with eosinophilic phenotype Adverse effects: Anaphylaxis Injection site reactions Increased risk of infections Generic Name Brand Name Benralizumab Fasenra Mepolizumab Nucala Reslizumab Cinqair Additional Therapies Cromolyn Mast cell stabilizer Alternative option in chronic asthma management Available as nebulizer solution Additional Therapies Theophylline Methylxanthine Non-specifically inhibit phosphodiesterase → bronchodilation Inhibit secretion of inflammatory mediators Dosing ≈ 10mg/kg/day (max 900mg/day); complicated dosing Narrow therapeutic range: 5 – 15 mcg/mL Side effects: N/V, GERD, nervousness, tremor, insomnia, HA, tachycardia, seizures, arrhythmias Metabolized by CYP 1A2 and 3A4 Levels increased by: CYP 1A2 or 3A4 inhibitors Levels decreased by: Tobacco smoking CYP 3A4 inducers Oral beta agonist (ie, theophylline and albuterol syrup) are not preferred for use in asthma per GINA guidelines Algorithm for slow titration of theophylline dosage and guide for final dosage adjustment based on serum theophylline concentration measurement. For infants younger than 1 year of age, the initial daily dosage can be calculated by the following regression equation: Dose (mg/kg) = (0.2) (age in weeks) + 5. Whenever side effects occur, dosage should be reduced to a previously tolerated lower dose. Citation: Chapter 43 Asthma, DiPiro JT, Yee GC, Posey L, Haines ST, Nolin TD, Ellingrod V. Pharmacotherapy: A Pathophysiologic Approach, 11e; 2020. Available at: https://accesspharmacy.mhmedical.com/content.aspx?bookid=2577&sectionid=228901475 Accessed: February 15, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved Patient Education  What about priming and cleaning your inhalers? Instructions for inhaler use from the NAEPP Expert Panel Report 3. (Source: National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. NIH Publication No. 07-4051. Revised August 2007.) Citation: Chapter 43 Asthma, DiPiro JT, Yee GC, Posey L, Haines ST, Nolin TD, Ellingrod V. Pharmacotherapy: A Pathophysiologic Approach, 11e; 2020. Available at: https://accesspharmacy.mhmedical.com/content.aspx?bookid=2577&sectionid=228901475 Accessed: February 15, 2021 Copyright © 2021 McGraw-Hill Education. All rights reserved Patient Self Monitoring The NAEPP has recommended a PEF monitoring system based on a traffic light scenario (based on percentage of normal predicted values or personal best values): the green zone is equal to 80% to 100%, the yellow zone is equal to 50% to 79%, and the red zone is less than 50%. The yellow zone is cautionary and requires increasing as-needed bronchodilator use and possibly beginning prednisone if not improved, whereas the red zone warrants contacting the patient's healthcare provider. Available Products Standard Electronic Personal Best Defined as the individuals highest PEFR over the course of two weeks, with the patient measuring PEFR two to four times daily and while the patient is feeling well Three attempts recorded in the Options: afternoon: Consider color 1) 498 L/min coordination 2) 425 L/min Limitation or 3) 463 L/min Advantage? Not as comprehensive as others Question Calculate the green, yellow and red zones from the following: Personal Best: 450 L/min ◦ >=360 L/min ◦ 359 L/min - 225 L/min ◦ < 225 L/min