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A patient with asthma is prescribed albuterol (Ventolin) for acute bronchospasm. Which nursing instruction is most crucial regarding the medication's use?

  • Discontinue other asthma medications to prevent potential drug interactions.
  • Increase the dose if the initial prescribed amount does not provide immediate relief.
  • Use the medication only as needed for acute symptoms rather than as a scheduled treatment. (correct)
  • Administer the medication at evenly spaced intervals to maintain consistent bronchodilation.

A patient is prescribed a nonselective adrenergic drug for bronchodilation. What potential side effect should the nurse monitor for most closely?

  • Hypotension
  • Increased anxiety (correct)
  • Bradycardia
  • Severe muscle weakness

A patient newly diagnosed with asthma is prescribed both albuterol (SABA) and salmeterol (LABA). How should the nurse instruct the patient to use these medications?

  • Alternate daily between albuterol and salmeterol to prevent tolerance.
  • Use salmeterol for immediate relief of acute symptoms and albuterol for long-term control.
  • Mix both medications in a nebulizer for simultaneous administration.
  • Use albuterol for immediate relief of acute symptoms and salmeterol for long-term control. (correct)

What is the primary mechanism of action of beta2-adrenergic agonists in treating asthma?

<p>Stimulating beta2-adrenergic receptors in bronchial smooth muscle. (D)</p> Signup and view all the answers

A patient taking high doses of albuterol reports experiencing palpitations and tremors. Which physiological effect is most likely contributing to these adverse effects?

<p>Stimulation of beta1 receptors due to loss of beta2 specificity. (D)</p> Signup and view all the answers

In COPD, what is the primary mechanism by which inhaled noxious particles lead to lung damage?

<p>Stimulation of an abnormal inflammatory response, leading to the release of mediators that damage lung tissue. (C)</p> Signup and view all the answers

Why does air trapping occur in individuals with COPD?

<p>Destruction of lung supporting structures and collapse of bronchioles, hindering exhalation. (B)</p> Signup and view all the answers

How does long-term exposure to occupational chemicals and dust contribute to the development of COPD?

<p>By causing chronic irritation and inflammation of the airways, leading to structural damage and impaired function. (D)</p> Signup and view all the answers

What is the underlying reason for the irreversible airflow limitations observed in COPD patients?

<p>Loss of elactis recoil (D)</p> Signup and view all the answers

In the context of COPD, what is the significance of pulmonary vascular changes?

<p>They contribute to pulmonary hypertension and reduced gas exchange due to thickening of blood vessels and decreased surface area. (D)</p> Signup and view all the answers

How does cigarette smoking impact the respiratory tract in the development of COPD?

<p>It leads to increased mucus production, hyperplasia of mucous glands, and decreased ciliary activity. (C)</p> Signup and view all the answers

Why can distinguishing between emphysema and chronic bronchitis be difficult in COPD patients?

<p>Emphysema and chronic bronchitis often coexist, and their symptoms can overlap, especially with comorbidities. (C)</p> Signup and view all the answers

What is the implication of dysfunctional cilia in the context of COPD?

<p>Reduced ability to clear mucus and debris, leading to increased risk of infections and airway obstruction. (D)</p> Signup and view all the answers

During an asthma exacerbation, which of the following mechanisms contributes directly to airflow obstruction in both large and small airways?

<p>Airway smooth muscle contraction, cellular edema, and mucous plugging. (B)</p> Signup and view all the answers

How does the late phase response in asthma contribute to sustained airway inflammation and hyperreactivity?

<p>It involves eosinophils and leads to worsening symptoms 3-10 hours after initial exposure, lasting for 24 hours. (D)</p> Signup and view all the answers

Which of the following is the most direct consequence of the destruction of the alveolar sacs (avioli sais) in emphysema?

<p>Reduced surface area for gas exchange. (B)</p> Signup and view all the answers

In the allergic cascade of asthma pathophysiology, what is the critical role of IgE antibodies produced by plasma cells?

<p>They bind to receptors on mast cells, sensitizing them for subsequent allergen exposure. (A)</p> Signup and view all the answers

What is the primary effect of increased mucus production in the respiratory tract of individuals with COPD?

<p>It contributes to airway obstruction and increased risk of infection by trapping pathogens and hindering mucociliary clearance. (C)</p> Signup and view all the answers

A patient with a history of asthma is exposed to a known allergen. Which sequence of events accurately describes the early phase response?

<p>Allergen cross-linking with IgE on mast cells, mediator release (histamine, prostaglandins, leukotrienes), leading to bronchoconstriction and vasodilation. (A)</p> Signup and view all the answers

How does obstruction in the small airways contribute to the pathophysiology of asthma?

<p>It causes airway closure and air-trapping, leading to hyperinflation. (D)</p> Signup and view all the answers

Which of the following best describes the process of sensitization to an allergen in the context of asthma?

<p>Initial exposure to an allergen, stimulating T cells to activate B cells, which differentiate into plasma cells producing IgE antibodies. (C)</p> Signup and view all the answers

What is the primary function of the pulmonary circulation in relation to the respiratory system?

<p>To facilitate gas exchange by bringing deoxygenated blood into close proximity with the alveoli. (C)</p> Signup and view all the answers

In advanced stages of COPD, dyspnea's presence shifts from occurring with exertion to when?

<p>At rest, indicating severely compromised lung function. (D)</p> Signup and view all the answers

What is the underlying mechanism that leads to the characteristic underweight presentation often observed in individuals with COPD, despite adequate caloric intake?

<p>Increased metabolic demand resulting from the increased work of breathing. (B)</p> Signup and view all the answers

Why does COPD frequently lead to an increased anterior-posterior chest diameter, resulting in a barrel chest?

<p>Air trapping and hyperinflation of the lungs limit diaphragmatic excursion. (B)</p> Signup and view all the answers

What compensatory mechanism does the body employ in response to chronic hypoxemia in COPD, and what physical manifestation does it produce?

<p>Increased erythropoietin production leading to polycythemia and cyanosis. (D)</p> Signup and view all the answers

What is the primary mechanism of action of beta2-adrenergic agonists in the treatment of COPD?

<p>Dilating the bronchioles through smooth muscle relaxation. (B)</p> Signup and view all the answers

How do anticholinergics improve respiratory function in individuals with COPD?

<p>By blocking muscarinic receptors in the airways, causing bronchodilation. (D)</p> Signup and view all the answers

Why is early-stage COPD often difficult to diagnose?

<p>Dyspnea only occurs during exertion and can be easily dismissed. (D)</p> Signup and view all the answers

In the physical examination of a patient with COPD, what causes the observed prolonged expiratory phase?

<p>Hyperinflation and airway collapse. (C)</p> Signup and view all the answers

What specific change to sputum production is a key indication that a patient may have COPD?

<p>An increase in thick, yellow-green, sputum production. (A)</p> Signup and view all the answers

Aside from physical symptoms, which factor, related to patient history, is most important when considering a COPD diagnosis?

<p>Exposure to known COPD risk factors. (A)</p> Signup and view all the answers

In the context of asthma, what physiological change primarily contributes to prolonged expiration?

<p>Bronchoconstriction and air trapping, leading to increased resistance during exhalation. (B)</p> Signup and view all the answers

Why might wheezing be an unreliable indicator of asthma severity during an acute attack?

<p>Severe airway obstruction can limit airflow, preventing the generation of wheezing sounds. (C)</p> Signup and view all the answers

Which of the following best describes the underlying pathology that differentiates chronic bronchitis from emphysema?

<p>Chronic bronchitis is defined by excessive mucus production and airway inflammation, while emphysema involves destruction of alveolar walls. (C)</p> Signup and view all the answers

What is the primary characteristic that distinguishes 'status asthmaticus' from a typical asthma exacerbation?

<p>Status asthmaticus is unresponsive to standard bronchodilator therapy and may require mechanical ventilation. (C)</p> Signup and view all the answers

How does the pathophysiology of emphysema directly lead to impaired gas exchange within the lungs?

<p>Destruction of alveolar walls reduces the surface area available for gas exchange. (D)</p> Signup and view all the answers

A patient with chronic bronchitis is likely to exhibit which specific pathological change in their airways?

<p>Increased number of goblet cells and damaged cilia. (C)</p> Signup and view all the answers

What is a key difference in the reversibility of airway obstruction between asthma and chronic bronchitis?

<p>Airway obstruction in asthma is typically reversible, whereas in chronic bronchitis, it is largely irreversible due to structural damage. (C)</p> Signup and view all the answers

Which factor is most likely to trigger an 'extrinsic' asthma exacerbation?

<p>Exposure to allergens such as pollen or pet dander. (B)</p> Signup and view all the answers

In a patient experiencing an acute asthma attack, which set of clinical signs would suggest the presence of hypoxemia?

<p>Restlessness, anxiety, increased pulse rate and blood pressure. (A)</p> Signup and view all the answers

Flashcards

Respiratory System Function

The main function of the respiratory system is gas exchange to provide O2 and remove CO2.

Alveoli Destruction

Irreversible destruction of the alveoli, impairing gas exchange.

Asthma

Recurrent and reversible shortness of breath due to airway narrowing.

Allergic Cascade: Sensitization

Initial exposure to an allergen that leads to the production of IgE antibodies.

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IgE Binding

IgE antibodies bind to mast cells.

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Early Phase Response

Mast cells release mediators (histamine, etc.) causing bronchoconstriction and inflammation.

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Late Phase Response

Worsening of asthma symptoms 3-10 hours after initial exposure, involving eosinophils.

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Asthma obstruction

The alveolar ducts/alveoli remain open, but airflow to them is obstructed.

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Asthma triggers

Exercise, respiratory infections, and allergens.

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Asthma symptoms

Wheezing, breathlessness, cough, and tight chest.

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Asthma expiration

Expiration may be prolonged.

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Asthma wheezing

Severe attacks may have no audible wheezing.

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Hypoxemia Signs (Asthma)

Restlessness, anxiety, increased pulse and blood pressure.

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Status asthmaticus

A prolonged asthma attack that does not respond to typical drug therapy.

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Chronic bronchitis

Chronic productive cough for three months in each of two successive years.

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Emphysema

Abnormal enlargement of airspaces distal to the terminal bronchioles with destruction of airspace walls.

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Beta2-Agonists: Mechanism

Stimulate beta2 adrenergic receptors in bronchial smooth muscle, causing bronchodilation.

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SABA

Provide rapid relief of bronchospasm; short duration.

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LABA

Provide long-term asthma control; slower onset, long duration.

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Beta2-Agonists: Indications

Relief of bronchospasm related to asthma and other pulmonary diseases.

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Beta2-Agonists: Side Effects

Tremors, tachycardia, vascular headache, insomnia, restlessness.

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Air Trapping

Trapping of air in the lungs due to airway obstruction or loss of elasticity.

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COPD Risk Factors

Cigarette smoking, occupational chemicals/dust, and air pollution.

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Smoking Effects on Respiratory Tract

Increased mucus production, hyperplasia of mucous glands, and decreased ciliary activity.

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COPD Development Factors

Dusts, vapors, irritants, fumes, and high levels of air pollution.

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COPD Defining Feature

Irreversible airflow limitations during forced exhalation due to loss of elastic recoil.

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Airflow Obstruction in COPD

Mucous hypersecretion, mucosal edema, and bronchospasm.

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Primary COPD Process

Inflammation from inhaled particles damages lung tissue and destroys parenchyma.

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COPD Lung Changes

Destruction of lung support structures, leading to bronchiolar collapse and air trapping.

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COPD Diagnosis

A disease that develops slowly, characterized by cough, sputum production, and dyspnea.

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COPD-related Dyspnea

Shortness of breath, initially with exertion, progressing to present at rest in advanced stages.

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Chest Breathing in COPD

Breathing pattern involving use of accessory muscles (intercostal) which increases the work of breathing and is metabolically demanding.

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COPD & Body Weight

Patients are characteristically underweight despite adequate caloric intake and experience chronic fatigue.

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COPD Auscultation Findings

Prolonged expiratory phase, wheezes, and decreased breath sounds upon auscultation.

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Barrel Chest

An increased anterior-posterior diameter of the chest, leading to a rounded appearance.

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Cyanosis in COPD

Bluish-red discoloration of the skin due to chronic hypoxemia.

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Overproduction of RBCs

Increased production of red blood cells to compensate for chronic hypoxemia.

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Bronchodilators

Medications that relax the smooth muscles of the airways, widening them and easing breathing.

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Beta2-Adrenergic Agonists

A type of bronchodilator that stimulates beta2-adrenergic receptors, leading to bronchodilation.

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Study Notes

  • Lower Respiratory Disorders cover diseases like asthma, emphysema, chronic bronchitis, pneumonia, and tuberculosis.

Respiratory System Review

  • The main function is not stated.
  • This is accomplished via ventilation, diffusion, and perfusion.
  • Conducting Airways Composition is an important factor to consider
  • Alveoli destruction is irreversible
  • There are Type I and Type II Alveolar cells
  • Pulmonary circulation facilitates gas exchange
  • Neurochemical control includes the respiratory center and chemoreceptors for CO2 & O2.
  • Mechanics of breathing involve major & accessory muscles, lung elasticity, airway resistance, alveolar surface tension, and work of breathing.
  • Gas transport involves O2 & CO2 transport and the distribution of ventilation.
  • Control of pulmonary circulation involves distributing pulmonary blood flow.

Asthma Pathophysiology

  • Shortness of breath is recurrent and reversible

  • Cascade occurs following exposure to an allergen

  • Sensitization to an allergen occurs through initial exposure.

  • T cells stimulate B cells (memory cells).

  • B cells develop into plasma cells.

  • Plasma cells produce IgE antibodies, that target that specific allergen

  • IgE binds to receptors on mast cells.

  • The early phase response occurs upon re-exposure to an allergen.

  • IgE of mast cells binds to the allergen and cross-links, releasing histamine, prostaglandins, and leukotrienes

  • These immune mediators cause bronchoconstriction, vasodilation, and increased capillary permeability.

  • The late phase response to an allergen begins at the same time as the early phase response.

  • Worsening symptoms appear 3-10 hours later and last for 24 hours, possibly involving eosinophils

  • The inflammatory and remodeling responses in asthma with activation of the epithelial mesenchymal trophic unit are shown in a diagram

Pathophysiology of Asthma

  • Airflow obstruction is related to contraction of airway smooth muscle, thickening of airway wall from cellular edema and plugging of the airways with mucus and debris

  • Obstruction in large airways leads to air flow limitation and decreased flow rates

  • Obstruction in small airways leads to airway closure and air-trapping/hyperinflation

  • Alveolar ducts/alveoli remain open, but airflow to them is obstructed

  • Factors causing obstruction include smooth muscle contraction, swollen mucosa, and mucus plugs which cause the bronchioles to narrow.

Asthma Types

  • Asthma can be intrinsic or extrinsic
  • Extrinsic asthma triggers include allergens and air pollutants
  • Triggers of occupational forms include drug and food additives
  • Other forms of asthma induced by exercise and respiratory infections
  • Potential causes include nasal/sinus problems

Clinical Manifestations of Asthma

  • Episodes are unpredictable and variable
  • Recurrent episodes include wheezing, breathlessness, cough, and tight chest
  • These episodes may be abrupt or gradual
  • Episodes can last from minutes to hours
  • Expiration may be prolonged resulting in a shortened breath
  • Inspiration-expiration ratio changes from 1:2 to 1:3 or 1:4
  • Air takes longer to move out
  • Wheezing is unreliable to gauge severity
  • A severe attack may have no audible wheezing, and usually begins upon exhalation
  • Difficulty with air movement can create a feeling of suffocation.
  • Patients may feel increasingly anxious
  • An acute attack usually reveals signs of hypoxemia: restlessness, anxiety, inappropriate behavior, increased pulse, and blood pressure.
  • Status asthmaticus is a prolonged asthma attack that does not respond to typical drug therapy which may last several minutes to hours and is a medical emergency requiring intubation and mechanical ventilation.

Chronic Bronchitis

  • Defined as a chronic productive cough for three months in each of two successive years in a patient whom other causes of chronic cough have been excluded which causes permanent structural damage
  • Continuous inflammation of the bronchi and bronchioles
  • Often occurs as a result of prolonged exposure to bronchial irritants/toxics (e.g., smoking)
  • An increase in the number of goblet cells with damaged cilia that leads to mucus production

Emphysema

  • Defined as abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls.
  • Air spaces enlarge from alveolar wall destruction
  • The surface area where gas exchange takes place is reduced
  • Effective respiration is impaired often as a result of air trapping

COPD

  • COPD has components of both chronic bronchitis and emphysema.
  • Chronic bronchitis involves chronic inflammation of bronchiole.
  • Emphysema involves destruction of alveoli sacs.
  • Risk factors for COPD include cigarette smoking, occupational chemicals/dust, and air pollution.
  • It is characterized by airflow limitation that is not fully reversible, and generally progressive
  • Represents an abnormal inflammatory response of lungs to noxious particles or gases
  • Smoking effects lead to increased mucus production
  • There is hyperplasia of mucus glands, where cells become larger
  • Ciliary activity is lost or decreased
  • Intense or prolonged exposure to dusts, vapors, irritants, or fumes can result in COPD
  • High levels of air pollution
  • Fumes from indoor heating or cooking with fossil fuels.
  • Defining features are irreversible airflow limitations during forced exhalation due to loss of elastic recoil
  • Airflow obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm.
  • Inhalation of noxious particles and inflammation are primary drivers of the disease
  • Mediators are released that cause damage to lung tissue.
  • Airways become inflamed and the parenchyma destroyed

COPD – Pathophysiology Continued

  • Supporting structures of lungs are destroyed.
  • Air goes in easily, but remains in the lungs.
  • Bronchioles tend to collapse.
  • Barrel-chest is associated with air-trapping.
  • Pulmonary vascular changes can occur
  • Blood vessels thicken.
  • Surface area for diffusion of O2 decreases, leading to a hypoxic state.
  • Common characteristics are mucous hypersecretion, dysfunction of cilia, hyperinflation of lungs, and abnormal gas exchange.
  • Commonly, emphysema and chronic bronchitis coexist
  • Distinguishing symptoms can be difficult with co-morbidities.
  • COPD often develops slowly and is considered when there is presence of a cough
  • Sputum with color change; Yellow/green color may indicate a bacterial infection
  • Dyspnea
  • Requires exposure to risk factors

COPD – Clinical Manifestations Continued

  • Chest breathing is common and dyspnea prompts medical attention as increased work of breathing is metabolically demanding.
  • Often present at rest with advanced disease.
  • Use of accessory and intercostal muscles is used to breath.
  • Characteristically underweight with adequate caloric intake, and chronic fatigue
  • Physical examination findings: prolonged expiratory phase, wheezes, decreased breath sounds, increased anterior-posterior diameter, and bluish-red color of skin.
  • Cyanosis indicates a hypoxic state.
  • Overproduction of RBCs to compensate for hypoxia.

Medications Used to Treat Asthma and COPD

  • Bronchodilators include Beta2-adrenergic agonists, anticholinergics, and xanthine derivatives.
  • Anti-inflammatory agents include leukotriene receptor antagonists, corticosteroids, and new asthma medications.

Bronchodilators: Beta2Agonists

  • They stimulate Beta2 adrenergic receptors in the bronchial smooth muscle throughout lungs to cause bronchodilation via relaxing/opening muscles

  • Three subtypes of drugs based on selectivity for receptors exist: nonselective adrenergic drugs, nonselective beta-adrenergic drugs, and selective beta2 drugs.

  • Non-selective drugs have more side effects.

  • Short-acting inhalers/nebulizers (SABA rescue inhalers): albuterol (Ventolin, Proventil), levalbuterol (Xopenex) and terbutaline (Brethine) have a rapid onset and are short-lived

  • Long-acting (LABA, maintenance): salmetrol (Serevent), formoterol (Foradil), arformoterol (Brovana) are prescribed for maintenance.

  • Indications: relief of bronchospasm related to asthma, bronchitis, and other pulmonary diseases

  • Used in treatment and prevention of acute and chronic attacks depending on their onset of action.

  • Further indications: hypotension, shock, uterine relaxation.

  • Adverse effects: tremors, tachycardia, vascular headache, insomnia, and restlessness

  • Overuse of Albuterol results in loss of its beta2-specific actions at larger doses activating beta1 receptors that causes nausea, increased anxiety, palpitations, tremors, and increased heart rate

  • Ensure that patients take medications exactly as prescribed, with no omissions or double doses.

  • Inform patient to report insomnia, jitteriness, restlessness, palpitations, or chest pain.

Bronchodilators (Anticholinergics):

  • Bronchial tree contains Acetylcholine which causes bronchial constriction and narrowing of the airways
  • Anticholinergics bind to the ACh receptors, preventing ACh from binding to reduce bronchial constriction and dilate, and causes a reduction of secretions
  • Main indication: Prevention of bronchospasm associated with COPD, allergen and exercise induced asthma.
  • Ipratopium bromide (Atrovent), tiotropium (Spiriva), aclidinium (Tudorza), and umeclidinium and vilanterol (Anoro Ellipta. are taken via inhaler or nebulizer
  • These have a slow and prolonged action
  • Used to prevent bronchoconstriction and NOT used for acute asthma exacerbations
  • Side effects include dry mouth or throat, hoarseness, nasal congestion, headache, coughing, anxiety, heart palpitations, and urinary retention.
  • Nursing implications include instructing patient to rinse mouth after medication administration.

Bronchodilators: Xanthine Derivatives

  • Example: theophylline (Theo-Dur, Elixohyliin) that can be administered orally, rectally, and intravenously - Emergency only
  • Mechanisms causes relaxation of bronchial smooth muscle resulting in bronchodilation by increasing camp.
  • Leads to smooth muscle relaxation, bronchodilation, and increased airflow.
  • Dilation of airways in asthmas, chronic bronchitis and emphysema.
  • Used as an adjunct drug in the management of COPD, but is not used as frequently because of potential for drug interactions and variables related to drug levels in the blood (toxicity)
  • Adverse effects include nausea, vomiting, anorexia, GERD, dysrhythmia, and seizures

SDOH

  • Albuterol is relatively cheap and can cost between $30 and $60 without insurance
  • With insurance it costs between $5 and $50 depending on copay
  • Ipatroprium bromide-without insurance costs $200
  • Theophylline costs $100 per month without insurance
  • Prescription access to provider is required
  • Consider environmental factors like exposure to pests, mold, air pollution (including secondhand smoke)

Anti-inflammatory Medications

Leukotriene Receptor Antagonists (LTRAs)

  • Has action on eosinophil reaction.
  • Route of administration is PO
  • Examples include montelukast (Singulair) (once daily dosing), zafirlukast (Accolate), zileuton (Zyflo)
  • Long term therapy of asthma in adults and children.
  • Also used for prevention of exercise induced bronchospasm, and management of seasonal allergies
  • Mode of Action modifies the immune response.
  • Leukotrienes are substances released when a trigger (allergen) starts a series of chemical reactions in the body and cause inflammation, bronchoconstriction, and mucus production.
  • LTRAs function by preventing leukotrienes from attaching to receptors on cells in the lungs and in circulation
  • Montelukast (Singulair)- Neuropsychiatric effects in children and adolescents
  • Zafirlukast (accolate)-headache, nausea, diarrhea, liver dysfunction
  • Zileuton(Zyflo)- headache, dyspepsia, nausea, dizziness, insomnia, liver dysfunction
  • Ensure that the drug is being used for chronic management, not acute episodes
  • Improvement should be seen in about a week
  • Assess liver function before beginning therapy for Seasonal allergies before beginning therapy
  • Teach patient to take medications every night on a continuous schedule, even if symptoms improve
  • An exception is if symptoms are related to sports or exercise, take two hours prior to activity

Corticosteroids

  • Anti-inflammatory properties.
  • Inhaled forms reduce systemic effects
  • Oral form is not for acute exacerbations
  • IV form can be used for acute asthma or COPD exac
  • May take several weeks before full effects are seen.
  • Stabilize membranes of cells that release harmful bronchoconstriction substances from leukocytes
  • Increases responsiveness of bronchial smooth muscle to beta-adrenergic stimulation
  • Beclomethasone dipropionate (Beclovent, Vanceril)
  • Budesonide (Pulmicort)
  • Triamcinolone acetonide (Azmacort)
  • Fluticasone (Flovent, Flonase)
  • Fluticasone and salmeterol (Advair)
  • Bronchospastic disorders are not controlled by conventional bronchodilators
  • Not considered first-line drugs for management
  • Pharyngeal irritation
  • Coughing
  • Dry mouth
  • Oral fungal infections/thrush
  • Systemic effects are rare because low doses are used for inhalation therapy
  • Teach patients to gargle and rinse the mouth with lukewarm water afterward to prevent the development of oral fungal infections
  • A beta-agonist bronchodilator should be used before the corticosteroid allows for delivery

Inhaled Corticosteroids: Nursing Implications

  • Teach patients to monitor disease with a peak flow meter.
  • Encourage use of a spacer device to ensure successful inhalations.
  • Teach patient how to keep inhalers and nebulizer equipment clean after uses.

Oral Corticosteroids

  • Example: prednisone, prednisolone.
  • Indications: short-term therapy following and acute asthma episode, copd exacerbation.
  • Long-term therapy for acute asthma.
  • Side effects of long term therapy: Suppression of adrenal gland function, bone loss, hyperglycemia, glycosuria, myopathy, peptic ulcer disease, infection, and fluid and electrolyte imbalance.

Intravenous Corticosteroids

  • hydrocortisone sodium succinate (Solu-cortef) and Methylprednisolone sodium succinate (Solu-mederol)
  • Short term IV agents used for acute exacerbations of COPD and status asthmaticus.
  • Similar to side effects of long-term oral therapy.
  • Monitor patients closely when switched to inhaled steroids after receiving systemic steroids due to adrenal insufficiency.
  • Fluticasone/Salmeterol, Budesonide/Formoterol are found in Inhalers
  • Ipratropium/Albuterol is found in Inhalers, Nebulizers
  • Combination inhaled corticosteroid and long-acting bronchodilator

SDOH

  • Disproportionate burden of COPD occurs in people of low socioeconomic status (SES) due to differences in health behaviors, social structure, environmental exposures, tobacco use, occupations with exposure to inhalant toxins
  • Leukotriene Receptor Antagonists are $8-$30 and are more expensive than than bronchodilators.
  • Inhaled corticosteroids cost $200 (without insurance).
  • Oral steroids start at $5 (much cheaper than others).

Newest Medications

  • Phosphodiesterase-4 inhibitor (FDA approval 2011), such as roflumilast (Daliresp) taken Orally is used for COPD exacerbations and can cause anxiety and depression
  • Monoclonal Antibody (Binds to IgE limits release of chemical mediators of inflammation), such as omalizumab (Xolair) is used for asthma and administered Subcutaneously every two to four weeks to as an Antiasthmatic that requires monitoring for anaphylaxis
  • Other mediations use the patient as last resort

Nursing Implications for medication

  • Encourage patients to take measures that promote good health to prevent relieve, or decrease symptoms of COPD.

  • Avoid exposure to conditions that precipitate bronchospasm, have adequate fluid intake, and comply with medical treatment.

  • Patients should also avoid excessive fatigue, heat, extremes in temperature, and caffeine

  • Advocate for vaccinations.

  • Encourage patients to get prompt treatment for flu or illnesses, and vaccinations

  • Encourage patients to check with their physician before taking any other medication.

  • Teach patients to take bronchodilators exactly as prescribed.

  • Ensure they know how to use devices and to demonstrate use of the devices.

  • Monitor for adverse effects.

  • Assessment should be done by reviewing skin color, checking baseline vital signs, listening to respirations (work of breathing), respiratory assessment including pulse oximetry, sputum production, known allergies, history of respiratory problems and other medications

Nursing impliations Continued

  • Decreased dyspnea
  • Decreased wheezing, restlessness, and anxiety
  • Improved respiratory patterns with return to normal rate and quality
  • Improved activity tolerance
  • Decreased symptoms and increased ease of breathing

Inhalers: Patient Education

  • Ensure that the patient is able to self-administer
  • Provide demonstration and return demonstration
  • Patient knows the correct time intervals for Inhalers
  • Provide a spacer if the patient has difficulty coordinating if they have to coordinate breathing.
  • Patient knows how to keep track of the number of doses in the inhaler device
  • Show the patients the red, yellow and green zones that should follow. and when to administer their medication.

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