Study Points

Chronic Obstructive Pulmonary Disease (COPD)

Course #98813 - $60-

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  1. Emphysema is defined as

    DEFINITIONS

    Emphysema is an enlargement of the air spaces (alveoli) distal to the terminal bronchioles, with destruction of their walls [40]. The destruction of air space walls reduces elastic recoil and the surface area available for the exchange of oxygen and carbon dioxide during breathing. These airways can collapse, leading to further limitation in airflow. Emphysema can be classified by location as panacinar/panlobular and centriacinar/centrilobular [41].

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  2. Which of the following is NOT a risk factor for the development of chronic obstructive pulmonary disease (COPD)?

    PATHOGENESIS

    RISK FACTORS FOR COPD

    Genetic predisposition
    Exposure to particles (e.g., tobacco smoke, organic and inorganic occupational dusts, outdoor air pollution, indoor air pollution from heating and cooking with biomass in poorly vented dwellings)
    Poor lung growth and development
    Oxidative stress
    Female sex
    Older age
    Respiratory infections
    Lower socioeconomic status
    Poor nutrition
    Comorbidities
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  3. What percentage of persons who smoke will develop clinically apparent COPD?

    PATHOGENESIS

    Cigarette smoking is the predominant and primary risk factor for COPD, and approximately 15% of all persons who smoke will develop clinically apparent COPD. Smokers of more than 40 pack-years exposure have a much higher likelihood of developing COPD than nonsmokers. The combined exposure to tobacco smoke and certain occupational dusts and chemicals magnifies the risk for COPD [6,7,8,9,10,11]. In developing countries, COPD has been attributed to chronic exposure to smoke from burning biomass fuels for indoor cooking and heating purposes. The COPD caused by smoking is associated with more rapid disease progression and more severe emphysema than COPD from biomass exposure, which is characterized primarily by airway-wall thickening and improved lung function in response to the use of bronchodilators [11]. Smokers with pre-existing airway reactivity also have a greater susceptibility to developing COPD.

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  4. Which of the following genetic disorders is an important cause of emphysema in nonsmokers?

    PATHOGENESIS

    It is believed that a variety of genes play an important role in COPD pathogenesis. A genetic disorder that causes alpha-1 antitrypsin deficiency is an important cause of emphysema in nonsmokers and increases susceptibility to disease in smokers. People with severe hereditary deficiency of alpha-1 antitrypsin are genetically predisposed to developing COPD. Alpha-1 antitrypsin deficiency stimulates neutrophil elastase activity, which leads to parenchymal destruction in the lungs and causes emphysema.

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  5. Which of the following is a structural change that occurs in the lung parenchyma of patients with COPD?

    PATHOLOGY

    INFLAMMATORY CELLS IN COPD

    Cell TypeCharacteristic Changes
    NeutrophilsElevated levels of neutrophils in sputum of normal smokers, with greater levels in those with COPD related to disease severity. Few neutrophils are seen in tissue. They may be important in mucus hypersecretion and the release of proteases.
    MacrophagesGreatly increased numbers of macrophages are seen in airway lumen, lung parenchyma, and bronchoalveolar lavage fluid. Derived from blood monocytes that differentiate within lung tissue, these cells produce increased inflammatory mediators and proteases in patients with COPD in response to cigarette smoke and may show defective phagocytosis.
    T-lymphocytes (T-cells)Both CD4+ and CD8+ cells are increased in the airway wall and lung parenchyma, with an increased CD8+:CD4+ ratio. Greater numbers of CD8+ T-cells (Tc1) and T helper 1 (Th1) cells, which secrete interferon-γ and express the chemokine receptor CXCR39. CD8+ cells may be cytotoxic to alveolar cells, contributing to their destruction.
    B-lymphocytes (B-cells)Elevated levels in peripheral airways and within lymphoid follicles, possibly as a response to chronic colonization and infection of the airways.
    EosinophilsElevated levels of eosinophil proteins in sputum and increased eosinophils in airway wall during exacerbations.
    Epithelial cellsMay be activated by cigarette smoke to produce inflammatory mediators.
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  6. In patients with COPD,

    PATHOLOGY

    It is suggested that neutrophils play a primary role in the generation of mucous metaplasia in chronic bronchitis and the destruction of lung tissue in emphysema. The neutrophilic inflammatory response appears to account for the excessive mucus secretion observed in response to an acute secretagogue and for augmentation of the bronchial mucus-producing apparatus observed in these patients [34,35]. There is a strong correlation between peripheral airway dysfunction in COPD and sputum neutrophil counts [36].

    Macrophages are the predominant inflammatory cells present in lavage fluid in patients with COPD [37]. Numerous studies have demonstrated a direct correlation between the number of alveolar macrophage in the lung tissue and the severity of lung destruction [38].

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  7. What role do chemokines play in the COPD disease process?

    PATHOLOGY

    INFLAMMATORY MEDIATORS INVOLVED IN COPD

    Cell TypeAction
    Lipid mediators (e.g., leukotriene B4)Attract neutrophils and T-lymphocytes
    Chemokines (e.g., interleukin-8)Attract neutrophils and monocytes
    Proinflammatory cytokines (e.g., tumor necrosis factor-α, interleukin-1ß, and interleukin-6)Amplify the inflammatory process and may contribute to some of the systemic effects of COPD
    Growth factors (e.g., transforming growth factor-ß)May induce fibrosis in small airways
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  8. The airway obstruction associated with COPD causes

    PATHOPHYSIOLOGY

    There is a direct correlation between degree of inflammation, fibrosis, and luminal exudates in small airways and the reduction in FEV1 and FEV1/forced vital capacity (FVC) ratio. The effect on airflow is pronounced in the smaller (<2 mm in diameter) conducting airways. The resultant peripheral airway obstruction produces alveolar hyperinflation and air trapping during expiration. Hyperinflation diminishes inspiratory capacity and increases functional residual capacity, which causes dyspnea and limitation of exercise capacity.

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  9. Which of the following is NOT one of the cardinal signs and symptoms of COPD?

    CLINICAL FEATURES

    The cardinal signs and symptoms of COPD are chronic cough, sputum production, breathlessness (shortness of breath and dyspnea), and limited exercise tolerance. Other common signs that may be present in COPD include:

    • Tachypnea

    • Pursed lips breathing

    • Prolonged expiration phase of breathing (compared with inspiration)

    • Active use of neck muscles during breathing

    • Increased resonance of the chest (by percussion) caused by hyperaeration and emphysematous change

    • Increased anteroposterior (A-P) diameter of the chest ("barrel chest")

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  10. In patients with COPD, clubbing of the fingers

    CLINICAL FEATURES

    Clubbing of the fingers may be present in patients with COPD, in part caused by chronic oxygen deprivation. However, it is relatively uncommon. Clubbing is more likely indicative of other chronic diseases such as congenital heart defect, bronchiectasis, infectious endocarditis, or cirrhosis of the liver.

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  11. Which of the following spirometry findings is indicative of airflow limitation that is not fully reversible?

    DIAGNOSIS AND CLINICAL ASSESSMENT

    A clinical diagnosis of COPD should be considered in the patient who presents with shortness of breath or dyspnea, chronic productive cough, and easy fatigue, especially if combined with a history of risk factor exposure (e.g., long-term exposure to tobacco or dust and chemicals, age, genetics). The diagnosis should then be confirmed by spirometry. The presence of a Tiffeneau index or postbronchodilator FEV1/FVC less than 0.70 and FEV1 less than 80% predicted confirms the presence of airflow limitation that is not fully reversible [199].

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  12. A comprehensive medical history of an individual presenting with COPD symptoms should include all of the following, EXCEPT:

    DIAGNOSIS AND CLINICAL ASSESSMENT

    As with any illness, a careful history is critical in determining the correct diagnosis. The goals of history taking are to identify possible causes of dyspnea and other symptoms and to screen for COPD risk factors. An inadequate history may result in misdiagnosis or delayed diagnosis, with ramifications on disease course. A comprehensive medical history of an individual presenting with COPD symptoms should include:

    • Long-term exposure to risk factors, such as smoking or occupational and environmental exposures

    • Past medical history, including asthma, allergy, respiratory infections in the past (especially in childhood), sinusitis or nasal polyps, and other respiratory illnesses

    • Family history of COPD or other chronic respiratory disease

    • Pattern of symptoms of COPD (e.g., development in adulthood, increasing dyspnea or breathlessness, frequent "winter colds," restricted social life)

    • History of previous hospitalizations or exacerbations for respiratory illnesses

    • Presence of comorbid conditions, such as chronic heart disease, malignancy, musculoskeletal disorders, or osteoporosis

    • Medical treatments

    • Impact of the disease on the patient's life, including restricted activity, absenteeism at work, financial impact, and depression or anxiety

    • Family and social support available

    • Possibilities for COPD risk factor reduction, particularly smoking cessation

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  13. When conducting a differential diagnosis, which of the following features is indicative of COPD rather than another condition?

    DIAGNOSIS AND CLINICAL ASSESSMENT

    DIFFERENTIAL DIAGNOSIS OF COPD

    DiagnosisSuggestive Featuresa
    COPD
    Onset in mid-life
    Symptoms slowly progressive
    Long history of tobacco smoking
    Breathlessness or dyspnea during exercise
    Largely irreversible airflow limitation
    Asthma
    Early onset, often in childhood
    Family history of asthma
    Symptoms at night/early morning and vary from day to day
    Presence of allergy, rhinitis, and/or eczema
    Largely reversible airflow limitation
    Bronchiectasis
    Copious amount of purulent sputum
    Generally associated with bacterial infection
    Coarse crackles or clubbing on auscultation
    Bronchial dilation and thickening of bronchial wall on chest x-ray/CT
    Congestive heart failure
    Fine basilar crackles on auscultation
    Dilated heart and pulmonary edema on chest x-ray
    Pulmonary function tests show volume restriction with no airflow limitation
    Tuberculosis
    Onset all ages
    Lung infiltrate visible on chest x-ray
    Microbiologic confirmation of Mycobacterium tuberculosis
    High local prevalence of tuberculosis
    Diffuse panbronchiolitis
    Majority of patients are men and nonsmokers
    Chronic sinusitis
    Diffuse small centrilobular nodular opacities and hyperinflation on chest x-ray and/or HRCT
    Obliterative bronchiolitis
    Onset in younger age, nonsmokers
    May have history of rheumatoid arthritis or exposure to fumes
    CT on expiration shows hypodense areas
    aThese signs/symptoms/features tend to be characteristic of the respective diseases but are not present in every case.
    CT = computed tomography, HRCT = high-resolution CT.
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  14. A patient with an FEV1 of 70% predicted on spirometry would be categorized as COPD stage

    ASSESSMENT OF COPD SEVERITY

    SPIROMETRIC CLASSIFICATION OF COPD SEVERITY BASED ON POSTBRONCHODILATOR FEV1a

    GOLD StageSpirometric Finding
    1 (mild)FEV1 ≥80% predicted
    2 (moderate)50% ≤ FEV1 <80% predicted
    3 (severe)30% ≤ FEV1 <50% predicted
    4 (very severe)FEV1 <30% predicted
    aIn patients with FEV1/FVC <0.70
    FEV1 = forced expiratory volume in one second, FVC = forced vital capacity, GOLD = Global Initiative for Chronic Obstructive Lung Disorder.
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  15. Which of the following is NOT one of the factors considered on the BODE index?

    ASSESSMENT OF COPD SEVERITY

    The BODE index is a multidimensional grading method used to assess clinical risk in patients with COPD based on four factors: body mass index (BMI), obstruction, dyspnea, and exercise (Table 10) [5,57]. It is a better prognostic marker of subsequent survival than any other component alone [5,57]. Each component of the BODE index is graded and a score out of 10 is obtained; higher scores are indicative of greater mortality risk. This method reflects the effect of both pulmonary and extrapulmonary factors on prognosis and survival in COPD.

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  16. Chest CT assessment of COPD is useful for revealing which of the following features?

    ASSESSMENT OF COPD SEVERITY

    Computed tomography (CT) of the chest has advanced understanding of COPD and has an important role in the clinical assessment of selected patients. Chest CT can identify the presence and extent of disease patterns that impact prognosis and influence the management of patients with COPD [10]. CT imaging features that are associated with adverse clinical outcomes include early interstitial lung abnormalities, bronchiectasis, presence and pattern of emphysema, airway wall thickness, and expiratory gas trapping [224]. The addition of expiratory CT scans has enabled measurement of small airway disease. Chest CT also may reveal extrapulmonary findings of importance, such as coronary artery calcification, cardiac chamber enlargement, and early-stage lung cancer. The presence of predominantly upper-lobe emphysema on CT imaging identifies the patient who is a good candidate for surgical lung-volume reduction [60].

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  17. Screening for alpha-1 antitrypsin deficiency is recommended for patients with COPD

    ASSESSMENT OF COPD SEVERITY

    White patients who experience COPD at a young age (i.e., younger than 45 years) or who have a positive family history of COPD may be screened for alpha-1 antitrypsin deficiency. A serum concentration of alpha-1 antitrypsin less than 15% to 20% of the normal expected value indicates a high probability of homozygous alpha-1 antitrypsin deficiency.

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  18. What is the main disadvantage of behavioral interventions for smoking cessation?

    RISK REDUCTION

    Behavioral interventions are nonpharmacologic treatments delivered directly to individual smokers [209]. The main disadvantage of this approach is that relatively few smokers (about 5%) are interested in attending specific classes at any given time [210]. Therefore, group sessions appear to be the most cost-effective approach to delivering smoking cessation interventions [211]. Although relatively few patients want to go to classes, healthcare professionals should still have a list of referral smoking cessation clinics in their area for those smokers who express an interest in attending them and for those who have failed to respond to other approaches. Simple computer-tailored cessation messages may also be an effective alternative for behavioral support, doubling the cessation rates. This concept has been incorporated into patient support programs provided by several manufacturers of smoking cessation products [210].

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  19. What pharmacotherapy for smoking cessation is approved for pregnant or nursing women?

    RISK REDUCTION

    The first-line pharmacologic interventions for smoking cessation are NRT, bupropion, and varenicline [217,218]. However, no pharmacotherapy has been approved for use among pregnant or nursing women. The five forms of NRT available are the patch, gum, lozenge, nasal spray, and inhaler.

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  20. Inhaled corticosteroids are recommended for patients with

    MANAGEMENT OF STABLE COPD

    GOLD GUIDELINES FOR STEPWISE MANAGEMENT OF COPD BY SEVERITY

    Treatment StepSymptom Grade
    Stage 0 (At Risk)Stage 1/A (Mild)

    Stage 2/B

    (Moderate)

    Stage 3/C (Severe)Stage 4/D (Very Severe)
    Step 1Avoidance of risk factors
    Step 2 Offer short-acting or long-acting bronchodilator to reduce breathlessness
    Step 3 

    Initiate regular treatment with one or a combination of long-acting bronchodilators

    Begin rehabilitation

    Step 4 

    Utilize single or combination long-acting bronchodilator

    Add inhaled corticosteroids if repeated exacerbations

    Step 5 

    Add macrolide in former smokers

    Consider roflumilast if patient has chronic bronchitis

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  21. Which of the following is a short-acting beta2-agonist?

    MANAGEMENT OF STABLE COPD

    MEDICATIONS COMMONLY USED IN THE MANAGEMENT OF COPD

    DrugInhaler (mcg)Solution for Nebulizer (mg/mL)OralVials for Injection (mg)Duration of Action (hours)
    Short-acting beta2-agonists
    Fenoterol100–200 (MDI)10.05% (syrup)4–6
    Levalbuterol45–90 (MDI)0.21, 0.426–8
    Salbutamol (albuterol)100, 200 (MDI & DPI)55 mg (pill), 0.024% (syrup)0.1, 0.54–6
    Terbutaline400, 500 (DPI)2.5 mg, 5 mg (pill)4–6
    Long-acting beta2-agonists
    Arformoterol0.007512
    Formoterol4.5–12 (MDI & DPI)0.0112
    Indacaterol75–300 (DPI)24
    Olodaterol5 (SMI)24
    Salmeterol25–50 (MDI & DPI)12
    Tulobuterol2 mg (transdermal)24
    Short-acting muscarinic antagonists
    Ipratropium bromide20, 40 (MDI)0.25–0.56–8
    Oxitropium bromide100 (MDI)1.57–9
    Long-acting muscarinic antagonists
    Aclidinium bromide322 (DPI)12
    Glycopyrronium bromide44 (DPI)24
    Tiotropium18 (DPI), 5 (SMI)24
    Umeclidinium62.5 (DPI)24
    Combination short-acting beta2-agonist plus muscarinic antagonist in one inhaler
    Fenoterol/ipratropium200/80 (MDI)1.25/0.56–8
    Salbutamol/ipratropium100/20 (SMI)6–8
    Combination long-acting beta2-agonist plus muscarinic antagonist in one inhaler
    Formoterol/aclidinium12/340 (DPI)12
    Indacaterol/glycopyrronium85/43 (DPI)24
    Olodaterol/tiotropium5/5 (SMI)24
    Vilanterol/umeclidinium25/62.5 (DPI)24
    Methylxanthines
    Aminophylline200–600 mg (pill)240Variable, up to 24
    Theophylline (SR)100–600 mg (pill)Variable, up to 24
    Inhaled corticosteroids
    Beclomethasone50–400 (MDI & DPI)0.2–0.4
    Budesonide100, 200, 400 (DPI)0.2, 0.25, 0.5
    Fluticasone50–500 (MDI & DPI)
    Combination long-acting beta2-agonist plus corticosteroid in one inhaler
    Formoterol/beclometasone6/100 (MDI & DPI)
    Formoterol/budesonide4.5/160 (MDI), 9/320 (DPI)
    Formoterol/mometasone10/200, 10/400 (MDI)
    Salmeterol/fluticasone50/100, 250, 500 (DPI)
    Vilanterol/fluticasone furoate25/100 (DPI)
    Systemic corticosteroids
    Prednisone5–60 mg (pill)
    Methylprednisolone4, 8, 16 mg (pill)
    Phosphodiesterase-4 inhibitors
    Roflumilast500 mcg (pill)24
    MDI = metered-dose inhaler, DPI = dry-powder inhaler, SMI = soft-mist inhaler, SR = sustained release.
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  22. Ipratropium bromide has a duration of action of

    MANAGEMENT OF STABLE COPD

    MEDICATIONS COMMONLY USED IN THE MANAGEMENT OF COPD

    DrugInhaler (mcg)Solution for Nebulizer (mg/mL)OralVials for Injection (mg)Duration of Action (hours)
    Short-acting beta2-agonists
    Fenoterol100–200 (MDI)10.05% (syrup)4–6
    Levalbuterol45–90 (MDI)0.21, 0.426–8
    Salbutamol (albuterol)100, 200 (MDI & DPI)55 mg (pill), 0.024% (syrup)0.1, 0.54–6
    Terbutaline400, 500 (DPI)2.5 mg, 5 mg (pill)4–6
    Long-acting beta2-agonists
    Arformoterol0.007512
    Formoterol4.5–12 (MDI & DPI)0.0112
    Indacaterol75–300 (DPI)24
    Olodaterol5 (SMI)24
    Salmeterol25–50 (MDI & DPI)12
    Tulobuterol2 mg (transdermal)24
    Short-acting muscarinic antagonists
    Ipratropium bromide20, 40 (MDI)0.25–0.56–8
    Oxitropium bromide100 (MDI)1.57–9
    Long-acting muscarinic antagonists
    Aclidinium bromide322 (DPI)12
    Glycopyrronium bromide44 (DPI)24
    Tiotropium18 (DPI), 5 (SMI)24
    Umeclidinium62.5 (DPI)24
    Combination short-acting beta2-agonist plus muscarinic antagonist in one inhaler
    Fenoterol/ipratropium200/80 (MDI)1.25/0.56–8
    Salbutamol/ipratropium100/20 (SMI)6–8
    Combination long-acting beta2-agonist plus muscarinic antagonist in one inhaler
    Formoterol/aclidinium12/340 (DPI)12
    Indacaterol/glycopyrronium85/43 (DPI)24
    Olodaterol/tiotropium5/5 (SMI)24
    Vilanterol/umeclidinium25/62.5 (DPI)24
    Methylxanthines
    Aminophylline200–600 mg (pill)240Variable, up to 24
    Theophylline (SR)100–600 mg (pill)Variable, up to 24
    Inhaled corticosteroids
    Beclomethasone50–400 (MDI & DPI)0.2–0.4
    Budesonide100, 200, 400 (DPI)0.2, 0.25, 0.5
    Fluticasone50–500 (MDI & DPI)
    Combination long-acting beta2-agonist plus corticosteroid in one inhaler
    Formoterol/beclometasone6/100 (MDI & DPI)
    Formoterol/budesonide4.5/160 (MDI), 9/320 (DPI)
    Formoterol/mometasone10/200, 10/400 (MDI)
    Salmeterol/fluticasone50/100, 250, 500 (DPI)
    Vilanterol/fluticasone furoate25/100 (DPI)
    Systemic corticosteroids
    Prednisone5–60 mg (pill)
    Methylprednisolone4, 8, 16 mg (pill)
    Phosphodiesterase-4 inhibitors
    Roflumilast500 mcg (pill)24
    MDI = metered-dose inhaler, DPI = dry-powder inhaler, SMI = soft-mist inhaler, SR = sustained release.
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  23. In the treatment of COPD, oral methylxanthines

    MANAGEMENT OF STABLE COPD

    Methylxanthines have weak bronchodilator and respiratory stimulant properties. Both of the available methylxanthines (aminophylline and theophylline) are administered orally and have variable durations of action (up to 24 hours). The inhaled bronchodilators are preferred over these oral agents, as the latter tends to be less predictable and more toxic. Although useful for some patients, the methylxanthines are a third-line option in the treatment of stable COPD [199].

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  24. Pulmonary rehabilitation programs address all of the following conditions, EXCEPT:

    MANAGEMENT OF STABLE COPD

    Pulmonary rehabilitation can address nonpulmonary conditions that are not addressed by the medical management of COPD, including:

    • Muscle weakness and wasting

    • Exercise deconditioning

    • Depression

    • Relative social isolation

    • Weight loss

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  25. Long-term oxygen therapy would usually be indicated for patients with stage 4 COPD and

    MANAGEMENT OF STABLE COPD

    Long-term oxygen therapy is usually indicated in stage 4 COPD for patients who have [199]:

    • PaO2≤7.3 kPa (55 mm Hg) or SaO2≤88%, with or without hypercapnia confirmed twice over a three-week period

    • PaO2 between 7.3 kPa (55 mm Hg) and 8.0 kPa (60 mm Hg) or SaO2 of 88%, if there is evidence of pulmonary hypertension, peripheral edema suggesting congestive cardiac failure, or polycythemia (hematocrit >55%)

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  26. Lung volume reduction surgery

    MANAGEMENT OF STABLE COPD

    Lung volume reduction surgery (LVRS) is a surgical procedure in which damaged parts of the lung are resected to reduce hyperinflation, thus improving efficacy of respiratory muscles. LVRS also improves expiratory flow rates by increasing the elastic recoil pressure of the lung. LVRS is considered for patients with bilateral emphysema on HRCT and severe obstruction with hyperinflation and air trapping [194]. As with bullectomy, certain characteristics may indicate the likelihood of a favorable or unfavorable outcome with LVRS (Table 16) [73].

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  27. Which of the following factors indicates that a COPD exacerbation should be treated in the hospital rather than at home?

    MANAGEMENT OF EXACERBATIONS

    FACTORS TO CONSIDER WHEN DECIDING WHERE TO TREAT THE PATIENT WITH COPD EXACERBATION

    FactorTreat at HomeTreat in Hospital
    Able to cope at homeYesNo
    BreathlessnessMildSevere
    General conditionGoodPoor/deteriorating
    Level of activityGoodPoor/confined to bed
    CyanosisNoYes
    Worsening peripheral edemaNoYes
    Level of consciousnessNormalImpaired
    Already receiving long-term oxygen therapyNoYes
    Social circumstancesGoodLiving alone/not coping
    Acute confusion NoYes
    Rate of onset Insidious or gradualRapid
    Significant comorbidity (particularly cardiac disease and insulin-dependent diabetes) NoYes
    SaO2 <90% NoYes
    Changes on chest radiograph NoPresent
    Arterial pH level≥7.35<7.35
    Arterial PaO2≥7 kPa<7 kPa
    PaO2 = partial pressure of oxygen, SaO2 = oxygen saturation.
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  28. Noninvasive intermittent ventilation is recommended for patients with

    MANAGEMENT OF EXACERBATIONS

    The selection criteria for NIV are based on clinical observations and gas exchange measurements. Patients with moderate-to-severe dyspnea with signs of increased breathing load (i.e., use of accessory muscles and paradoxical abdominal motion) and tachypnea (>25 breaths per minute) as well as moderate-to-severe acidosis (pH ≤7.35) and/or hypercapnia (PaCO2 >6.0 kPa OR 45 mm Hg) are considered candidates for NIV [199]. Relative contraindications include [199]:

    • Respiratory arrest

    • Life-threatening hypoxemia

    • Unstable cardiovascular status (e.g., cardiac arrhythmias, myocardial infarction, hypotension)

    • Altered mental status or inability to cooperate (e.g., low Glasgow coma score)

    • High aspiration risk, vomiting

    • Viscous or copious secretions

    • Recent history of facial or gastroesophageal surgery

    • Craniofacial trauma

    • Bowel obstruction

    • Fixed nasopharyngeal abnormalities

    • Severe burns

    • Morbid obesity

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  29. Assessment of pulmonary artery pressure is only recommended for patients with

    MONITORING AND ASSESSMENT

    Only patients with respiratory failure require assessment of pulmonary artery pressure; otherwise, its measurement is not recommended. The development of respiratory failure is indicated by a PaO2 less than 8.0 kPa (60 mm Hg) with or without PaCO2 greater than 6.7 kPa (50 mm Hg) in arterial blood gas measurements while breathing air at sea level. Patients may be screened with pulse oximetry and arterial blood gases if SaO2 is less than 92%.

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  30. What is the most common comorbid condition in patients with COPD?

    COMORBIDITIES

    Pneumonia is the most common comorbid condition in patients with COPD. Pneumonia can present as a part or a trigger of COPD exacerbations; however, there are important clinical differences between pneumonia and acute COPD exacerbations without pneumonia. COPD exacerbation with pneumonia has a more rapid onset of symptoms, more severe illness, longer length of hospital stay, and higher rate of ICU admission and mortality compared to an exacerbation without pneumonia [144].

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