COPD - Readings

Question 1

What is COPD?

Answer 1

Chronic obstructive pulmonary disease (COPD) is a treatable and preventable disease characterized by progressive airflow limitation that is not fully reversible and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases.

Question 2

IS COPD the First, second, third or 4th leading cause of death in the US?

Answer 2

4th

Question 3

What is the primary cause of COPD?

Answer 3

The primary cause of COPD is cigarette smoking, implicated in 75% of diagnosed cases in the United States. Other risks include genetic predisposition, environmental exposures (including occupational dust and chemicals), and air pollution.

Question 4

What are the only management strategies proven to slow COPD?

Answer 4

Smoking cessation and avoidance

Question 5

When is oxygen therapy indicated?

Answer 5

Oxygen therapy can reduce mortality in selected patients with COPD. Oxygen therapy is indicated for patients with a resting PaO2 of less than 55 mm Hg (7.3 kPa) or a PaO2 of less than 60 mm Hg (8.0 kPa) and evidence of right-sided heart failure, polycythemia, or impaired neurologic function.

Question 6

What is the mainstay of drug therapy for COPD?

Answer 6

Inhaled bronchodilators are the mainstay of drug therapy for COPD and are used to relieve patient symptoms and improve exercise tolerance and quality of life. Guidelines recommend short-acting bronchodilators as initial therapy for patients with occasional symptoms and all patients as rescue therapy to relieve symptoms.

Question 7

What is the treatment for patients with persistent COPD symptoms?

Answer 7

For patients experiencing persistent symptoms, either a long-acting β2-agonist (LABA) or long-acting anticholinergic (LAMA) offers significant benefits, and both are of comparable efficacy. If a patient has continued symptoms, combining long-acting bronchodilator agents (LABA plus LAMA) is recommended.

Question 8

Which is more effective at reducing exacerbation frequency, SABA or LAMA?

Answer 8

LAMA
If a patient has continued exacerbations or has more severe disease, combining long-acting bronchodilator agents (LABA plus LAMA) is recommended.

Question 9

Which patients may benefit from ICS?

Answer 9

Patients with frequent and severe exacerbations may benefit from ICS therapy, although the risk of pneumonia is increased.

Question 10

What is the typical treatment for AECOPD?

Answer 10

Treatment of acute exacerbations includes intensification of bronchodilator therapy and a short course of systemic corticosteroids.

Antimicrobial therapy should generally be used during AECOPD if the patient exhibits at least two of the following: increased dyspnea, increased sputum volume, and increased sputum purulence. A C-reactive protein (CRP) test may be helpful to guide the decision to treat a COPD exacerbation with antibiotics.

Question 11

What are the two phenotypes of COPD?

Answer 11

The two principal conditions are chronic bronchitis and emphysema, which are phenotypes. Chronic bronchitis is associated with chronic or recurrent episodes of excessive mucus secretion into the bronchial tree with a cough present on most days for at least 3 months of the year for at least 2 consecutive years in a patient in whom other causes of chronic cough have been excluded.

emphysema also has been defined as abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls without obvious fibrosis.1

Differentiating COPD as either chronic bronchitis or emphysema as distinct subsets of COPD is no longer considered relevant because both are caused by a common risk factor (cigarette smoking), and most patients exhibit features of both. Emphasis is placed on the pathophysiologic features of small airways disease and parenchymal destruction as contributors to chronic airflow limitation.

Question 12

WHat is the pathogenesis of COPD?

Answer 12

Chronic inflammation affects the integrity of the airways, causes damage, and promotes the destruction of the parenchymal structures. The underlying problem is persistent exposure to noxious particles or gases that sustain the inflammatory response. The airways of both the lung and the parenchyma are susceptible to inflammation, and the result is the chronic airflow limitation that characterizes COPD (Fig. 45-1).

Question 13

Describe the diagram about COPD

Answer 13

Question 14

How can the inflammation be differentiated between COPD and asthma?

Answer 14

The inflammation seen in COPD is often referred to as neutrophilic in nature, but macrophages and CD8+ lymphocytes also play major roles.1,18 In a small subset of patients with COPD, there may be inflammation common to both COPD and asthma, and such patients may be classified as having “asthma-COPD overlap syndrome.”

Question 15

Review the complete pathogenesis of COPD

Answer 15

Other processes proposed to play a major role in the pathogenesis of COPD include increased oxidative stress and imbalance between destructive and protective defense systems in the lungs (proteases and antiproteases).1,20 Altered interaction between airway oxidants and antioxidants is responsible for the increased oxidative stress present in COPD. Increases in oxidant markers (eg, hydrogen peroxide and nitric oxide) are seen in the epithelial lining fluid and are generated by cigarette smoke or noxious particles.1

Oxidants react with and damage various proteins and lipids, leading to cell and tissue damage. Oxidants also promote inflammation directly and exacerbate the protease–antiprotease imbalance by inhibiting antiprotease activity.20 These processes may be the result of ongoing inflammation or occur because of environmental pressures and exposures (Fig. 45-1).

Pathologic changes of COPD are widespread, affecting large and small airways, lung parenchyma, and the pulmonary vasculature.1 An inflammatory exudate is often present that leads to an increase in the number and size of goblet cells and mucus glands. Mucous secretion is increased, and ciliary motility is impaired. There is also a thickening of smooth muscle and connective tissue in the airways. Inflammation is present in central and peripheral airways. The chronic inflammation results in a repeated injury and repair process that leads to scarring and fibrosis. Diffuse airway narrowing is present and is more prominent in smaller peripheral airways. Airflow obstruction is attributed to airway inflammation, while the blood gas abnormalities result from impaired gas transfer due to parenchymal damage and loss of alveolar-capillary networks.

Mucus hypersecretion is present early in the course of the disease and is associated with an increased number and size of mucus-producing cells. The presence of chronic inflammation perpetuates the process, although resulting airflow obstruction and chronic airflow limitation may be reversible or irreversible. The various causes of airflow obstruction are summarized in Table 45-3.

Question 16

When are significant changes in ABGS present?

Answer 16

Significant changes in ABGs usually are not present until airflow limitation is very severe

Question 17

Describe the course of hypoxia in COPD?

Answer 17

Initially, when present, hypoxemia is associated with exertion. As the disease progresses, hypoxemia develops at rest. Hypoxemia is attributed to hypoventilation (V) of lung tissue relative to perfusion (Q) of the area.

Question 18

How does respiratory acidosis occur in COPD?

Answer 18

As COPD progresses and gas exchange worsens, patients may exhibit chronic hypercapnia and are referred to as carbon dioxide retainers. In such patients, central respiratory response to chronically increased PaCO2 is blunted. These changes in PaO2 and PaCO2 are subtle and progress over a period of many years. As a result, serum pH usually is near normal because the kidneys compensate by retaining bicarbonate. If acute respiratory distress develops, such as seen with significant pneumonia or COPD exacerbation with respiratory failure, PaCO2 may rise sharply, and the patient presents with a worsening respiratory acidosis.

Question 19

What are the vascular changes that occur in COPD?

Answer 19

The vascular changes of COPD include loss of pulmonary capillary beds, thickening of pulmonary vessels, and vasoconstriction of pulmonary arteries in response to hypoxemia.1,21 Chronic hypoxemia and permanent changes in pulmonary vasculature lead to increases in pulmonary pressures, especially during exercise.

Question 20

What type of heartfailure can occur in COPD?

Answer 20

right-sided heart failure, or cor pulmonale, develops and is characterized by right ventricle hypertrophy in response to increased pulmonary vascular resistance. Pulmonary hypertension is the most common cardiovascular complication of COPD and can result in significant morbidity.

Question 21

What happens to functional residual capacity inpts with COPD exhibiting thoracic hyperinflation.

Answer 21

For patients with COPD exhibiting thoracic hyperinflation, there is an increase in functional residual capacity (FRC), which is the amount of air left in the lung after exhalation at rest.

Question 22

What are systemic consequences of COPD?

Answer 22

Systemic effects include cardiovascular events associated with ischemia, cachexia, weight loss, osteoporosis, anemia, and muscle wasting.1 There has been interest in measuring C-reactive protein as a marker to assess systemic inflammation and its correlation with disease severity; however, it is premature to recommend its use in practice for chronic management.22 Instead, C-reactive protein may have a role in identifying patients with acute exacerbation of COPD who should receive treatment with antibiotics.

Question 23

What are the symptoms of COPD?

Answer 23

Symptoms

Chronic cough—may be intermittent; may be unproductive

Chronic sputum production

Dyspnea—worse with exercise; progressive over time

Decreased exercise tolerance or decline in physical activity

Chest tightness or wheezing

Question 24

What are Risk factors for COPD?

Answer 24

Risk Factors

Tobacco smoke exposure

Indoor air pollution (eg, burning wood and biofuel for cooking or heating)

Occupational and environmental hazards (eg, organic and inorganic dusts, chemical fumes)

α1-Antitrypsin deficiency

Question 25

What is found on physical examination?

Answer 25

Shallow breathing

Increased resting respiratory rate

Pursed lips during exhalation

Use of accessory respiratory muscles

Cyanosis of mucosal membranes (seen in later stages of disease)

Question 26

What diagnostic tests are done for COPD?

Answer 26

Spirometry with postbronchodilator testing

Radiograph of chest (to rule out other diagnoses)

Arterial blood gas (not routinely obtained in chronic management; has utility in acute decompensation). Lab abnormalities may include pH <7.35, PaO2 <80 mm Hg (10.6 kPa), PaCO2 >50 mm Hg (6.7 kPa), and bicarbonate >26 mEq/L (mmol/L)

Question 27

What is the hallmark finding in pts with COPD?

Answer 27

Patients with all levels of severity of COPD exhibit the hallmark finding of airflow obstruction; specifically, a reduction in FEV1/FVC ratio to less than 70% (0.70). FVC is the total volume of air exhaled after maximal inhalation and FEV1 is the total volume of air exhaled in 1 second. A fixed ratio of less than 70% (0.70) may be problematic because normal aging may affect this result; however, it continues to be the current standard.

Question 28

Describe the various categories of severity of airflow obstruction in COPD?

Answer 28

Question 29

What is typically the most troublesome complaint for pts with COPD?

Answer 29

Dyspnea

Question 30

Describe the BODE, ADO, and COTE index in terms of prognostics in COPD

Answer 30

Question 31

What is the major focus in terms of COPD prevention?
What about goals for those who have it?

Answer 31

1. Prevention is KEY - limiting exposure to cigarette smoke
2. Slow or prevent disease progression

Question 32

What do treatments for COPD ultimately do?

Answer 32

Unfortunately, most treatments for COPD have not been shown to improve survival or to slow the progressive decline in lung function. However, many therapies do improve pulmonary function and quality of life as well as reduce the risk of COPD exacerbations and duration of hospitalization.

Question 34

What are the benefits of smoking cessation in pts with COPD?

Answer 34

Smoking cessation leads to decreased symptomatology and slows the rate of decline of pulmonary function even after significant abnormalities in pulmonary function tests have been detected. As confirmed by the Lung Health Study, smoking cessation is the only intervention proven to affect long-term decline in FEV1 and slow the progression of COPD

Question 35

What is the 5 step strategy for smoking cessation?

Answer 35

Question 36

Describe the different treatments/dose, duration and AE for smoking cessation

Answer 36

Question 37

Describe the role of pulmonary rehab in COPD management?

Answer 37

Exercise training is beneficial in the treatment of COPD to improve exercise tolerance and to reduce symptoms of dyspnea and fatigue.1 Pulmonary rehabilitation programs are an integral component in the management of COPD and should include exercise training along with smoking cessation, breathing exercises, optimal medical treatment, psychosocial support, and health education. Pulmonary rehabilitation has no direct effect on lung function or gas exchange. Instead, it optimizes other body systems so that the impact of poor lung function is minimized. Exercise training reduces the CNS response to dyspnea, ameliorates anxiety and depression, reduces thoracic hyperinflation, and improves skeletal muscle function.35

Question 38

What are the surgical options for COPD?

Answer 38

Various surgical options have been employed in the management of COPD.1 These include bullectomy, lung volume reduction surgery (LVRS), and lung transplantation. Presence of bullae may contribute to complaints of dyspnea, and their removal can improve lung function and reduce symptoms, although there is no evidence of a mortality benefit. Lung volume reduction surgery removes sections of lung to reduce hyperinflation and may improve survival in selected patients. Lung transplantation, either single or double, may improve exercise capacity and health status but median survival is only 5.5 years after transplant.1

Question 39

What is the role of oxygen in COPD?

Answer 39

The use of supplemental oxygen therapy increases survival in COPD patients with chronic hypoxemia at rest. Patients receiving oxygen therapy for at least part of the day have lower rates of mortality than those not receiving oxygen

Question 40

What vaccinations are indicated in COPD?

Answer 40

• Pneumococcal, influenzae, COVID, Tdap, SHINGLES

Question 41

What is the recommended treatment for patients:
A. Less symptoms, less risk of exacerbation
B. MOre symptoms, less risk
C. Less symptoms, more risk
D. More symptoms, more risk

Answer 41

A. Offer bronchodilator, either short- or long-acting depending on symptoms
B.Start either LAMA or LABA for symptom control
C. Start long-acting bronchodilator for exacerbation prevention

LAMA is preferred over LABA for initial monotherapy

D. LAMA is preferred over LABA for initial monotherapy

For severe breathlessness, may start with dual LAMA/LABA. If less symptoms, may start only LAMA monotherapy and add LABA at a later time

If blood eosinophils ≥300 cells/microliter (0.3 × 109/L), start ICS/LABA as initial dual therapy

Question 42

What do bronchodialators do for COPD patients?

Answer 42

For patients with COPD, clinical benefits of bronchodilators include increased exercise capacity, decreased air trapping in lungs, and relief of symptoms such as dyspnea. However, the use of bronchodilators does not produce significant improvements in pulmonary function measurements of expiratory airflow such as FEV1. Bronchodilator classes available for the treatment of COPD include short- and long-acting β2-agonists, short- and long-acting anticholinergics, and methylxanthines

Question 43

What are the benefits of short acting bronchodialators?
Long acting broncho dialator benefits?

Answer 43

Short-acting bronchodilators relieve symptoms and increase exercise tolerance. Long-acting bronchodilators relieve symptoms, reduce exacerbation frequency, and improve quality of life and health status

Question 44

How do B2 agonists work?

Answer 44

β2-agonists cause bronchodilation by stimulating adenyl cyclase to increase the formation of cyclic adenosine monophosphate (cAMP), which is responsible for mediating the relaxation of bronchial smooth muscle. In addition, β2-agonists may improve mucociliary clearance within the airways. In COPD patients, short-acting β2-agonists exert a rapid onset of effect, although response generally is less than that seen in asthma. Short-acting inhaled β2-agonists cause only a small improvement in FEV1 acutely but may improve respiratory symptoms and exercise tolerance despite the small improvement in spirometric measurements.

Question 45

What are side effects of B2 agonists?

Answer 45

Inhaled β2-agonists are generally well tolerated. They can cause sinus tachycardia and rhythm disturbances in predisposed patients, but these are rarely reported. Skeletal muscle tremors can occur initially but generally subside as tolerance develops. Older patients may be more sensitive and may experience palpitations, skeletal muscle tremors, and “jittery” feelings after β2-agonist use.

Question 46

How do Short acting anticholinergic inhalers work?

Answer 46

When given by inhalation, anticholinergics, also referred to as antimuscarinics, produce bronchodilation by competitively inhibiting muscarinic receptors, subtypes M1, M2, and M3, in bronchial smooth muscle and mucus glands. This activity blocks acetylcholine, with the net effect being a reduction in cyclic guanosine monophosphate (cGMP), which normally acts to constrict bronchial smooth muscle and decreased mucus secretion.

Question 47

What are adverse effects of ipratropium?

Answer 47

Lack of systemic absorption of ipratropium greatly diminishes anticholinergic adverse effects such as blurred vision, constipation, urinary retention, nausea, and tachycardia associated with the prototype anticholinergic, atropine. The most frequent patient complaints with ipratropium are dry mouth, nausea, and an occasional metallic taste. In rare instances, inhaled anticholinergics may precipitate narrow-angle glaucoma symptoms. Compared to albuterol, ipratropium has a lower incidence of skeletal muscle tremor and tachycardia.

Question 48

What is the onset of action of Aclidinium,glycopyrrolate and umecldinium vs. Teotropium?

Answer 48

Aclidinium, glycopyrrolate, and umeclidinium have a faster onset of action (5-15 minutes) compared to tiotropium (80 minutes); however, none of these agents are recommended for acute relief of symptoms.

Question 49

Which are better for reductions in exacerbations, lamas, or LABAs?

Answer 49

When evaluating exacerbation outcomes, LAMAs (primarily tiotropium) provide a greater reduction in exacerbation frequency compared to LABAs and should be considered as first-line monotherapy for patients at high risk for exacerbation (Tables 45-13 and 45-14).

Question 50

When are combination regimens of bronchodialators used in COPD treatment?

Answer 50

Combination regimens of bronchodilators are often used in the treatment of COPD as symptoms worsen over time. Combining bronchodilators with different mechanisms of action allows the lowest possible effective doses to be used and reduces potential adverse effects from individual agents.1 Short-acting bronchodilators may be combined for patients experiencing persistent symptoms, although step-up to long-acting bronchodilator monotherapy is usually preferred (Tables 45-13 and 45-14).

Current clinical practice guidelines recommend combining long-acting bronchodilators for patients who have persistent symptoms or recurrent exacerbations on bronchodilator monotherapy (Tables 45-13 and 45-14). Combination of long-acting bronchodilators (LAMA/LABA) provides significant improvement in lung function, symptoms, and quality-of-life measures compared with LABA or LAMA monotherapy.1,53 In addition, dual long-acting bronchodilator therapy has been shown to decrease the frequency of moderate-to-severe exacerbations compared to either LAMA or LABA monotherapy.

Question 51

When might a methylxanthine such as theophylline be considered in apatient?

Answer 51

Because of the risk for drug interactions and significant intrapatient and interpatient variability in dosage requirements, theophylline therapy generally is considered for patients who are intolerant or unable to use an inhaled bronchodilator.

Question 52

Describe the dosing and therapeutic range for Theophylline?

Answer 52

Therapy can be initiated at 200 mg twice daily and titrated upward every 3 to 5 days to the target dose. Most patients require daily doses of 400 to 900 mg. Dosage adjustments generally should be made based on serum concentration results. Traditionally, the therapeutic range of theophylline has been 10 to 20 mcg/mL (mg/L; 55-111 µmol/L); however, because of the frequency of dose-related adverse effects and a lack of a clear benefit when used in higher concentrations, a more conservative therapeutic range of 8 to 15 mcg/mL (mg/L; 44-83 µmol/L) is now targeted, especially in the elderly. When concentrations are measured, trough measurements should be obtained.

Theophylline is a challenging medication to dose, monitor, and manage due to the significant intrapatient and interpatient variability in pharmacokinetics and the potential for drug interactions and toxicities. Consequently, inhaled bronchodilator therapy is currently preferred based on superior efficacy and safety, as well as ease of use. Current guidelines recommend theophylline only when inhaled bronchodilators are unavailable or unaffordable.1

Question 53

What are the mechanisms by which ICS are maybe beneficial in COPD?

Answer 53

(a) reduction in capillary permeability to decrease mucus, (b) inhibition of release of proteolytic enzymes from leukocytes, and (c) inhibition of prostaglandins. The benefits of chronic systemic corticosteroid therapy in the chronic management of COPD are not clear, and the risk of toxicity is significant.

Question 54

What is the issue with using long-term oral corticosteroids?

Answer 54

Long-term adverse effects associated with systemic corticosteroid therapy include osteoporosis, muscular atrophy, thinning of the skin, development of cataracts, and adrenal suppression and insufficiency

Question 55

When are ICS used?

Answer 55

Inhaled corticosteroids may be considered in patients with chronic stable COPD who are at high risk of exacerbation (category C or D) and used short-term as systemic therapy for acute exacerbations (Tables 45-13, 45-14, and 45-22).

Question 56

When is Dual therapy of LAMA/LABA or ICS/LABA considered?

Answer 56

For most patients with recurrent exacerbations despite optimal long-acting bronchodilator monotherapy, combination therapy with dual long-acting bronchodilators (LAMA/LABA) is preferred over combination therapy with ICS/LABA (Table 45-14).1,61

Question 56

When is ICS withdrawal recommended, considered, recommended against?

Answer 56

Question 57

When is triple therapy indicated in COPD?

Answer 57

For patients with persistent symptoms and recurrent exacerbations on dual inhaled therapy, triple therapy with LAMA/LABA/ICS is recommended as initial escalation therapy for patients with blood eosinophil counts greater than 100 cells/μL (0.1 × 109/L)

Compared to dual therapy with either LAMA/LABA or ICS/LABA, triple therapy with LAMA/LABA/ICS provides additional benefit in reducing the frequency of moderate-to-severe exacerbations in patients with COPD.

Given the risk of adverse effects with ICS, clinicians may consider bypassing triple inhalation therapy (LAMA/LABA/ICS) for those patients with persistent exacerbations and lower blood eosinophil count (<100 cells/μL [0.1 × 109/L]) in favor of oral alternatives such as roflumilast or azithromycin.1

Question 58

How do Phosphodiesterase 4 inhibitors work?

Answer 58

Phosphodiesterase 4 (PDE4) is the major phosphodiesterase found in airway smooth muscle cells and inflammatory cells and is responsible for degrading intracellular cAMP. Inhibition of PDE4 results in relaxation of airway smooth muscle cells and diminished inflammatory mediators such as TNF-α and IL-8.

Question 59

When is the PD4I Roflumilast indicated?

Answer 59

Roflumilast, an oral PDE4 inhibitor available in the United States, is recommended for patients with recurrent exacerbations despite treatment with triple inhalation therapy (LAMA/LABA/ICS) (Table 45-14).1 It may also be considered as escalation therapy for patients with recurrent exacerbations on dual long-acting bronchodilators (LAMA/LABA) who are not candidates for ICS, such as those with low blood eosinophil count (<100 cells/μL [0.1 × 109/L]) or who are at higher risk of adverse effects associated with ICS.

Question 60

Should Roflumilast and Theophylline be used together?

Answer 60

NO! Similar mechanisms of action.

Question 61

What are common adverse effects of Roflumilast?

Answer 61

Roflumilast has bothersome adverse effects that may limit therapy in some patients.70 Major effects include diarrhea, nausea, decreased appetite, weight loss, headache, and neuropsychiatric effects such as suicidal thoughts, insomnia, anxiety, and new or worsened depression. Most symptoms such as diarrhea, nausea, and headache occur early after initiation and usually resolve over time. The starting dose should be 250 mcg orally for 4 weeks and then increase to a maintenance dose of 500 mcg orally once a day to avoid adverse effects that may lead to early discontinuation of therapy. Weight loss (average of 2 kg) may be of concern in patients with low BMI, and discontinuation may be necessary if significant weight loss is observed.

Question 62

What are the benefits of chronic azithromycin therapy in COPD?

Answer 62

In certain pulmonary conditions such as cystic fibrosis and bronchiectasis, chronic therapy with macrolide antibiotics, specifically azithromycin, has proven clinical benefit due to their anti-inflammatory and antimicrobial properties. Studies evaluating chronic azithromycin therapy (either 250 mg orally daily or 500 mg orally three times a week for 12 months) in patients with COPD have reported lower rates of exacerbations among treated patients.71,72 In a subgroup analysis, patients who continued to smoke did not have a reduction in exacerbation frequency with azithromycin. Therapy with azithromycin was associated with a higher rate of colonization with macrolide-resistant bacteria and hearing deficits. In 2012, a retrospective, observational study reported an increase in cardiac events with short courses of azithromycin.73 The Food and Drug Administration (FDA) has since updated product labeling to include a precaution about QT prolongation.

Given limited evidence supporting the use of long-term treatment with azithromycin, it would be prudent to wait for more safety data before routinely recommending this therapy for more than 12 months in patients with COPD who are at high risk for exacerbations. Current guidelines recommend considering the addition of chronic azithromycin for patients with recurrent exacerbations despite optimal therapy and who are not active smokers (Table 45-14). Clinicians may choose to consider azithromycin for individual patients at high risk for exacerbations but must carefully weigh the risks and benefits of therapy.

Question 63

What is the patholophysiology behind COPD xeacerbations?

Answer 63

There is limited data about the pathophysiology of COPD exacerbation due to the chronic nature of the disease and the poor health of patients. Inflammatory mediators, including neutrophils and eosinophils, may be increased in sputum during an exacerbation. Airflow limitation may not change remarkably during an exacerbation compared to chronic baseline limitation.1 Lung hyperinflation, if present, is worsened during an exacerbation, which contributes to increasing dyspnea and poor gas exchange.

The primary physiologic change is often a worsening of ABG values due to poor gas exchange and increased muscle fatigue. For a patient experiencing a severe exacerbation, profound hypoxemia and hypercapnia can be accompanied by respiratory acidosis and respiratory failure.

Question 64

Describe the difference between mild, moderate and severe acute exacerbation in COPD?

Answer 64

Question 65

Describe the symptoms, physical examination, and diagnostic tests seen in clinical presentation of COPD exacerbation

Answer 65

Symptoms

Increased sputum volume

Acutely worsening dyspnea

Chest tightness

Presence of purulent sputum

Increased need for bronchodilators

Malaise, fatigue

Decreased exercise tolerance

Physical Examination

Fever

Wheezing, decreased breath sounds

Diagnostic Tests

Sputum sample for Gram stain and culture

Chest radiograph to evaluate for new infiltrates

Question 67

What are the goals of therapy for AECOPD?

Answer 67

AECOPD are to minimize the negative consequences of the acute exacerbation (ie, reduce symptoms, prevent hospitalization, shorten hospital stay, prevent acute respiratory failure or death), and prevent future exacerbations

Question 68

What factors warrent hospital treatment in AECOPD?

Answer 68

– presence of high-risk comorbidity
- Suboptimal response to outpatient management
- Marked worsening of dyspnea
- inability to eat or sleep due to symptoms
- mental status changes
- lack of home support for care
- uncertain diagnosis

Question 69

When are antibiotics recommended in AECOPD?

Answer 69

AB are recommended if these three cardial symptoms present OR if two are present as long as one of them is increased sputum purulence.
- Dyspnea
- Increased sputum production
- increased sputum purulence

ALso recommended if pts require mechanical ventilation
Treatment duration is 5-7 days

Question 70

How long are corticosteroids used for in AECOPD?

Answer 70

Oral or IV therapy may be used for a total duration of 5-7 days. If IV is used, it should be changed to oral after improvement in pulmonary status. Longer courses of therapy are associated with increased risk of pneumonia and adverse effects

Question 71

Describe bronchodilators in regards for AECOPD?

Answer 71

MDIs and DPIs equal in efficacy to nebulization

β-Agonists also may increase mucociliary clearance

Long-acting β-agonists or long-acting antimuscarinics should not be used for quick relief of symptoms or on an as-needed basis

Question 72

How is controlled oxygen therapy used in COPD?

Answer 72

Titrate oxygen to desired O2 sat of >90%

• Monitor arterial blood gas for the development of hypercapnia

Question 73

WHen would we use non-invasive mechanical ventilation?

Answer 73

Consider for patients with acute respiratory failure

Not appropriate for patients with altered mental status, severe acidosis, respiratory arrest, or cardiovascular instability

Question 74

What are the benefits of Noninvasive positive-pressure ventilation (NPPV)

Answer 74

NPPV has been associated with lower mortality, lower intubation rates, and shorter hospital stays for COPD exacerbations. A recent analysis regarding NPPV in patients with respiratory failure, in general, included a subset of patients with COPD and reported that the risk of hospital-based mortality and long-term mortality was reduced by 56%

Not all patients with COPD exacerbations are appropriate candidates for NPPV. Patients with altered mental status may not be able to protect their airway and thus may be at increased risk for aspiration. Patients with severe acidosis (pH < 7.25), respiratory arrest, or cardiovascular instability should not be considered for NPPV. Patients who fail a trial of NPPV or those considered poor candidates should be considered for intubation and mechanical ventilation if appropriate based on the patient’s goals of care.

Question 75

What are the benefits of corticosteroids in AECOPD?

Answer 75

Treatment with systemic corticosteroids in AECOPD has been shown to improve oxygenation, recovery time, shorten hospitalization, and reduce the risk of relapse

Adverse effects such as hyperglycemia, insomnia, and hallucinations may occur at higher doses. Depending on the patient’s clinical status, treatment may be initiated at a lower dose or tapered more quickly if these effects occur.

Question 76

Why are sputum gram stain and culture use questionable in AECOPD?

Answer 76

Utility of sputum Gram stain and culture is questionable, as some patients have chronic bacterial colonization of the bronchial tree between exacerbations

Question 77

WHat are the 4 most common organisms for acute exacerbation of COPD?

Answer 77

Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae, and Haemophilus parainfluenzae.

More virulent bacteria may be present for patients with more complicated AECOPD, including drug-resistant pneumococci, β-lactamase–producing H. influenzae and M. catarrhalis, and enteric gram-negative organisms, including Pseudomonas aeruginosa

Question 78

What is the recommended AB therapy for uncomplicated exacerbations (<4 exacerbations per year) no comorbid illness?

Answer 78

Pathogens: S. Pneumoniae, H. Influenzae, M. Catarrhalis, H. Parainfluenzae - Resistance uncommon

AB - Macrolide, Second or third gen cephalosporin, doxycycline

Therapies not recommendeda: TMP/SMX, amoxicillin, first-generation cephalosporins, and erythromycin

Question 79

What is the recommended AB therapy for complicated exacerbations (Age > 65, and>4 exacerbations per year, presence of comorbid illness)

Answer 79

PAthogens - S.pneumoniae, H.influ, M. Cata,H. Parinfluenzae, PLUS drug resistance pneumococci, B-lactamase producing H.influenzae, and M. Catarrhalis

Recommended ABS: Amoxicillin/clavulanate

Fluoroquinolone with enhanced pneumococcal activity (levofloxacin, gemifloxacin, and moxifloxacin)

Question 80

What about AB therapy for AECOPD if there are presence of risk factors for colonization and infection with MDR pathogens?

Need for chronic corticosteroid therapy

Recent hospitalization (90 days)

Recent antibiotic treatment (90 days)

Resident of long-term care facility

Answer 80

Pathogens: S. pneumoniae, H. influenzae, M. catarrhalis, H. parainfluenzae, Resistance uncommon
Some enteric gram-negativesAs above plus P. aeruginosa

USE Fluoroquinolone with enhanced pneumococcal and P.Aeruginosa activity (Levofloxacin)

IV therapy if required: β-lactamase–resistant penicillin with antipseudomonal activity third- or fourth-generation cephalosporin with antipseudomonal activity

Question 81

What is the issue with controlled oxygen therapy?

Answer 81

Oxygen therapy should be provided for patients with significant hypoxemia during an exacerbation (eg, oxygen saturation less than 90% [0.90]). Caution must be used, however, because many patients with COPD rely on mild hypoxemia to trigger their drive to breathe. In healthy individuals, drive to breathe is triggered by carbon dioxide accumulation. For patients with COPD who retain carbon dioxide due to disease progression, hypoxemia rather than hypercapnia becomes the main trigger for the respiratory drive.

Overly aggressive administration of oxygen to patients with chronic hypercapnia may result in respiratory depression and respiratory failure. Oxygen therapy should be used to achieve a PaO2 of greater than 60 mm Hg (8.0 kPa) or oxygen saturation of greater than 90% (0.90). An ABG should be obtained after oxygen initiation to monitor carbon dioxide retention resulting from hypoventilation.

Question 82

From the Canadian Thoracic society guidelines, review the Chart

Answer 82

integrated comprehensive management of Copd includes confirming Copd diagnosis with postbronchodilator spirometry, evaluation and on-going monitoring of dyspnea/symptom burden and risk of exacerbations and use of both pharmacologic and nonpharmacologic interventions (see figure 3) to alleviate dyspnea/ symptoms, improve health status, prevent aeCopd and reduce mortality. the approach should not be viewed as “stepwise” and may not necessarily occur in the order they appear for all patients. self-Management education includes optimizing inhaler device technique and [re-]review, assessment and review of medication adherence, breathing and cough techniques, early recognition of aeCopd, written aeCopd action plan and implementation (when appropriate), promoting physical activity and/or exercise, and other healthy habits including diet and smoking cessation. **inhaled Maintenance/preventative pharmacotherapies are long-acting muscarinic antagonists (laMa) and/or long-acting ẞ2-agonists (laBa) with or without inhaled corticosteroids (iCs). iCs monotherapy should not be used in Copd management. *other pharmacotherapies include oral therapies (prophylactic macrolide, and pde-4 inhibitor, mucolytic agents for patients with chronic bronchitis), alpha-1-antitrypsin augmentation therapy for documented severe a1at deficiency, and opioids for severe refractory dyspnea (see prior Cts Guideline).13 ǂsurgical therapies may include lung transplantation and lung volume reduction (including with endoscopic valves). Abbreviations. a1at, alpha-1 antitrypsin; aeCopd, acute exacerbation of Copd; Cat, Copd assessment test; Copd, chronic obstructive pulmonary disease; Cts, Canadian thoracic society; mMrC, modified Medical research Council; prn, as-needed; niV, noninvasive ventilation.

Question 83

IN which COPD patients can we consider Starting initial monotherapy with either LAMA or LABA

Answer 83

In individuals with stable COPD, at low risk of exacerbations§, with low symptom burden and health status impairment (CAT <10, mMRC 1), and only mildly impaired lung function (FEV1 ≥ 80% predicted), we recommend starting initial monotherapy with either LAMA or LABA

Question 84

When would we start LAMA/LABA dual therapy?

Answer 84

In individuals with stable COPD, at low risk of exacerbations§, with a moderate to high symptom burden/health status impairment (CAT ≥10, mMRC ≥2) and impaired lung function (FEV1 < 80% predicted), we recommend starting LAMA/LABA dual therapy as initial maintenance therapy.

Question 85

When would be consider LAMA/LABA/IC therapy in COPD?

Answer 85

In individuals with stable COPD, at low risk of exacerbations§, with a moderate to high symptom burden and/or health status impairment (CAT ≥10, mMRC ≥2) and impaired lung function (FEV1 < 80% predicted) despite LAMA/LABA dual therapy or ICS/LABA combination therapy, we recommend step-up to a LAMA/LABA/ICS triple combination therapy.

Question 86

Do we ever consider step down therapy in patients who are on triple or dual therapy

Answer 86

NO!

However, stepping down may be considered in patients in whom the step up did not result in improved symptoms or health status or because of adverse effects that are of significant importance. no studies of step-down have assessed the impact on dyspnea

Question 87

Do we ever consider ICS monotherapy in COPD patients?

Answer 87

NO!

Higher risk of pneumonia

Question 88

When might we start dual therapy vs triple therapy in a patient with stable COPD?

Answer 88

Stable COPD at LOW RISK of exacerbations but high symptom burden (CAT>10, mMRC >2) and FEV1<80% predicted - DUAL thearpy LABA/LAMA

Stable COPD at HIGH RISK of exacerbations but high symptom burden (CAT>10, mMRC >2) and FEV1<80% predicted - TRIPLE THERAPY - LABA/LAMA/ICS

Question 89

When is macrolide maintenace therapy started in COPD patients?

Answer 89

-. In individuals with stable COPD, at a high risk of exacerbations*, with a moderate to high symptom burden and/or health status impairment (CAT ≥10, mMRC ≥2) and impaired lung function (FEV1 < 80% predicted) who continue to exacerbate (either moderate or severe) despite being on LAMA/ LABA/ICS triple combination therapy, we recommend the addition of macrolide maintenance therapy

Question 90

WHen might we consider adding Roflumilast or N-Acetylcysteine?

Answer 90

In individuals with stable COPD, with a Chronic Bronchitic Phenotype at a high risk of exacerbations*, with a moderate to high symptom burden and/ or health status impairment (CAT ≥10, mMRC ≥2) and impaired lung function (FEV1 < 80% predicted) who continue to exacerbate despite being on LAMA/LABA/ICS triple combination therapy, we suggest the addition of either Roflumilast or N-Acetylcysteine

Question 91

When is COPD patient considered HIGH RISK of Exacerbation??

Answer 91

*patients are considered at “High risk of aeCopd” if ≥2 moderate aeCopd or ≥ 1 severe exacerbation in the last year

Question 92

Why is LAMA/LABA duel therapy preferred over ICS/LABA therapy?

Answer 92

Greater improvements in lung function, and lower rates of pneumonia!!

Question 93

Why don’t we consider stepping down therapy in COPD patients in generaL??

Answer 93

Withdrawing ICS may result in worsening of health status and lung function. Stepping down may be considered in patients when there are concerns that the step-up may not have been justified in the first place or because of adverse effects. No studies of step-down have assessed the impact on dyspnea. Based on evidence, we do not suggest adding any of the oral medications to improve dyspnea, exercise tolerance, physical activity levels and/or health status (rec. PICO P.1.E.). Additionally, in all individuals with stable COPD and a low risk of exacerbations, we recommend against treatment with ICS monotherapy

Question 94

When might ICS/LABA therapy be preferred of LABA/LAMA in COPD patient?

Answer 94

If they have ASTHMA ALSO!

Question 95

Do high dose ICS in triple therapy help?

Answer 95

high doses of ICS64 are not typically necessary to achieve optimum benefit in COPD, as shown by a relatively flat dose-response curve65,66 and greater incidence of adverse effects with higher inhaled ICS doses.

Question 96

MEMORIZE THE DISEASE SEVERITY treatment chart bitch!

Answer 96