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Chronic Obstructive Pulmonary Disease (COPD)

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Title: Chronic Obstructive Pulmonary Disease (COPD)


1
Chronic Obstructive Pulmonary Disease (COPD)
  • John Noviasky, PharmD

2
Background
  • Not reversible Limitation of Expiratory Airflow
  • Progressive and associated with abnormal
    inflammatory response of lungs to noxious
    substances
  • COPD most commonly refers to chronic bronchitis
    and emphysema (NOT Asthma)

3
Epidemiology
  • 16 million have COPD
  • 14 million chronic bronchitis
  • 2 milion have emphysema
  • 14 million physician visits and 600k
    hospitalizations/year
  • 30 billion dollars/year
  • Disabling disease
  • Chronic Bronchitis - 12 days/yr
  • Emphysema - 68 days/yr

4
Epidemiology
  • 4th leading cause of death
  • 107k in 1998, not including deaths from pneumonia
    and flu which are COPD complications
  • Disease can vary from chronic productive cough to
    severe, disabling dyspnea

5
Risk Factors
  • EnvironmentalOccupational
  • Grain, coal, asbestos, Pollution
  • Behavioral
  • 20 of smokers develop COPD
  • Genetic-Alpha1-antitrypsin deficiency (1),
    disease at young age
  • Other - Asthma, respiratory infections

6
Smoking-(figure 24-1)
  • Accelerated loss of lung function
  • gt35yo FEV1 decline about 20-30ml/yr
  • IF smoking, then 50-120ml/yr
  • Not all smokers get COPD, protective mechanism
    unknown (genetic?)
  • Smoke-
  • increases and activity of secretory cells
  • attracts neutrophils/macrophages - destructive
    enzymes released

7
Smoking-(figure 24-1)
  • Releases Oxygen Free radicals
  • increased concentration of inflammatory mediators
    and inhibit antiprotease activity
  • sustains chronic inflammation and susceptibility
    to damage by protease enzymes

8
Pathophysiology
  • Airflow limitation related to small airway and
    parenchymal disease
  • Chronic Bronchitis
  • Inflammation of Bronchioles
  • Mucus Hypersecretion
  • Presence of chronic productive cough for 3
    months/yr over 2 years (not asthma, not CHF,
    GERD)
  • Figure 24-2

9
Pathophysiology
  • Emphysema
  • Abnormal permanent enlargement of airspaces
    distal to terminal bronchioles, accompanied by
    destruction of their walls
  • Loss of elastic recoil and surface area for gas
    exchange
  • Figure 24-2

10
Large vs Small Airways
  • Large airways (tracheabranchs of bronchi)
  • AKA Central airways
  • Location of airway wall inflammation and
    hypersecretion seen in chronic bronchitis
  • As response to inflammation
  • increase in s (hyperplasia) and enlargement
    (hypertrophy) of submucosal glands and goblet
    cells which produce mucus

11
Large vs Small Airways
  • Smaller bronchi down to terminal bronchioles make
    up peripheral airways and site of increased air
    resistance seen in asthma and chronic bronchitis
  • IF just bronchitis and mucus production then
    still no airflow impairment (smokers cough) and
    little effect on pulmonary function testing
  • With prolonged inflammation, edema, mucus
    secretion- airway narrowing and airflow
    obstruction

12
Large vs Small Airways
  • Increased Mucus - excellent medium for recurrent
    infections - lead to further damage
  • Smokers Mucus - looks like a blanket
    compared to normal gel-like substance
  • Increased mucus combined with impaired ciliary
    function-reduced mucociliary clearance, pooling
    of secretions and increased trapping of
    bacteria - recurrent infections

13
Parenchymal Destruction
  • Lung Parenchyma
  • Made of thousands of acini (gas xchange units),
    looks like bunch of grapes
  • Each acinus contains respiratory bronchioles,
    alveolar ducts, alveolar sacs
  • Emphysema - destruction of alveolar walls and
    enlargement of terminal airspaces
  • As septal walls are destroyed, grapelike
    appearance becomes more rounded and surface area
    (for airway xchange) is reduced

14
Parenchymal Destruction
  • Inflammation
  • Important to progression of COPD
  • Inflammatory mediators and cellular components
    cause mucus hypersecretion and loss of alveolar
    structure and airway remodeling

15
Clinical Consequences
  • As result of morphologic change
  • Worsened obstruction
  • hyperinflation of the lungs
  • increased sputum production
  • reduced elastic recoil
  • recurrent respiratory infections
  • altered gas exchange
  • Respiratory muscle fatigue, ventilatory
    disorders, cardiovascular compromise, and poor
    QOL

16
Comparison with Asthma
  • Mechanism of Inflammation varies
  • Asthma - eosinophilic inflammation
  • Chronic Bronchitis - Neutrophilic
  • Mucus Hypersecretion and cough
  • important to chronic bronchitis, not to emphysema
  • may be seen in acute asthma attack
  • With bronchodilators, FEV1 is more reversible in
    asthma than COPD
  • Table 24-1

17
DiagnosisPatient Assessment
  • Guidelines- table 24-2 24-3(goldcopd.com)
  • Spirometry - for diagnosis and assessment of
    disease severity
  • Diagnosis based on subjective and objective data
  • Tobacco use - raises suspicion
  • Careful medical history
  • symptoms of cough, sputum production, dyspnea,
    wheezing
  • Early detection and intervention is important
  • Once changes occur, irreversible

18
DiagnosisPatient Assessment
  • Cough an sputum production may be present for
    years prior to airflow limitations (and not
    everyone w/symptoms go on to COPD)
  • DOE (Dyspnea on Exertion) may not be present
    until sixth or seventh decade
  • PE -
  • early on, may not have physical signs
  • Later on, barrel chest, rales, rhonchi, prolonged
    expiratory phase, decreased breath sounds,
    cyanosis, edema, pursed lip breathing

19
Spirometry Testing
  • Should be performed when pt is stable
  • Indicators for COPD
  • Decreased FEV1
  • Reduction in FEV1 to FVC ratio to lt75
  • PEF (peak expiratory flow) roughly correlate to
    FEV1, However in advanced emphysema, FEV1 can be
    quite impaired and PEF only moderately affected

20
Spirometry Testing
  • IF FEV1 lt1 L
  • 5 year Mortality 50
  • IF FEV1 lt 0.5 L
  • Mean survival lt 2yrs

21
ABG Testing
  • In stable condition
  • pH is normal
  • hypoxemia present
  • mild to moderate hypercapnia (carbon dioxide
    retention) , gets worse when FEV lt 0.8L
  • During acute exacerbation
  • pH is acidotic
  • Hypercapnia worsens

22
Other Testing
  • HB and HCT
  • May be elevated secondary to chronic hypoxia
  • Alpha1-antitrypsin concentration
  • Should be determined for pt lt50 yo developing
    COPD, or if have emphysema w/o smoking history,
    patients with family history of deficiency

23
Management Strategies
  • Table 24-4

24
Natural Course
  • Generally develops and worsens over 20-40 yrs
  • Influenced by genetic predisposition, exposure to
    inhaled irritants (tobacco smoke, pollutants),
    and repeated infections
  • Typical course for smoker
  • Asymptomatic for first two decades (may have more
    frequent viral or bacterial infections)
  • After 25-30 yrs, dyspnea may be noted and
    morning cough, irreversible damage has occurred

25
General Management
  • Goals Table 24-5
  • Generally, benefits of medication are less in
    COPD than in Asthma
  • Side effects are more frequent
  • comorbidities are more common and complicate
    treatment
  • Functional Status Goal
  • Asthma- normal functioning, including exercise
  • COPD- less ambitious, e.g. walk through house w/o
    severe SOB

26
General Management
  • PFT Goal
  • Asthma- gt80 of patients predicted normal or
    personal best (green zone)
  • COPD- may have baseline lt50 of normal and this
    patient personal best may be in the red zone
  • Overall, the goal is to obtain the best possible
    QOL that is attainable

27
General Management
  • Assess and monitor disease
  • Reduce the risk factors
  • smoking, immunize as appropriate

28
General Management
  • Manage stable COPD
  • pulmonary rehab (table 24-6), proper coughing
    techniques, postural drainage, chest percussion
    (mobilize mucus-may not be that effective)
  • Manage exacerbations
  • Adequate hydration (not done in stable COPD)
  • guaifenesin and iodide - supposed to thin
    secretions - not effective

29
Pharmacotherapy
  • Current Medications do not alter progression of
    disease
  • Symptomatic relief and minimize airflow
    obstruction
  • Realistic goals should be set
  • FEV1 (although pts may not have noticeable
    change), dyspnea, exercise tolerance, QOL,
    exacerbation rates,
  • Other Measures-utilization of healthcare,
    mortality
  • Therapy trials should be continued for weeks to
    months before assessing efficacy

30
Pharmacotherapy Bronchodilators
  • Reduce bronchial airway smooth muscle tone
  • patients are able to exhale more fully
  • None shown more effective than another
  • Inhalation better than oral route
  • First Line
  • Short Acting B2-agonist or anticholinergic
    (ipraptropium)-variable effect -some pts may have
    better outcome from one over the other
  • Should be given prn or scheduled, dependent on
    symptom frequency

31
Pharmacotherapy Bronchodilators
  • While gold standard for significant improvement
    is 12 to15 FEV1 improvement
  • patients often feel better because now able to
    empty the lungs and reduce thoracic overinflation
  • Long acting bronchodilators
  • easier than short-acting

32
Pharmacotherapy Bronchodilators
  • Theophylline - Long debated
  • Was assumed that only functioned as
    bronchodilator (not that effective)
  • Other mechanisms - stimulate diaphragm
    contractility and anti-inflammatory effects
  • When Theo withdrawn, pts can deteriorate
  • Reserved as near-last therapy

33
Pharmacotherapy Systemic Corticosteroids (CS)
  • Controversial and disappointing
  • Only 10-30 benefit
  • Difficult to determine who will benefit
  • Risk is substantial
  • Only indicated for short-term use during acute
    exacerbations

34
Pharmacotherapy Inhaled Corticosteroids (CS)
  • Minimizes risks compared to systemic CS
  • Does not seem to deter progression of disease
  • Recommended in symptomatic patients with FEV1
    lt50 and repeated exacerbations requiring
    antibiotics or systemic CS
  • No established role for cromolyn or leukotriene
    modifiers

35
Pharmacotherapy Antibiotics (abx)
  • Patients with COPD are chronically colonized
  • 50 of Acute exacerbations of COPD are infectious
  • Virus, gram (streptococcus pneumoniae), gram -
    (Haemophilus influenza)
  • 1st Amoxicillin, bactrim, doxycycline
  • 2nd B-lactamase stable penicillins, 2nd/3rd
    generation cephalosporins, extended macrolides,
    anti-pneumococcal FQ
  • No evidence of benefit from prophylactic abx

36
Pharmacotherapy (cont)
  • Antibiotics should be given when documented
    infection (gram stain, CXR shows pneumonia)
  • Oxygen therapy
  • well documented efficacy
  • O2 saturation gt90
  • Alpha1 antitrypsin
  • Is available for those with deficiency
  • not well tolerated
  • expensive

37
Acute Exacerabtions
  • 2 to 4 acute exacerbations yearly
  • increased dyspnea, cough, sputum production
  • May require hospitalization
  • Treatment
  • Supplemental oxygen
  • intense bronchodilator regimens
  • systemic CS, abx

38
Section 1
  • What sign does EB have that is typical of early
    stage of COPD
  • What breath sounds suggest increased mucus
    secretion?
  • What risk category is EB according to GOLD?
  • Can lung damage occur before COPD symptoms
    develop?

39
Section 2
  • What is the primary risk factor present in EB?
    Other risk factors?
  • What is the acceleration of FEV1 decline that
    occurs with smoking?
  • What are other environmental causes of COPD?
  • What is a pack-year?

40
Section 3
  • Is there overlap between chronic bronchitis and
    emphysema?
  • Should we test EB for Alpha1 antitrypsin?

41
Section 4
  • What is the gold standard for assessment and
    staging of COPD severity?

42
Section 5
  • What are goals for EB?
  • What should education strategy include for EB?

43
Section 6
  • What is the only intervention with beneficial
    impact on COPD progression?
  • What pharmacotherapy can be considered for
    smoking cessation?

44
Section 7
  • Which vaccinations should be considered for EB?
  • How many people die from the Flu every year?
  • Does lung disease put you at higher risk of death
    from flu?
  • How often should flu vaccine be given to COPD
    patient?
  • Is nasal flu vaccine an option for EB?

45
Section 7
  • What does the 23 in Pneumovax 23 stand for?
  • How often should Pneumovax be administered to pts
    with COPD?

46
Section 8
  • What does EB productive cough indicate?
  • What pharmacologic therapy has been demonstrated
    to modify the progressive decline in lung
    function found in COPD?
  • What is the primary pharmacologic therapy for
    COPD?
  • Can subjective benefit be seen with
    bronchodilators without objective benefit (e.g.
    PFT)?

47
Section 8
  • How do the B2 agonists produce bronchodilation?
  • Are bronchodilators more effective in asthma or
    COPD and why?
  • Which route of delivery is more effective for
    bronchodilators, oral or inhaled, and why?
  • What is the onset of action of B2 agonists
    ipraptropium, when do they reach maximal
    effectiveness, what is duration of action?

48
Section 8
  • What are some common adverse effects found with
    B2 agonists?
  • How do the anticholinergics (ipraptropium) work
    in bronchodilation?
  • How does the bronchodilation of anticholinergics
    compare to B2 agonists?
  • What is the primary inhaled anticholinergic in
    use?

49
Section 8
  • What is typical starting dose of ipraptropium,
    maximal dose?
  • What are some side effects of inhaled
    anticholinergics (ipraptropium)?
  • What structural feature decreases absorption
    through lung tissue thereby decreasing systemic
    effects?
  • What are other anticholinergics that have been
    used clinically in COPD?

50
Section 8
  • How does atropine compare to ipraptropium as far
    as Side effects and why?

51
Section 9
  • What tests can help us to determine whether B2
    agonists or anticholinergics should be used in pt
    with COPD?
  • How long should drug trial be conducted to
    determine efficacy in a patient?
  • If a partial response is obtained after 2 weeks,
    how should dosage be increased?
  • What is advantage of B2 agonist over
    anticholinergic?

52
Section 10
  • According to guidelines, should inhaled therapy
    be prescribed on prn or routine basis?

53
Section 11
  • What symptoms does EB have that are consistent
    with chronic bronchitis (CB)?
  • What organisms are colonized in patients with CB?
  • What leads to pulmonary hypertension?
  • What is cor pulmonale?

54
Section 12
  • What does an FEV1 of 1.5L indicate as far as
    severity of disease?
  • Why hasnt the FVC declined as much as FEV1 in
    EB?
  • What is the change in FEV1 with bronchodilator
    therapy and is this significant?
  • What is the definition of reversible airflow
    obstruction with use of bronchodilator?

55
Section 12
  • What is alternate absolute improvement in FEV1
    that can be considered significant?
  • Does improvement on spirometry always correlate
    to patients QOL?

56
Section 15
  • What is the advantage of using combination
    therapy?
  • Are long acting B2 agonists superior to short
    acting B2 agonists in COPD?
  • Are higher than recommended doses of salmeterol
    and formoterol useful and safe?
  • Can the long-acting B2 agonists be used as prn
    therapy?

57
Section 15
  • How does tiotropium differ from ipraptropium in
    mechanism of action?
  • How often is tiotropium dosed?
  • How does tiotropium compare to ipraptropium in
    efficacy?
  • In clinical studies, how does tiotropium (18 mcg
    daily) compare to salmeterol (50 mcg BID)?

58
Section 15
  • When should theophylline (T) be considered in
    patient with COPD?
  • List some downsides to using T
  • What is target serum concentration of T?
  • How long should theophylline trial continue?
  • What did one study find when patients
    discontinued theophylline?
  • What are possible MofA of T?

59
Section 16
  • List signs of theophylline (T) toxicity in CK
  • How much is T concentration increased with
    concomitant use of Ciprofloxacin?

60
Section 17
  • What are alternative treatments for elevated
    theophylline (T) concentration?

61
Section 18
  • Why isnt long-term treatment with systemic
    corticosteroids (SC) recommended?
  • What percentage of patients experience a clinical
    response to SC?
  • What occurred in one study which withdrew SC in
    patients with COPD? Reference 120

62
Section 19
  • What did a meta-analysis find regarding effect of
    inhaled corticosteroids (IC) on FEV1?
  • What did one study find regarding d/c of IC?
  • Do IC modify the progression of COPD?
  • Why are IC less effective in COPD than asthma?
  • According to GOLD, when should IC be used?
  • How long should therapeutic trial of IC be
    conducted?

63
Section 20
  • What did the TRISTAN study find in regards to
    efficacy of salmeterol(S)/fluticasone(F)/ SF?

64
Section 22
  • If AZ exacerbation continues, what could develop?
  • What is the mortality rate for patients requiring
    hospitalization? 1yr mortality rate? Risk of
    rehospitalization?
  • What are primary treatment of acute COPD?
  • How much supplemental O2 should be used?

65
Section 22
  • What are maximal doses of B2 agonists and
    ipraptropium?
  • Can intravenous theophylline be used in acute
    COPD?
  • What did the SCCOPE trial find
  • regarding treatment failures?
  • 2 week vs 8 week regimen?
  • Can switching to inhaled corticosteroid aid in
    tapering of systemic corticosteroid?

66
Section 23
  • How often are COPD exacerbations have an
    infectious bacterial nature?
  • When are abx most beneficial?
  • What organisms should be covered by abx therapy?

67
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