Chronic Obstructive Pulmonary
Disease (COPD)
 Chronic obstructive pulmonary disease (COPD) is a leading
cause of morbidity and mortality worldwide.
 COPD is the most prevalent manifestation of obstructive
lung disease and mainly comprises chronic bronchitis and
emphysema.
 Chronic obstructive pulmonary disease (COPD) is a disease
state characterized by airflow limitation that is not fully
reversible.The airflow limitation is usually both progressive
and associated with an abnormal inflammatory response of
the lungs to noxious particles or gases.
(Pharmacotherapy principles and practice by dipirio)
 COPD has been defined (National Institute for
Health and Clinical Excellence, 2010) as:
 Airflow obstruction with a reduced FEV1/FVC ratio of less
than 0.7.
 If FEV1 is ≥ 80% of predicted normal, a diagnosis of COPD
should only be made in the presence of respiratory
symptoms, for example breathlessness or cough.
COPD: An umbrella term
• Umbrella term used to describe progressive lung diseases
which include:
• Emphysema
• Chronic bronchitis
COPD is also known as:
 Chronic Obstructive Lung Disease (COLD)
 Chronic Lower Respiratory Disease (CLRD)
Types of COPD
 Emphysema
 Permanent and destructive enlargement of airspaces
distal to the terminal bronchioles without obvious
fibrosis and with loss of normal architecture
 Always involves clinically significant airflow limitation.
 “pink puffer”
 Chronic Bronchitis
 Presence of a cough productive of sputum not
attributable to other causes on most days for at least 3
months over 2 consecutive years
 May be present in the absence of airflow limitation.
 “blue bloater”
Etiology
 Most cases of COPD are caused by inhaling pollutants; that
includes tobacco smoking (cigarettes, pipes, cigars, etc.), and
second-hand smoke.
 Fumes, chemicals and dust found in many work environments
are contributing factors for many individuals who develop
COPD.
 Genetics can also play a role in an individual’s development of
COPD—even if the person has never smoked or has ever been
exposed to strong lung irritants in the workplace.
Sign & Symptoms
 Symptoms of COPD can be different for each person, but
the common symptoms are:
 Shortness of breath
 Frequent coughing (with and without sputum or phlegm)
 Increased breathlessness
 Feeling tired, especially when exercising or doing daily
activities
 Wheezing
 Tightness in the chest
Pathogenesis of COPD
 Increased number of activated polymorphonuclear cells
and macrophages produce elastases (such as human
leukocyte elastase), resulting in lung destruction.
 Increased oxidative stress caused by free radicals in
cigarette smoke, the oxidants released by phagocytes,
and polymorphonuclear leukocytes all may lead to
apoptosis or necrosis of exposed cells
Classification of COPD
Risk Factors
Smoking
 COPD most often occurs in people 40 years of
age and older who have a history of smoking.
These may be individuals who are current or
former smokers. While not everybody who
smokes gets COPD, most of the individuals who
have COPD (about 90% of them) have smoked.
However, only one in five smokers will get
significant COPD.
Environmental Factors
 COPD can also occur in those who have had long
term exposure and contact with harmful pollutants in
the workplace. Some of these harmful lung irritants
include certain chemicals, dust, or fumes. Heavy or
long-term contact with secondhand smoke or other
lung irritants in the home, such as organic cooking
fuel, may also cause COPD. Individuals who have
worked for many years around these irritants are at
risk for developing mild COPD
Genetic Factors
 Even if an individual has never smoked or been exposed to
pollutants for an extended period of time, they can still
develop COPD. Alpha-1 Antitrypsin Deficiency (AATD) is
the most commonly known genetic risk factor for
emphysema. Alpha-1 Antitrypsin related COPD is caused by a
deficiency of the Alpha-1 Antitrypsin protein in the
bloodstream. Without the Alpha-1 Antitrypsin protein, white
blood cells begin to harm the lungs and lung deterioration
occurs. The World Health Organization and the American
Thoracic Society recommends that every individual diagnosed
with COPD be tested for Alpha-1.
 Alpha 1-antitrypsin deficiency is a genetic condition
that is responsible for about 2% cases of COPD.
 In this condition, the body does not make enough of
a protein, alpha 1-antitrypsin.
 This protein protects the lungs from damage caused
by protease enzymes, such as elastase and trypsin,
that can be released as a result of an inflammatory
response to tobacco smoke.
 Almost 90% of COPD deaths occur in low- and
middle-income countries, where effective strategies
for prevention and control are not always
implemented or accessible.
Physical Exam
 RR, HR, O2 saturation
 Gen: Barrel-chest, accessory muscle use
 CV: Quiet heart sounds
 Resp: Decreased breath sounds, wheezing, rhonchi, crackles
 CBC:  Hgb/Hct
 ABG: pH, pCO2
 Chemistry: HCO3
Diagnosis
• A simple diagnostic test called "spirometry“ measures how much
air a person can inhale and exhale, and how fast air can move
into and out of the lungs
• Spirometry can detect
COPD long before its
Symptoms appear.
Pharmacotherapy Plans
1.Bronchodilators:
A. 𝜷𝟐 agonists
Anticholinergics
Recommendations
 Inhaled therapy is preferred.
 The choice between beta2-agonists, anticholinergics, theophylline, or
combination therapy depends on the availability of medications and each
patient’s individual response in terms of symptom relief and side
effects.
 Bronchodilators are prescribed on an as-needed or on a regular basis to
prevent or reduce symptoms.
 LA inhaled bronchodilators are convenient and more effective at
producing maintained symptom relief than short-acting bronchodilators.
 LA inhaled bronchodilators reduce exacerbations and related
hospitalizations and improve symptoms and health status, and
tiotropium improves the effectiveness of pulmonary rehabilitation.
 Combining bronchodilators of different pharmacological classes
may improve efficacy and decrease the risk of side effects compared to
increasing the dose of a single bronchodilator
Methyl xanthines
Recommendations
 Methylxanthines are less effective and less well tolerated
than inhaled long-acting bronchodilators and are not
recommended if those drugs are available and
affordable.
 Addition of theophylline to salmeterol produces a
greater increase in FEV1 and relief of breathlessness than
salmeterol alone. Low-dose theophylline reduces
exacerbations but does not improve post- bronchodilator
lung function.
Inhaled corticosteroids
Recommendations
• In COPD patients with FEV1 < 60% predicted, regular treatment
with inhaled corticosteroids improves symptoms, lung function,
and quality of life, and reduces the frequency of exacerbations.
• Inhaled corticosteroid therapy is associated with an
increased risk of pneumonia.
• Withdrawal from treatment with inhaled corticosteroids
may lead to exacerbations in some patients.
• Based on efficacy and side effects, inhaled bronchodilators
are preferred over oral bronchodilators.
• Long-term monotherapy with inhaled corticosteroids is
not recommended.
• Long-term treatment with oral corticosteroids is also not
recommended
Other pharmacological treatments
 Vaccines
 Alpha-1AntitrypsinAugmentationTherapy
 Antibiotics
 Mucolytics
Mucolytic agents
 Patients with viscous sputum may benefit from
mucolytics (e.g. carbocysteine), but overall
benefits are very small.
Vaccines
 Influenza vaccines can reduce serious illness and death in
COPD patients.
 Vaccines containing inactivated viruses are recommended,
and should be given once each year.
 Pneumococcal polysaccharide vaccine is recommended for
COPD patients 65 years and older, and has been shown to
reduce community-acquired pneumonia in those under age
65 with FEV1< 40% predicted.
Alpha-1 Antitrypsin AugmentationTherapy
Not recommended for patients with COPD that is unrelated to
alpha-1 antitrypsin deficiency.
Antibiotics
 Not recommended except for treatment of infectious
exacerbations and other bacterial infections.
 Drugs include doxycycline, trimethoprim-
sulfamethoxazole and amoxicillin-clavulanate
potassium.
 Treatment with augmented penicillins,
fluoroquinolones, third-generation
cephalosporins or aminoglycosides may be
considered in patients with more severe exacerbations
Non pharmacological treatments
 Rehabilitation
 Oxygen therapy
 Ventilatory support
 Surgical treatments
 Palliative Care, End-of-life Care, and Hospice Care
Rehabilitation
 Patients at all stages of disease benefit from exercise training
programs with improvements in exercise tolerance and
symptoms of dyspnea and fatigue.
 Benefits can be sustained even after a single pulmonary
rehabilitation program.
 The minimum length of an effective rehabilitation program is
6 weeks; the longer the program continues, the more
effective the results.
Oxygen therapy
 Long-term administration of oxygen (> 15 hours per day) to
patients with chronic respiratory failure has been shown to
increase survival in patients with severe, resting hypoxemia.
 Long-term oxygen therapy is indicated for patients who have:
o PaO2 between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg).
Ventilatory support
 Combination of non-invasive ventilation with long-term
oxygen therapy may be of some use in a selected subset
of patients, particularly in those with pronounced
daytime hypercapnia.
 It may improve survival but does not improve quality of
life.
Surgical treatment
 Advantage of lung volume reduction surgery (LVRS)
over medical therapy is more significant among patients
with upper-lobe predominant emphysema and low
exercise capacity prior to treatment.
 LVRS is costly relative to health-care programs not
including surgery.
 In appropriately selected patients with very severe
COPD, lung transplantation has been shown to
improve quality of life and functional capacity.

COPD

  • 1.
  • 2.
     Chronic obstructivepulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide.  COPD is the most prevalent manifestation of obstructive lung disease and mainly comprises chronic bronchitis and emphysema.  Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible.The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. (Pharmacotherapy principles and practice by dipirio)
  • 3.
     COPD hasbeen defined (National Institute for Health and Clinical Excellence, 2010) as:  Airflow obstruction with a reduced FEV1/FVC ratio of less than 0.7.  If FEV1 is ≥ 80% of predicted normal, a diagnosis of COPD should only be made in the presence of respiratory symptoms, for example breathlessness or cough.
  • 4.
    COPD: An umbrellaterm • Umbrella term used to describe progressive lung diseases which include: • Emphysema • Chronic bronchitis COPD is also known as:  Chronic Obstructive Lung Disease (COLD)  Chronic Lower Respiratory Disease (CLRD)
  • 5.
    Types of COPD Emphysema  Permanent and destructive enlargement of airspaces distal to the terminal bronchioles without obvious fibrosis and with loss of normal architecture  Always involves clinically significant airflow limitation.  “pink puffer”  Chronic Bronchitis  Presence of a cough productive of sputum not attributable to other causes on most days for at least 3 months over 2 consecutive years  May be present in the absence of airflow limitation.  “blue bloater”
  • 6.
    Etiology  Most casesof COPD are caused by inhaling pollutants; that includes tobacco smoking (cigarettes, pipes, cigars, etc.), and second-hand smoke.  Fumes, chemicals and dust found in many work environments are contributing factors for many individuals who develop COPD.  Genetics can also play a role in an individual’s development of COPD—even if the person has never smoked or has ever been exposed to strong lung irritants in the workplace.
  • 7.
    Sign & Symptoms Symptoms of COPD can be different for each person, but the common symptoms are:  Shortness of breath  Frequent coughing (with and without sputum or phlegm)  Increased breathlessness  Feeling tired, especially when exercising or doing daily activities  Wheezing  Tightness in the chest
  • 8.
    Pathogenesis of COPD Increased number of activated polymorphonuclear cells and macrophages produce elastases (such as human leukocyte elastase), resulting in lung destruction.  Increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells
  • 9.
  • 10.
    Risk Factors Smoking  COPDmost often occurs in people 40 years of age and older who have a history of smoking. These may be individuals who are current or former smokers. While not everybody who smokes gets COPD, most of the individuals who have COPD (about 90% of them) have smoked. However, only one in five smokers will get significant COPD.
  • 11.
    Environmental Factors  COPDcan also occur in those who have had long term exposure and contact with harmful pollutants in the workplace. Some of these harmful lung irritants include certain chemicals, dust, or fumes. Heavy or long-term contact with secondhand smoke or other lung irritants in the home, such as organic cooking fuel, may also cause COPD. Individuals who have worked for many years around these irritants are at risk for developing mild COPD
  • 12.
    Genetic Factors  Evenif an individual has never smoked or been exposed to pollutants for an extended period of time, they can still develop COPD. Alpha-1 Antitrypsin Deficiency (AATD) is the most commonly known genetic risk factor for emphysema. Alpha-1 Antitrypsin related COPD is caused by a deficiency of the Alpha-1 Antitrypsin protein in the bloodstream. Without the Alpha-1 Antitrypsin protein, white blood cells begin to harm the lungs and lung deterioration occurs. The World Health Organization and the American Thoracic Society recommends that every individual diagnosed with COPD be tested for Alpha-1.
  • 13.
     Alpha 1-antitrypsindeficiency is a genetic condition that is responsible for about 2% cases of COPD.  In this condition, the body does not make enough of a protein, alpha 1-antitrypsin.  This protein protects the lungs from damage caused by protease enzymes, such as elastase and trypsin, that can be released as a result of an inflammatory response to tobacco smoke.  Almost 90% of COPD deaths occur in low- and middle-income countries, where effective strategies for prevention and control are not always implemented or accessible.
  • 14.
    Physical Exam  RR,HR, O2 saturation  Gen: Barrel-chest, accessory muscle use  CV: Quiet heart sounds  Resp: Decreased breath sounds, wheezing, rhonchi, crackles  CBC:  Hgb/Hct  ABG: pH, pCO2  Chemistry: HCO3
  • 15.
    Diagnosis • A simplediagnostic test called "spirometry“ measures how much air a person can inhale and exhale, and how fast air can move into and out of the lungs • Spirometry can detect COPD long before its Symptoms appear.
  • 16.
  • 18.
  • 19.
  • 20.
    Recommendations  Inhaled therapyis preferred.  The choice between beta2-agonists, anticholinergics, theophylline, or combination therapy depends on the availability of medications and each patient’s individual response in terms of symptom relief and side effects.  Bronchodilators are prescribed on an as-needed or on a regular basis to prevent or reduce symptoms.  LA inhaled bronchodilators are convenient and more effective at producing maintained symptom relief than short-acting bronchodilators.  LA inhaled bronchodilators reduce exacerbations and related hospitalizations and improve symptoms and health status, and tiotropium improves the effectiveness of pulmonary rehabilitation.  Combining bronchodilators of different pharmacological classes may improve efficacy and decrease the risk of side effects compared to increasing the dose of a single bronchodilator
  • 21.
  • 22.
    Recommendations  Methylxanthines areless effective and less well tolerated than inhaled long-acting bronchodilators and are not recommended if those drugs are available and affordable.  Addition of theophylline to salmeterol produces a greater increase in FEV1 and relief of breathlessness than salmeterol alone. Low-dose theophylline reduces exacerbations but does not improve post- bronchodilator lung function.
  • 23.
  • 24.
    Recommendations • In COPDpatients with FEV1 < 60% predicted, regular treatment with inhaled corticosteroids improves symptoms, lung function, and quality of life, and reduces the frequency of exacerbations. • Inhaled corticosteroid therapy is associated with an increased risk of pneumonia. • Withdrawal from treatment with inhaled corticosteroids may lead to exacerbations in some patients. • Based on efficacy and side effects, inhaled bronchodilators are preferred over oral bronchodilators. • Long-term monotherapy with inhaled corticosteroids is not recommended. • Long-term treatment with oral corticosteroids is also not recommended
  • 25.
    Other pharmacological treatments Vaccines  Alpha-1AntitrypsinAugmentationTherapy  Antibiotics  Mucolytics
  • 26.
    Mucolytic agents  Patientswith viscous sputum may benefit from mucolytics (e.g. carbocysteine), but overall benefits are very small.
  • 27.
    Vaccines  Influenza vaccinescan reduce serious illness and death in COPD patients.  Vaccines containing inactivated viruses are recommended, and should be given once each year.  Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older, and has been shown to reduce community-acquired pneumonia in those under age 65 with FEV1< 40% predicted. Alpha-1 Antitrypsin AugmentationTherapy Not recommended for patients with COPD that is unrelated to alpha-1 antitrypsin deficiency.
  • 28.
    Antibiotics  Not recommendedexcept for treatment of infectious exacerbations and other bacterial infections.  Drugs include doxycycline, trimethoprim- sulfamethoxazole and amoxicillin-clavulanate potassium.  Treatment with augmented penicillins, fluoroquinolones, third-generation cephalosporins or aminoglycosides may be considered in patients with more severe exacerbations
  • 29.
    Non pharmacological treatments Rehabilitation  Oxygen therapy  Ventilatory support  Surgical treatments  Palliative Care, End-of-life Care, and Hospice Care
  • 30.
    Rehabilitation  Patients atall stages of disease benefit from exercise training programs with improvements in exercise tolerance and symptoms of dyspnea and fatigue.  Benefits can be sustained even after a single pulmonary rehabilitation program.  The minimum length of an effective rehabilitation program is 6 weeks; the longer the program continues, the more effective the results.
  • 31.
    Oxygen therapy  Long-termadministration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival in patients with severe, resting hypoxemia.  Long-term oxygen therapy is indicated for patients who have: o PaO2 between 7.3 kPa (55 mmHg) and 8.0 kPa (60 mmHg).
  • 32.
    Ventilatory support  Combinationof non-invasive ventilation with long-term oxygen therapy may be of some use in a selected subset of patients, particularly in those with pronounced daytime hypercapnia.  It may improve survival but does not improve quality of life.
  • 33.
    Surgical treatment  Advantageof lung volume reduction surgery (LVRS) over medical therapy is more significant among patients with upper-lobe predominant emphysema and low exercise capacity prior to treatment.  LVRS is costly relative to health-care programs not including surgery.  In appropriately selected patients with very severe COPD, lung transplantation has been shown to improve quality of life and functional capacity.