Asthma and COPD

Isabelita M. Samaniego MD, MOH, FPAFP Ma. Eufemia M. Collao, MD, DPAFP FCM 3 – College of Medicine Pamantasan ng Lungsod ng Maynila

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Session Objectives

To describe the symptomatology in asthma & COPD To describe the disease severity according to lung function based on GINA and GOLD. To describe the definition of disease control & treatment objectives for asthma & COPD To describe the national objectives for health for asthma & COPD.
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Symptomatomatology
 

Asthma Intermittent & feeling well in between Frequent to persistent & rarely feeling completely well Intermittent cough frequently dry

 

COPD Frequent cough usually wet mostly in the morning. Can become so well that asthma is seemingly cured Never full recovery usually getting progressively worse
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Disease Severity According to lung function GINA & GOLD
Asthma
None Step 1= PEFR or FEV1 > 80% ( Intermittent) Step 2 = PEFR or FEV1 > 80% ( Mild persistent)

COPD
Stage 0 =FEV1> 80% ( At risk) =FEV1/FVC>70% Stage 1 = FEV1 > 80% ( Mild) = FEV1/FVC < 70% Stage 2= 50% < FEV1 < 80% Moderate =FEV1/FVC < 70%

Step 3 = PEFR < 60% orFEV1 < 80% (Moderate Persistent)

Stage 3 = 30% < FEV1 < 50% Severe =FEV1/FVC < 70%

Step 4 PEFR or FEV1 < 60% ( Severe persistent)
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Stage 4=FEV1 < 30% ( Very severe) = FEV1/FVC < 70% Chronic Resp. & heart failure

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Definition of Disease Control & Treatment Objectives for Asthma & COPD  
Asthma= GINA COPD= GOLD
   

  

Minimal episodes No emergency visits Minimal need for prn B2 agonist No limitations on activities, including exercise PEF variability <20% ( Near normal PEF) Minimal or no adverse effects from medicine.

       

Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status Prevent & treat exacerbations Prevent & treat complications Reduce mortality Minimize side effects

Summary : To prevent the progression of the disease ( lung function deterioration) & to improve the health status or quality of life of patients as much as possible.

Summary: To achieve total absence of symptoms of wheeze, breathlessness & cough, normal or near normal lung function.

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Goal

To reduce asthma-related mortality and morbidity

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Health Status Objectives

Limit the prevalence of asthma to no more than 12% Increase the awareness of patient and family on factors that trigger or precipitate asthma to 30% Increase knowledge of the signs and symptoms of asthma by patients, families and the general public to 50%

Risk Reduction Objectives

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Services and Protection Objectives

Establish baseline data on the prevalence of asthma in the Philippines in 2000 Expand the coverage of asthma clubs in coordination with the National Asthma Movement to 75% Operationalize Asthma Education Prevention and Control Programs in 2000

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Philippine Report on Asthma 2004

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Epidemiolgy

Asthma is a common disease

Highest prevalence in UK, Australia, NZ

Increasing trend for all ages, sex, and racial groups
 

Prevalence increasing by 4%/yr Higher among children than adults (esp males), blacks than whites, impoverished children

International Study of Asthma and Allergies in Children ( ISAAC) , 1995
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Philippine Picture

No available nationwide data on asthma prevalence. Limited reports: prevalence of 12% in children 13-14y/o and 17-22% in older age grps Lung Center (1996) reported a prevalence of 22% in adults

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Current Concepts

During the last four decades, asthma has been considered primarily as a dse of airway smooth muscle. But, based on the National Institute of Health guidelines (1997) concept shifted to airway inflammation
  

Release of inflammatory mediators from eosinophils and masts cells – persistent bronchial inflammation – structural abn:
 


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fibrosis, inc sm muscle mass & mucus glands, inc epithelial shedding and thickening of the reticular basement membrane, fiibronectin deposition in the subepithelial layer
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Asthma

Definition: A chronic reactive airway disorder that produces episodic reversible airway obstruction via bronchospasm, increased mucous secretions and mucosal edema Classifications:

Extrinsic Asthma (atopic asthma)

Results from sensitivity to specific external allergens No extrinsic substance can be identified; usually preceded by severe respiratory infection

Intrinsic Asthma (non-atopic asthma)

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It causes recurring episodes of wheezing, breathlessness, chest tightness, and coughing particularly at night or in the early morning Common risk factors:
    

Domestic dust mites, Animals with fur, Coakroach Pollens and molds, Occupational irritants Tobacco smoke, Respiratory (viral) infections Exercise, Strong emotional expressions Chemical irritants and drugs

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Severity can be intermittent, or it can be persistently mild, moderate or severe; treatment decisions are based on severity Should take into account stepwise approach to pharmacologic treatment to achieve and maintain control of asthma Attacks are episodic, but airways inflammation is chronically present Medications should be taken daily to maintain to control symptoms, improve lung function and prevent attacks Asthma requires a partnership between the patient and health care professional
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Current Concepts on Asthma as a Disease
  

Airway thickening by 50-300% of normal Leading to airway remodelling Resulting to:
 

Inc airway hyperresponsiveness Non-reversibility of airway obstruction and residual obstruction after bronchodilator and anti-inflammatory therapy Accelerated dec in FEV in some asthmatic patients
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Diagnosis of Asthma

 

 

History, PE, and objective measurements of variable airflow obstruction and/or bronchial hyperresponsiveness But, Hx and PE may not be reliable at times. Thus, an objective measure is needed to dx accurately Screening strats: Hx, PE Strats for confirmation: FEV1, PEFR, Airway hyperresponsiveness

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History

Asthma should be suspected in any patient who has any of the following:
   

Cough: worsens at night Wheeze Difficulty in breathing Chest tightness
 

Dxc accuracy increases as more symptoms are present Dx is strengthened if:
  

(+) hx of waxing and waning of symptoms provoked usu by allergens, irritants, exercise, viral infection; (+)FHx; improvement after use of anti-asthma meds
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Physical Examination

Note that PE may be normal in px with asthma Wheezes are characteristic but not specific for asthma Thus, px may have normal auscultation but has significant airway obstruction A better parameter for significant airway obstruction: prolonged forced expiratory time (6 secs or more) = correlates with moderate to severe a.o.
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Forced Expiratory Volume in 1 second (FEV 1)

Spirometry to document airflow obstruction in asthma Variable airflow obstruction documented via:
 

Spontaneous variability in FEV Improvement noted 15 mins after inhaled B2agonist administration
 

Significant: 12% (200ml at least) improvement in FEV1 Or: at least 20% improvement in FEV1 after a week with or without oral steroids, or after 2 wks of inhaled steroids
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Peak Expiratory Flow Rate
In the absence of spirometry, home measurement of PEF may be used + Response to B2-agonist  PEF variability is computed as

mean percentage difference b/w postbronchodilator pm value & prebronchodilator am value x several wks or Minimum am pre-bronchodilator PEF x 1wk (Min%/ Max) asthma if variability of 20% or more
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Peak Expiratory Flow Rate
 

May also be used in clinics, ER and hospital If with an improvement of 20% or more in the PEFR 15 mins after administration of 200400ug of inhaled salbutamol or other equivalent, may be used as indicator of asthma PEFR is more suited for monitoring rather than for diagnosis Thus, it is more of an adjunct to spirometry; not as substitute
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Airway Hyperresponsiveness

If asthma is still suspected in patients with normal FEV1 Documentation via:

Methacholine or histamine inhalation challenge Best to use if the pretest probability of having asthma based on sx is 30-70% A negative test is more reliable in excluding a dx of asthma
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Asthma Classification

According to
 

Etiology And severity (clinical condition on presentation whether the patient is in acute state or chronic state)

Etiology: limited because no environmental cause can be identified

A rigorous search for a SPECIFIC environmental cause should be part of the initial assessment
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Severity:
 

Acute state (in exacerbation) Chronic state

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New Classification of Chronic Asthma Severity
Parameter S E V E R I T Y Persistent Intermittent Daytime Sx
Nocturnal awakening less than wkly Less than monthly Less than wkly More than 80% Prn B2 agonist MildModerate

Severe daily nightly
Several times daily Less than 60 ICS+LABA+ OCS 28

wkly
Monthlywkly Wkly-daily

Rescue B2 use PEF or FEV Control
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60-80
LABA + ICS

Six-Part Program to Manage and Control Asthma
1) 2) 3) 4)

5)

6)

Educate patients to develop a partnership in asthma care Assess and monitor asthma severity Avoid exposure to risk factors Establish individual medication plans for longterm management in children and adults Establish individual plans to manage asthma attacks Provide regular follow-up care

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Goals for successful management of asthma
      

Minimal or no symptoms, including nighttime symptoms Minimal asthma episodes or attacks No emergency visits to physicians or hospitals Minimal need for reliever medications No limitations on physical activities and exercise Nearly normal lung function Minimal or no side effects from medications
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Part 1: Educate Patients to develop a partnership in asthma  Patient can learn to: care
 

avoid risks factors and take medications correctly Understand the difference between “controllers” and “reliever” medications Monitor their status using symptoms and if available PEF Recognize signs that asthma is worsening and take action Seek medical help as appropriate
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Part 1: Educate Patients to develop a partnership in asthma  Asthma management plans should cover: care
 

Prevention steps for long-term control: asthma risk factors to avoid & daily medication to take Action steps to stop attacks

Ongoing education presented at every patient visit, is the key to success in all aspects of asthma management

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Part 2: Assess and monitor Asthma Severity

Monitoring includes review of symptoms and if possible measurement of lung function Regular visits (1-6 months interval) even after control of asthma is established Addressing patient’s concern, fears and expectations related to asthma to ensure compliance and adherence to asthma management

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Part 3: Avoid Exposure to Risk Factors Immunotherapy, directed at  Specific
treating an underlying allergy to grass and other pollen, domestic mites, animal dander, or alternaria, may be considered when avoiding allergens is not possible or appropriate medications fail to control asthma symptoms. Primary prevention of asthma is not yet possible, but promising leads are being actively investigated
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Part 4: Establish Individual Medication Plans for Long-term Management in Children and Adults

Stepwise Approach

Used to classify asthma and severity and guide treatment The number and frequency of medications increase (step up) as the need for asthma therapy increases, and decreases (step down) when asthma is under control

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Gain Control

First approach: Establish control promptly with a high level of therapy and then step down.

Ex: Add a short course oral glucocorticosteroid and /or a higher dose if inhaled glucocorticosteroid + long-acting B2 agonist to the therapy that corresponds with the patient’s level of asthma severity

Second approach: Start treatment at the step most appropriate to the level of asthma severity and step up if necessary

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Step up: if control is not achieved and sustained. Improvement should be achieved within 1 month. Review patient’s medication technique, compliance and avoidance of risk factors Step down: if control is sustained for at least 3 months; follow a gradual stepwise reduction in treatment. Goal is to decrease treatment to the least medication necessary to maintain control
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Review treatment every 3 to 6months once asthma is under control Consult with an asthma specialist when other conditions complicate asthma (sinusitis), the patient does not respond to therapy, or treatment at 3 or 4 required

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Acute Asthma Management
Initial Assessment History, PE, PEF or FEV1 Initial Therapy Bronchodilators; O2 if needed Good Response Observe for at least 1 hour If Stable Discharge Incomplete/Poor Response Add Systemic Glucocorticosteroid Respiratory Failure

Admit to ICU

Good Response

Poor Response Admit to Hospital

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Stepwise approach to long-term management of asthma

Criteria in the choice of treatment:
   

 

Severity of asthma Current treatment Pharmacological properties Availability of the various forms of asthma treatment Economic considerations Cultural preference Differing health care system

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Part 5: Establish Individual Plans to Manage Asthma attacks

Mild attacks can be treated at home if patient is prepared and has a personal asthma management plan that includes action steps Moderate attacks may require, and severe attacks usually require, care in a clinic or hospital Monitor response to treatment
 

Evaluate symptoms, if possible, peak flow In hospital: assess O2 saturation, consider arterial blood gas measurement, exhaustion, etc
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Part 6: Provide Regular Followup Care

Once asthma control is established, regular follow-up visits, at 1-6 months intervals as appropriate During visits, monitor and review treatment plans, medications and level of asthma control

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Goal

Morbidity and Mortality from lifestyle-related diseases are reduced and the quality of life of those who are suffering from such diseases is improved.

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National Objective

Mortality from degenerative or lifestylerelated diseases is reduced. Mortality rate from COPD per 100,000 population Less than 20.8 deaths per 100,000 population (PHS, 2000)

Indicator

Target

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Strategic Thrusts for 2005 to 2010

  

Implement sound, long-term and sustained Healthy Lifestyle promotion programs Promote information, education and advocacy campaigns Translate and implement provisions of the tobacco laws as local ordinances and develop community infrastructure supportive of healthy lifestyle Pursue training of clinicians and other frontline healthcare providers Manage risk behaviors and risk factors Strengthen networking and collaboration Support and implement financial risk protection measures

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Definition

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 Diagnosis should be considered in any patient who has symptoms of cough, sputum production, or dyspnea, and/or history of exposure to risk factors for the disease.
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Components of COPD that may coexist  Emphysema with Chronic Bronchitis
 

Small airway disease ( Obstructive Bronchiolitis) Chronic Asthma with only partial reversibility

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Risk Factors
     

Smoking – 85% Coal Isocyanates Silica Cadmium Other dust

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Classification of Severity of COPD 
Stage 0: At Risk
 

Normal spirometry Chronic symptoms (cough, sputum production)

Stage I: Mild COPD
  

FEV1/FVC < 70% FEV1 80% predicted With or without chronic symptoms (cough, sputum production)
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Stage II Moderate
 

FEV1/FVC ,70%; 50% FEV1<80% predicted w/ or w/o chromic symptoms

Stage III Severe COPD
 

FEV1/FVC ,70%; 30% FEV1<50% predicted w/ or w/o chromic symptoms

Severe IV Severe COPD
 

FEV1/FVC ,70%; 30% FEV1<50% predicted Plus chronic respiratory failure
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Stages of COPD
( Australian New Zealand Guidelines)COPDX

Stage Mild

Postbronchodilator FEV1 60-80% predicted 40-59% predicted < 40% predicted

Moderate Severe

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EPIDEMIOLOGY

Prevalence and morbidity data greatly underestimate the total burden of COPD because the disease is usually not diagnosed until it is clinically apparent and moderately advanced Mortality data also underestimate COPD as a cause of death because the disease is more likely to be cited as a contributory than as an underlying cause of death, or may not be cited at all
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G lobal Initiative for Chronic
bstructive O ung L isease

D
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GOLD Structure
GOLD Executive Committee
Sonia Buist, MD – Chair Roberto Rodriguez-Roisin, MD – Co-Chair

Science Committee
Klaus Rabe, MD, PhD - Chair

Dissemination/Implementation Task Group
Christine Jenkins, MD - Chair

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GOLD Executive Committee
S. Buist, Chair, US N. Khaltaev, Switzerland WHO A. Anzueto, US ATS M. Lopez, Uruguay ALAT P. Calverley, UK E. Nizankowska, Poland T. DeGuia, Philippines K. Rabe, Netherlands Y. Fukuchi, Japan APSR C. Jenkins, Australia R. Rodriguez-Roisin, Spain T. van der Molen, J. Kiley, US NHLBI A. Kocabas, Turkey Netherlands

C. Van Weel, Netherlands
WONCA

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GOLD Science Committee
K. Rabe, Chair A. Agusti, A. Anzueto P. Barnes S. Buist P. Calverley

M. Decramer Y. Fukuchi P. Jones R. RodriguezRoisin J. Vestbo J. Zielinski
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Description of Levels of Evidence
Evidence Category A B C D
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Sources of Evidence
Randomized controlled trials (RCTs). Rich body of data Randomized controlled trials (RCTs). Limited body of data Nonrandomized trials Observational studies. Panel consensus judgment

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GOLD Structure
GOLD Executive Committee
Sonia Buist, MD – Chair Roberto Rodriguez-Roisin, MD – Co-Chair

Science Committee
Klaus Rabe, MD, PhD - Chair

Dissemination/Implementation Task Group
Christine Jenkins, MD - Chair

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GOLD National Leaders -

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Slovenia Ireland Germany Australia Yugoslavia Croatia Canada Philippines Brazil Austria Taiwan United States Portugal Thailand ROC Malta Norway Greece Moldova China Syria South Africa United Kingdom Hong Kong ROC Italy New Nepal Chile Israel Zealand Argentina Mexico Pakista Russia United Arab Emirates n Peru Japan GOLD National Poland Korea Netherland Leaders Egypt s Switzerland India Venezuela Georgia France Macedonia Czech Iceland Denmark Turkey Belgium Slovakia Republic Singapore Spain Columbia Ukraine Romania Uruguay 01/09/09 61 Sweden Kyrgyzstan Vietnam Albania

Saudi Arabia

Bangladesh

GOLD Website Address http://www.goldcopd.o rg

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GOLD Objectives
Increase awareness of COPD among health professionals, health authorities, and the general public.
s

Improve diagnosis, management and prevention of COPD.
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Stimulate research in COPD.

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Global Strategy for Diagnosis, Management and Prevention of COPD
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Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical

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Definition of COPD
s

COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious 01/09/09 65 particles or gases.

s

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Classification of COPD Severity by Spirometry Stage I: Mild FEV /FVC < 0.70
1

FEV1 > 80% predicted Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted FEV1/FVC < 0.70 30% < FEV1 < 50% predicted FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted plus

Stage III: Severe

Stage IV: Very Severe
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“At Risk” for COPD
s

COPD includes four stages of severity classified by spirometry. A fifth category--Stage 0: At Risk--that appeared in the 2001 report is no longer included as a stage of COPD, as there is incomplete evidence that the individuals who meet the definition of “At Risk” (chronic cough and sputum production, normal spirometry) necessarily progress on to Stage I: Mild COPD. The public health message is that chronic cough and sputum are not normal remains important - their 67 01/09/09 presence should trigger a search for underlying

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Global Strategy for Diagnosis, Management and Prevention of COPD
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Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical

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Burden of COPD: Key Points

COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing. COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries. The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population. 01/09/09 69

Burden of COPD: Prevalence

Many sources of variation can affect estimates of COPD prevalence, including e.g., sampling methods, response rates and quality of spirometry. Data are emerging to provide evidence that prevalence of Stage I: Mild COPD and higher is appreciably higher in: - smokers and ex-smokers - people over 40 years of age - males
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COPD Prevalence Study in Latin America
The prevalence of postbronchodilator FEV1/FVC < 0.70 increases steeply with age in 5 Latin American Cities
01/09/09 Source: Menezes AM et al. Lancet 2005 71

Burden of COPD: Mortality

COPD is a leading cause of mortality worldwide and projected to increase in the next several decades. COPD mortality trends generally track several decades behind smoking trends. In the US and Canada, COPD mortality for both men and women have been increasing. In the US in 2000, the number of COPD deaths was greater among women than men.
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Percent Change in AgeAdjusted Death Rates, U.S., 1965-1998
Proportion of 1965 Rate 3.0 2.5 2.0 1.5 1.0 0.5 0

Coronary Heart Disease

Stroke

Other CVD

COPD

All Other Causes

–59%

–64%

–35%

+163%

–7%
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1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998

Source: NHLBI/NIH/DHHS

Of the six leading causes of death in the United States, only COPD has been increasing Source: Jemal A. et al. JAMA steadily since
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COPD Mortality by Gender,
U.S., 1980-2000
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Number Deaths x 1000
60 50 40 30 20 10 0 1980
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Men

Women

1985

1990

1995

2000
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Source: US Centers for Disease Control and

Global Strategy for Diagnosis, Management and Prevention of COPD
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Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical

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Risk Factors for COPD
Genes Exposure to particles ● Tobacco smoke ● Occupational dusts, organic and inorganic ● Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings ● Outdoor air pollution
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Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Nutrition Comorbidities
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Risk Factors for COPD
Nutrition Infections Socio-economic status

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Aging Populations

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Global Strategy for Diagnosis, Management and Prevention of COPD
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Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical

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Changes in Large Airways of COPD Patients
Mucus hypersecretion Neutrophils in sputum

Goblet cell hyperplasia

Squamous metaplasia of epithelium No basement membrane thickening ↑ Macrophages ↑ CD8+ lymphocytes Little increase in airway smooth muscle

Mucus gland hyperplasia

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Source: Peter J. Barnes, 81 MD

Changes in the Lung Parenchyma in COPD Patients

Alveolar wall destruction

Loss of elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes
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Source: Peter J. Barnes, 82 MD

Changes in Pulmonary Arteries in COPD Patients

Endothelial dysfunction

Intimal hyperplasia

Smooth muscle hyperplasia

↑ Inflammatory cells (macrophages, CD8+ lymphocytes)
Source: Peter J. Barnes, 83 MD

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Pathogenesis of COPD Cigarette smoke
Biomass particles Particulates Host factors Amplifying mechanisms

LUNG INFLAMMATION
Anti-oxidants Anti-proteinases

Oxidative stress

Proteinases
Repair mechanisms

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COPD PATHOLOGY

Source: Peter J. Barnes,

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Inflammatory Cells Involved in COPD

Cigarette smoke (and other irritants)

Epithelial cells

Alveolar macrophage
Chemotactic factors

Fibroblastlymphocyte

CD8+

Neutrophil

Monocyte

PROTEASESCathepsins
MMPs

Neutrophil elastase

Mucus hypersecretion Fibrosis Alveolar wall destruction (Obstructive (Emphysema) bronchiolitis)
01/09/09 85 Source: Peter J. Barnes, MD

Oxidative Stress in COPD Macrophage
Anti-proteases SLPI α 1-AT Proteolysis

Neutrophil

NF-κ B IL-8 TNF-α

↓ HDAC2 ↑Inflammation Steroid resistance

O2-, H202 OH., ONOO-

Neutrophil recruitment

Isoprostanes ↑ Mucus secretion
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Plasma leak

Bronchoconstriction

Source: Peter J. Barnes, 86 MD

Differences in Inflammation and its Consequences: Asthma and COPD

ASTHMA
Allergens
Y

Cigarette smoke
Y Y

COPD

Ep cells

Mast cell Alv macrophage Ep cells

CD4+ cell (Th2)

Eosinophil

Bronchoconstricti on AHR

CD8+ cell (Tc1)

Neutrophil

Small airway narrowing Alveolar destruction

Reversible
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Airflow Limitation

Irreversible
87 Source: Peter J. Barnes,

Air Trapping in COPD Inspiration Normal
small airway

Mild/moderate COPD

Severe COPD

alveolar attachments Expiration

loss of elasticity

loss of alveolar attachments

closure

↓ Health status
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Dyspnea ↓ Exercise capacity

Air trapping Hyperinflation
Source: Peter J. Barnes,
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Pulmonary Hypertension in COPD
Chronic hypoxia Pulmonary vasoconstriction Muscularization Pulmonary hypertension Cor pulmonale Intimal hyperplasia Fibrosis Obliteration Edema Death
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Source: Peter J. Barnes, MD

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Inflammation in COPD Exacerbations
Bacteria Viruses Non-infective Pollutants

Macrophages

Epithelial cells

TNF-α

IL-8

IL-6

Neutrophils

Oxidative stress
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Source: Peter J. Barnes,

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Global Strategy for Diagnosis, Management and Prevention of COPD
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Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical

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Four Components of COPD Management
1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD
q q q

Education Pharmacologic Non-pharmacologic
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• Manage exacerbations
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GOALS of COPD

MANAGEMENT
VARYING EMPHASIS WITH DIFFERING SEVERITY • Relieve symptoms

• Prevent disease progression • Improve exercise tolerance • Improve health status • Prevent and treat complications • Prevent and treat
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Four Components of COPD Management
• Assess and monitor disease • Reduce risk factors • Manage stable COPD
q q q

Education Pharmacologic Non-pharmacologic
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• Manage exacerbations
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Management of Stable COPD

A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible.
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Assess and Monitor COPD: Key Points

Comorbidities are common in COPD and

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Diagnosis of COPD
SYMPTOMS cough sputum shortness of breath EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution

SPIROMETRY
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² ² ²

Management of Stable COPD

Assess and Monitor COPD: Spirometry
Spirometry should be performed after the administration of an adequate dose of a shortacting inhaled bronchodilator to minimize variability. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly. 01/09/09 97

Spirometry: Normal and Patients with COPD

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Differential Diagnosis: COPD and Asthma
COPD
• Onset in mid-life
ASTHMA

• Onset early in life (often
childhood)

• Symptoms slowly progressive • • •
Long smoking history Dyspnea during exercise Largely irreversible airflow limitation

• Symptoms vary from day to day • Symptoms at night/early morning • Allergy, rhinitis, and/or eczema
also present

• Family history of asthma • Largely reversible airflow
limitation
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COPD and CoMorbidities
COPD patients are at increased risk for:
• • • • • •

Myocardial infarction, angina Osteoporosis Respiratory infection Depression Diabetes Lung cancer

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100

COPD and CoMorbidities
COPD has significant extrapulmonary (systemic) effects including:
• • •

Weight loss Nutritional abnormalities Skeletal muscle dysfunction

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101

Four Components of COPD Management
• Assess and monitor disease • Reduce risk factors • Manage stable COPD
q q q

Education Pharmacologic Non-pharmacologic
102

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• Manage exacerbations

Management of Stable COPD

Reduce Risk Factors: Key Points  Reduction of total personal exposure to
tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD.

 Smoking cessation is the single most
effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its
103

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Brief Strategies to Help the Patient Willing to Quit Smoking
• ASK • ADVISE • ASSESS • ASSIST • ARRANGE
01/09/09

Systematically identify all tobacco users at every visit. Strongly urge all tobacco users to quit. Determine willingness to make a quit attempt. Aid the patient in quitting. Schedule follow-up contact.
104

Management of Stable COPD

Reduce Risk Factors: Smoking Cessation

 Counseling delivered by physicians and
other health professionals significantly increases quit rates over self-initiated strategies. Even a brief (3-minute) period of counseling to urge a smoker to quit results in smoking cessation rates of 5-10%.

 Numerous effective pharmacotherapies for
smoking cessation are available and pharmacotherapy is recommended when 01/09/09
105

Management of Stable COPD

Reduce Risk Factors: Indoor/Outdoor Air Pollution

 Reducing the risk from indoor and outdoor
air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients.

 Reduction of exposure to smoke from
biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.
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Four Components of COPD Management
• Assess and monitor disease • Reduce risk factors • Manage stable COPD
q q q

Education Pharmacologic Non-pharmacologic
107

01/09/09

• Manage exacerbations

Management of Stable COPD

Manage Stable COPD: Key Points approach to managing stable COPD  The overall
should be individualized to address symptoms and improve quality of life.

For patients with COPD, health education plays an important role in smoking cessation (Evidence A) and can also play a role in improving skills, ability to cope with illness and health status. None of the existing medications for COPD have been shown to modify the long-term decline in lung function that is the hallmark of this disease (Evidence A). Therefore, pharmacotherapy for COPD is used to decrease symptoms and/or complications.
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Management of Stable COPD

Pharmacotherapy: Bronchodilators  Bronchodilator medications are central to the
symptomatic management of COPD (Evidence A). They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations.

 

The principal bronchodilator treatments are ß2agonists, anticholinergics, and methylxanthines used singly or in combination (Evidence A). Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators 01/09/09 109

Management of Stable COPD

Pharmacotherapy: Glucocorticosteroids

The addition of regular treatment with inhaled glucocorticosteroids to bronchodilator treatment is appropriate for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations (Evidence A). An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more 01/09/09

110

Management of Stable COPD

Pharmacotherapy: Glucocorticosteroids  The dose-response relationships and long-term safety of inhaled glucocorticosteroids in COPD are not known.

Chronic treatment with systemic glucocorticosteroids should be avoided because of an unfavorable benefit-torisk ratio (Evidence A).
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Management of Stable COPD

Pharmacotherapy: Vaccines

In COPD patients influenza vaccines can reduce serious illness (Evidence A). Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted (Evidence B).
112

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Management of Stable COPD

All Stages of Disease Severity

Avoidance of risk factors - smoking cessation
- reduction of indoor pollution - reduction of occupational exposure

Influenza vaccination
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Therapy at Each Stage of COPD
I: Mild II: Moderate III: Severe IV: Very Severe
 FEV1/FVC < 70%  FEV1/FVC < 70%  FEV1/FVC < 70%  FEV1/FVC < 70%  FEV1 > 80% predicted  50% < FEV1 < 80% predicted  30% < FEV1 < 50% predicted  FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure

Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations
Add long term oxygen if chronic respiratory failure. Consider surgical 114 treatments

01/09/09

Management of Stable COPD

 

Other Pharmacologic Treatments

Antibiotics: Only used to treat infectious exacerbations of COPD Antioxidant agents: No effect of nacetylcysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids

01/09/09

Mucolytic agents, Antitussives, Vasodilators: Not recommended in

115

Management of Stable COPD

Non-Pharmacologic Treatments
Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue (Evidence A). Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase
116

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Four Components of COPD Management
1. Assess and monitor disease 2. Reduce risk factors 3. Manage stable COPD
q q
Revised 2006

Education Pharmacologic Non-pharmacologic
117

q

01/09/09

• Manage exacerbations

Management COPD Exacerbations

Key Points
An exacerbation of COPD is defined as: “An event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”

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118

Management COPD Exacerbations

Key Points
The most common causes of an
exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified (Evidence B).

Patients experiencing COPD exacerbations
with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment (Evidence 01/09/09 119 B).

Manage COPD Exacerbations

Key Points

Inhaled bronchodilators inhaled ß2-agonists

(particularly

with or without anticholinergics) and oral glucocortico- steroids are effective treatments for exacerbations of COPD (Evidence
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120

Management COPD Exacerbations

Key Points

Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality (Evidence A). Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect 01/09/09 121

Global Strategy for Diagnosis, Management and Prevention of COPD
s

s s s

s
01/09/09

s

Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management Practical

122

Translating COPD Guidelines into Primary Care

KEY POINTS

Better dissemination of COPD guidelines and their effective implementation in a variety of health care settings is urgently required. In many countries, primary care practitioners treat the vast majority of patients with COPD and may be actively involved in public health campaigns and in bringing messages about reducing exposure to risk factors to both patients and the public.
123

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Translating COPD Guidelines into Primary Care

KEY POINTS

Spirometric confirmation is a key component of the diagnosis of COPD and primary care practitioners should have access to high quality spirometry. Older patients frequently have multiple chronic health conditions. Comorbidities can magnify the impact of COPD on a patient’s health status, and can complicate the management of COPD.
124

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Global Strategy for Diagnosis, Management and Prevention of COPD SUMMARY
s

s s s

s
01/09/09

Definition, Classification Burden of COPD Risk Factors Pathogenesis, Pathology, Pathophysiology Management
125

s

Global Strategy for Diagnosis, Management and Prevention of COPD: Summary

 COPD is increasing in
prevalence in many countries of the world.

 COPD is treatable and
preventable.

 The GOLD program offers a
01/09/09

strategy to identify patients and to treat them according to

126

Global Strategy for Diagnosis, Management and Prevention of COPD: Summary

  

COPD can be prevented by avoidance of risk factors, the most notable being tobacco smoke. Patients with COPD have multiple other conditions (comorbidities) that must be taken into consideration. GOLD has developed a global network to raise awareness of COPD and disseminate information on diagnosis
127

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WORLD COPD DAY
November 14, 2007

Raising COPD Awareness Worldwide
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128

Global Initiative for Chronic Obstructive Lung Disease  Conducted in collaboration with the US National (GOLD)

Heart Lung and Blood Institute (NHLBI) and WHO. Goal:
To increase awareness of COPD and decrease morbidity and mortality from the disease to improve prevention and management of COPD through a concerted worldwide effort of people involved in all facets of health care and health care policy, and to encourage a renewed research interest in this extremely prevalent disease
129

Aims :

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GOLD Workshop Report: 4 Components of COPD Management Plan
1) 2) 3) 4)

Assess and monitor disease Reduce risk factors Manage stable COPD Manage exacerbations

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130

Component 1: Assess and Monitor Disease
 

KEY POINTS: Diagnosis of COPD is based on history of exposure to risk factors and the presence of airflow limitation that is not fully reversible, w/ or without the presence of symptoms Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation, even if they do not have dyspnea
131

01/09/09

For the diagnosis and assessment of COPD, Spirometry is the gold standard, as it is the most reproducible, standardized, and objective way of measuring airflow limitation. Health care workers involved in the diagnosis and management of COPD patients should have access to spirometry Measurement of arterial blood gas tensions should be considered in all patients with FEV<40% predicted or clinical signs suggestive of respiratory failure or right heart failure
132

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Component 2: Reduce Risk Factors  KEY POINTS:

Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD Smoking cessation is the single most effective- and cost effective – way in most people to reduce the risk of developing COPD and stop its regression
133

01/09/09

Brief tobacco dependence counseling is effective and every tobacco user should be offered at least this treatment at every visit to a health care provider  Several effective pharmacotherapies for tobacco dependence are available and at least one of these medications should be added to counseling if necessary and in the absence of contraindications  Progression of many occupationally induced respiratory disorders can be reduced or controlled through a variety of strategies aimed at reducing the burden of inhaled particles and gases 01/09/09 134

Component 3: Manage Stable COPD
 

KEY POINTS: The overall approach to managing stable COPD should be characterized by a stepwise increase in treatment, depending on the severity of the disease Health education can play a role in improving skills, ability to cope with illness, and health status

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135

Pharmacotherapy for COPD is used to decrease symptoms and/or complications Bronchodilator medications are central to the symptomatic management of COPD, which are given on as-needed basis or on a regular basis to prevent or reduce symptoms Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators, but more expensive Addition of regular treatment with inhaled glucocortisteroids to bronchodilator treatment is appropriate for symptomatic COPD patients - stage III and IV- and repeated exacerbations
136

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Component 4: Manage Exacerbations
 

KEY POINTS: Most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but 1/3 of the cause of severe exacerbations cannot be identified Inhaled bronchodilators are effective treatment for exacerbation of COPD

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137

Those with clinical symptoms of infections benefit from antibiotic treatment Non-invasive intermittent positive pressure ventilation (NIPPV) in exacerbations improves the blood gases and pH, reduces hospital mortality decreases the need for invasive mechanical ventilation and intubation and decreased the length of hospital stay

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138

  

 

  

Symptomatic therapyA) Short acting bronchodilators B) Long acting inhaled anticholinergic agents ( tiotropium) C) Salmeterol – long acting B 2 agonist, formoterol Moderate- Severe COPD- FEV1 < 50% predicted with two exacerbation per year. Inhaled corticosteroids Combined B 2 agonist and inhaled corticosteroids Theophyllines, mucolytics may still have a role

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139

Pulmonary Rehabilitation – 7-8 weeks improve exercise capacity and quality of life. Oxygen therapy –appropriate for patients who are hypoxemic at rest ( PaO2 less than or equal to 5.5 mm Hg or 56 to 59 mm Hg with evidence of end organ effects of the hypoxemia ) Treatment of exacerbation

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140

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141