asthma and copd

04/08/23 1

Asthma and COPD

Isabelita M. Samaniego MD, MOH, FPAFPMa. Eufemia M. Collao, MD, DPAFP

FCM 3 – College of MedicinePamantasan 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 COPD

NoneStage 0 =FEV1> 80%

( At risk) =FEV1/FVC>70%

Step 1= PEFR or FEV1 > 80%

( Intermittent)

Stage 1 = FEV1 > 80%

( Mild) = FEV1/FVC < 70%

Step 2 = PEFR or FEV1 > 80%

( Mild persistent)

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)

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 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.Summary:

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

COPD= GOLD Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status Prevent & treat exacerbations Prevent & treat complications Reduce mortality Minimize side effectsSummary :

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.

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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% Risk Reduction Objectives

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%

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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:

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 Intrinsic Asthma (non-atopic asthma)

No extrinsic substance can be identified; usually preceded by severe respiratory infection

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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 B2-

agonist 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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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 post-bronchodilator pm value & pre-bronchodilator am value x several wks or

Minimum am pre-bronchodilator PEF x 1wk (Min%/ Max)

asthma if variability of 20% or more

Peak Expiratory Flow Rate

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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 200-400ug 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 SeverityParameter S E V E R I T Y

Persistent

Intermittent Mild-Moderate

Severe

Daytime Sx less than wkly wkly daily

Nocturnal awakening

Less than monthly

Monthly- wkly

nightly

Rescue B2 use

Less than wkly Wkly-daily Several times daily

PEF or FEV More than 80% 60-80 Less than 60

Control Prn B2 agonist LABA + ICS ICS+LABA+ OCS

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Six-Part Program to Manage and Control Asthma

1) Educate patients to develop a partnership in asthma care

2) Assess and monitor asthma severity

3) Avoid exposure to risk factors

4) Establish individual medication plans for long-term management in children and adults

5) Establish individual plans to manage asthma attacks

6) 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 care Patient can learn to:

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 care Asthma management plans should cover:

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 Specific Immunotherapy, directed at

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 ManagementInitial Assessment

History, PE, PEF or FEV1

Initial TherapyBronchodilators; O2 if needed

Incomplete/Poor Response

Add SystemicGlucocorticosteroid

Good Response

Observe for at least 1 hour

If Stable Discharge Good Response Poor Response

Admit to Hospital

Respiratory Failure

Admit toICU

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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 Follow-up 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 lifestyle-

related diseases is reduced. Indicator

Mortality rate from COPD per 100,000 population

Target Less than 20.8 deaths per 100,000

population (PHS, 2000)

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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 coexistwith Chronic Bronchitis Emphysema 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)COPDXStage Postbronchodilator FEV1

Mild 60-80% predicted

Moderate 40-59% predicted

Severe < 40% predicted

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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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lobal Initiative for Chronic

bstructive

ung

isease

lobal Initiative for Chronic

bstructive

ung

isease

G

OLD

G

OLD

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GOLD Structure

GOLD Executive CommitteeSonia Buist, MD – Chair

Roberto Rodriguez-Roisin, MD – Co-Chair

Science Committee

Klaus Rabe, MD, PhD - Chair

Science Committee


Dissemination/ImplementationTask Group

Christine Jenkins, MD - Chair



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GOLD Executive Committee

S. Buist, Chair, US

A. Anzueto, US ATS

P. Calverley, UK

T. DeGuia, Philippines

Y. Fukuchi, Japan APSR

C. Jenkins, Australia

J. Kiley, US NHLBI

A. Kocabas, Turkey

N. Khaltaev, Switzerland WHO

M. Lopez, Uruguay ALAT

E. Nizankowska, Poland

K. Rabe, Netherlands

R. Rodriguez-Roisin, Spain

T. van der Molen, Netherlands

C. Van Weel, Netherlands WONCA

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GOLD Science Committee

K. Rabe, Chair A. Agusti, A. AnzuetoP. BarnesS. BuistP. Calverley

M. DecramerY. Fukuchi P. JonesR. Rodriguez-RoisinJ. VestboJ. Zielinski

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Evidence Category

Sources of Evidence

A Randomized controlled trials (RCTs). Rich body of data

B Randomized controlled trials(RCTs). Limited body of data

C Nonrandomized trialsObservational studies.

D Panel consensus judgment

Description of Levels of Evidence

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GOLD Structure

GOLD Executive CommitteeSonia Buist, MD – Chair

Roberto Rodriguez-Roisin, MD – Co-Chair

Science Committee


Science Committee






GOLD National Leaders - GNL

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United StatesUnited States

United Kingdom

ArgentinaArgentina

AustraliaAustraliaBrazilBrazil Austria

CanadaCanada

Chile

Belgium

ChinaChina

DenmarkDenmark

ColumbiaColumbia

CroatiaCroatia

EgyptEgypt

Germany

Greece

IrelandIreland

ItalyItaly

SyriaSyria

Hong Kong ROC

Japan

IcelandIndiaIndia

KoreaKorea

KyrgyzstanUruguayUruguay

MoldovaMoldova

NepalNepal

Macedonia

Malta

Netherlands

New Zealand

PolandPoland

NorwayNorway

Portugal

GeorgiaGeorgia

Romania

Russia

SingaporeSlovakia

Slovenia Saudi ArabiaSaudi Arabia

South AfricaSouth Africa

Spain

SwedenSweden

ThailandThailand

SwitzerlandSwitzerland

UkraineUkraine

United Arab EmiratesUnited Arab Emirates

Taiwan ROC

VenezuelaVenezuela

Vietnam

Peru

Yugoslavia

Albania

Bangladesh

France

Mexico

Turkey Czech Republic

Pakistan

Israel

GOLD National Leaders

Philippines

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GOLD Website Address

http://www.goldcopd.org

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GOLD Objectives

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

Improve diagnosis, management and prevention of COPD.

Stimulate research in COPD.

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Global Strategy for Diagnosis, Management and Prevention of COPD


Definition, Classification

Burden of COPD Risk Factors Pathogenesis,

Pathology, Pathophysiology

Management Practical

Considerations





Considerations

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Definition of COPD

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 particles or gases.

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Classification of COPD Severity

by SpirometryStage I: Mild FEV1/FVC < 0.70

FEV1 > 80% predicted

Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or

FEV1 < 50% predicted plus chronic respiratory failure

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“At Risk” for COPD

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 presence should trigger a search for underlying cause(s).

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Considerations





Considerations

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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.

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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 post-bronchodilator FEV1/FVC < 0.70 increases steeply with age in 5 Latin American Cities

Source: Menezes AM et al. Lancet 2005

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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 Age-Adjusted Death Rates, U.S., 1965-1998

Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998

00

0.50.5

1.01.0

1.51.5

2.02.0

2.52.5

3.03.0

Proportion of 1965 Rate Proportion of 1965 Rate

1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998 1965 - 19981965 - 1998

–59%–59% –64%–64% –35%–35% +163%+163% –7%–7%

CoronaryHeart

Disease

CoronaryHeart

Disease

StrokeStroke Other CVDOther CVD COPDCOPD All OtherCauses

All OtherCauses

Source: NHLBI/NIH/DHHSSource: NHLBI/NIH/DHHS

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Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970

Source: Jemal A. et al. JAMA 2005

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COPD Mortality by Gender,U.S., 1980-2000

0

10

20

30

40

50

60

70

1980 1985 1990 1995 2000

Men

Women

Num

ber

Death

s x

100

0N

um

ber

Death

s x

100

0

Source: US Centers for Disease Control and Prevention, 2002

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Considerations





Considerations

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Risk Factors for COPD

Lung growth and development

Oxidative stress

Gender

Age

Respiratory infections

Socioeconomic status

Nutrition

Comorbidities

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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Risk Factors for COPD

NutritionNutrition

InfectionsInfections

Socio-economic Socio-economic statusstatus

Aging PopulationsAging Populations

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Considerations





Considerations

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Mucus gland hyperplasia

Goblet cellhyperplasia

Mucus hypersecretion Neutrophils in sputum

Squamous metaplasia of epithelium

↑ Macrophages

No basement membrane thickening

Little increase in airway smooth muscle

↑ CD8+ lymphocytes

Changes in Large Airways of COPD Patients

Changes in Large Airways of COPD Patients

Source: Peter J. Barnes, MD

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Alveolar wall destruction

Loss of elasticity

Destruction of pulmonarycapillary bed

↑ Inflammatory cells macrophages, CD8+ lymphocytes

Changes in the Lung Parenchyma in COPD Patients


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Endothelial dysfunction

Intimal hyperplasia

Smooth muscle hyperplasia

↑ Inflammatory cells (macrophages, CD8+ lymphocytes)

Changes in Pulmonary Arteries in COPD Patients


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LUNG INFLAMMATIONLUNG INFLAMMATION

COPD PATHOLOGYCOPD PATHOLOGY

OxidativeOxidativestressstress ProteinasesProteinases

Repair Repair mechanismsmechanisms

Anti-proteinasesAnti-proteinasesAnti-oxidantsAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeCigarette smokeBiomass particlesBiomass particles

ParticulatesParticulates

Pathogenesis of COPD


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Cigarette smoke Cigarette smoke (and other irritants)(and other irritants)

PROTEASES PROTEASES Neutrophil elastaseNeutrophil elastaseCathepsinsCathepsinsMMPsMMPs

Alveolar wall destructionAlveolar wall destruction(Emphysema)(Emphysema)

Mucus hypersecretionMucus hypersecretion

CD8CD8+ +

lymphocytelymphocyte

Alveolar Alveolar macrophagemacrophage

EpithelialEpithelialcellscells

FibrosisFibrosis(Obstructive(Obstructivebronchiolitis)bronchiolitis)

FibroblastFibroblast

MonocyteMonocyteNeutrophilNeutrophil

Chemotactic factorsChemotactic factors

Inflammatory Cells Involved in COPD


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Anti-proteases

SLPI 1-AT

Proteolysis

OO22--, H, H220022

OHOH.., ONOO, ONOO--

Mucus secretion

Plasma leak Bronchoconstriction

NF-NF-BB

IL-8IL-8

NeutrophilNeutrophilrecruitmentrecruitment

TNF-TNF-

IsoprostanesIsoprostanes

↓ ↓ HDAC2HDAC2

↑↑InflammationInflammationSteroidSteroid

resistanceresistance

Macrophage NeutrophilOxidative Stress in COPD


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Differences in Inflammation and its Consequences: Asthma and COPD

YYYYYY

Mast cellMast cell

CD4+ cellCD4+ cell(Th2)(Th2)

EosinophilEosinophil

AllergensAllergens

Ep cellsEp cells

ASTHMAASTHMA

BronchoconstrictiBronchoconstrictionon

AHRAHR

Alv macrophageAlv macrophage Ep cellsEp cells

CD8+ cellCD8+ cell(Tc1)(Tc1)

NeutrophilNeutrophil

Cigarette smokeCigarette smoke

Small airway narrowingSmall airway narrowingAlveolar destructionAlveolar destruction

COPDCOPD

Reversible IrreversibleAirflow LimitationAirflow Limitation


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NormalNormalInspiration

Expiration

alveolar attachments

Mild/moderateMild/moderateCOPD COPD

loss of elasticity

Severe Severe COPD COPD

loss of alveolar attachments

closure

small small airwayairway

Dyspnea↓ Exercise capacity

Air trappingAir trappingHyperinflationHyperinflation

↓ ↓ HealthHealthstatusstatus

Air Trapping in COPD


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Chronic hypoxiaChronic hypoxia

Pulmonary vasoconstrictionPulmonary vasoconstriction

MuscularizationMuscularization

Intimal Intimal hyperplasiahyperplasia

FibrosisFibrosis

ObliterationObliteration

Pulmonary hypertensionPulmonary hypertension

Cor pulmonaleCor pulmonale

Death

EdemaEdema

Pulmonary Hypertension in COPD


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Macrophages

TNF- IL-8 IL-6

Bacteria Viruses Non-infective Pollutants

Epithelial cells

Oxidative stressOxidative stress

Neutrophils

Inflammation in COPD Exacerbations


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Considerations





Considerations

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Four Components of COPD ManagementFour Components of COPD Management

1. Assess and monitor disease

2. Reduce risk factors

3. Manage stable COPD Education Pharmacologic Non-pharmacologic

4. Manage exacerbations





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• Relieve symptoms • Prevent disease progression• Improve exercise tolerance• Improve health status• Prevent and treat complications• Prevent and treat exacerbations• Reduce mortality

GOALS of COPD MANAGEMENTVARYING EMPHASIS WITH DIFFERING SEVERITY

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Four Components of COPD ManagementFour Components of COPD Management









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Management of Stable COPD

Assess and Monitor COPD: Key PointsA 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.

Comorbidities are common in COPD and should be actively identified.

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SYMPTOMScoughcough

sputumsputumshortness of breathshortness of breath

EXPOSURE TO RISKFACTORS

tobaccotobaccooccupationoccupation

indoor/outdoor pollutionindoor/outdoor pollution

SPIROMETRYSPIROMETRY

Diagnosis of COPDDiagnosis of COPD

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Assess and Monitor COPD: Spirometry

Spirometry should be performed after the administration of an adequate dose of a short-

acting 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.

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Spirometry: Normal and Patients with COPD

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Differential Diagnosis: Differential Diagnosis: COPD and AsthmaCOPD and Asthma

COPD ASTHMA

• Onset in mid-life

• Symptoms slowly progressive

• Long smoking history

• Dyspnea during exercise

• Largely irreversible airflow limitation

• Onset early in life (often childhood)

• 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 Co-Morbidities

COPD patients are at increased risk for: • Myocardial infarction, angina• Osteoporosis• Respiratory infection• Depression• Diabetes• Lung cancer

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COPD and Co-Morbidities

COPD has significant extrapulmonary

(systemic) effects including:

• Weight loss

• Nutritional abnormalities

• Skeletal muscle dysfunction

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Four Components of COPD Management









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Reduce Risk Factors: Key PointsReduction 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 progression (Evidence A).

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Brief Strategies to Help the Patient Willing to Quit Smoking

• ASK Systematically identify all tobacco users at every visit.

• ADVISE Strongly urge all tobacco users to quit.

• ASSESS Determine willingness to make a quit attempt.

• ASSIST Aid the patient in quitting.

• ARRANGE Schedule follow-up contact.

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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 counseling is not sufficient to help patients quit smoking.

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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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Manage Stable COPD: Key Points The overall approach to managing stable COPD

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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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 ß2-agonists, 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 (Evidence A).

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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 effective than the individual components (Evidence A).

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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-to-risk ratio (Evidence A).

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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).

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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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IV: Very Severe III: Severe II: Moderate I: Mild

Therapy at Each Stage of COPD

FEV1/FVC < 70%

FEV1 > 80% predicted

FEV1/FVC < 70%

50% < FEV1 < 80% predicted

FEV1/FVC < 70%

30% < FEV1 < 50% predicted

FEV1/FVC < 70%

FEV1 < 30% predicted

or FEV1 < 50% predicted plus chronic respiratory failure

Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation

Add inhaled glucocorticosteroids if repeated exacerbations

Active reduction of risk factor(s); influenza vaccinationAdd short-acting bronchodilator (when needed)

Add long term oxygen if chronic respiratory failure. Consider surgical treatments

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Other Pharmacologic Treatments Antibiotics: Only used to treat

infectious exacerbations of COPD

Antioxidant agents: No effect of n-acetylcysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids

Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD

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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 survival (Evidence A).

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Revised 2006

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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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Key PointsThe 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 B).

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Manage COPD Exacerbations

Key Points

Inhaled bronchodilators

(particularly inhaled ß2-agonists

with or without anticholinergics)

and oral glucocorticosteroids

are effective treatments for

exacerbations of COPD (Evidence

A).

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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 the quality of life and prognosis of patients with COPD.

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Considerations





Considerations

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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.

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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.

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Global Strategy for Diagnosis, Management and Prevention of COPDSUMMARY





Considerations





Considerations

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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 strategy to identify patients and to treat them according to the best medications available.

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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 and treatment.

Global Strategy for Diagnosis, Management and Prevention of COPD:

Summary

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WORLD COPD DAYNovember 14, 2007

WORLD COPD DAYNovember 14, 2007

Raising COPD Awareness WorldwideRaising COPD Awareness Worldwide

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

Heart Lung and Blood Institute (NHLBI) and WHO. Goal:

To increase awareness of COPD and decrease morbidity and mortality from the disease

Aims : 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

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GOLD Workshop Report: 4 Components of COPD Management Plan1) Assess and monitor disease

2) Reduce risk factors

3) Manage stable COPD

4) Manage exacerbations

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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

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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

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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

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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

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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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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

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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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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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Symptomatic therapy- A) 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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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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asthma and copd

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