Gold Slides 07

7/30/2019 Gold Slides 07

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lobal Initiative for Chronic

bstructive

ung

isease

GOL

D


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GOLD Structure

GOLD Executive Committee

Roberto Rodriguez-Roisin, MD Chair

Klaus Rabe, MD, PhD Co-Chair

Science Committee

Peter Calverley - Chair

Dissemination/Implementation

Task GroupChristine Jenkins, MD - Chair


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GOLD Science Committee

P. Calverley, ChairA. Agusti,A. AnzuetoP. BarnesM. Decramer

Y. Fukuchi

P. JonesK. RabeR. Rodriguez-RoisinJ. VestboJ. Zielinski


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EvidenceCategory

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 Committee

Roberto Rodriguez-Roisin, MDChair

Klaus Rabe, MD, PhD Co-Chair

Science Committee

P. Calverley - Chair

Dissemination/Implementation

Task GroupChristine Jenkins, MD - Chair

GOLD National Leaders - GNL


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United States

United Kingdom

Argentina

Australia

Brazil

AustriaCanada

Chile

Belgium

China

Denmark

Columbia

Croatia

Egypt

Germany

Greece

Ireland

Italy

Syria

Hong Kong ROC

Japan

Iceland

India

Korea

KyrgyzstanUruguay

Moldova

Nepal

Macedonia

Malta

Netherlands

New Zealand

Poland

Norway

Portugal

Georgia

Romania

Russia

SingaporeSlovakia

Slovenia Saudi Arabia

South Africa

Spain

Sweden

Thailand

Switzerland

Ukraine

United Arab Emirates

Taiwan ROC

Venezuela

Vietnam

Peru

Yugoslavia

Albania

Bangladesh

France

Mexico

Turkey CzechRepublic

Pakistan

Israel

GOLD National Leaders

Philippines


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GOLD Website Address

http://www.goldcopd.org


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lobal Initiative for Chronic

bstructive

ung

isease

GOL

D


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GOLD Objectives

Increase awareness of COPD among

health professionals, healthauthorities, and the general public.

Improve diagnosis, managementand 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


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Definition of COPD

COPD is a preventable and treatable disease withsome significant extrapulmonary effects that maycontribute to the severity in individual patients.

Its pulmonary component is characterized by airflowlimitation that is not fully reversible.

The airflow limitation is usually progressive andassociated with an abnormal inflammatory responseof the lung to noxious particles or gases.


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Classification of COPD Severityby Spirometry

Stage I: Mild FEV1/FVC < 0.70

FEV1 > 80% predicted

Stage II: Moderate FEV1/FVC < 0.7050% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.7030% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70FEV1 < 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 byspirometry.

A fifth category--Stage 0: At Risk--that appeared in the 2001report is no longer included as a stage of COPD, as there isincomplete evidence that the individuals who meet thedefinition 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 sputumare not normal remains important - their presence should

trigger a search for underlying cause(s).


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Burden of COPD

Risk Factors


Management



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Burden of COPD: Key Points

COPD is a leading cause of morbidity and mortalityworldwide and results in an economic and socialburden that is both substantial and increasing.

COPD prevalence, morbidity, and mortality varyacross countries and across different groups withincountries.

The burden of COPD is projected to increase in thecoming decades due to continued exposure toCOPD risk factors and the changing age structure

of the worlds population.


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Burden of COPD: Prevalence

Many sources of variation can affect estimates ofCOPD prevalence, including e.g., sampling methods,response rates and quality of spirometry.

Data are emerging to provide evidence thatprevalence ofStage I: Mild COPDand higher isappreciably higher in:

- smokers and ex-smokers- people over 40 years of age- males


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COPD Prevalence Study in LatinAmerica

The prevalenceof post-bronchodilator

FEV1/FVC < 0.70increases steeplywith age in 5Latin American

Cities

Source: Menezes AM et al. Lancet2005


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Burden of COPD: Mortality

COPD is a leading cause of mortality worldwide andprojected to increase in the next several decades.

COPD mortality trends generally track severaldecades behind smoking trends.

In the US and Canada, COPD mortality for bothmen and women have been increasing.

In the US in 2000, the numberof COPD deaths wasgreater among women than men.


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

0

0.5

1.0

1.5

2.0

2.5

3.0

Proportion of 1965 Rate

1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998

59% 64% 35% +163% 7%

CoronaryHeart

Disease

Stroke Other CVD COPD All OtherCauses

Source: NHLBI/NIH/DHHS


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Of the sixleading causes

of death in theUnited States,only COPD has

been increasingsteadily since1970

Source: Jemal A. et al. JAMA2005


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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

Numb

erDeaths

x1000

Source: US Centers for Disease Control and Prevention, 2002


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Burden of COPD

Risk Factors


Management



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Risk Factors for COPD

Lung growth and development

Oxidative stress

Gender

Age

Respiratory infections

Socioeconomic status

NutritionComorbidities

Genes

Exposure to particles

Tobacco smoke

Occupational dusts, organicand inorganic

Indoor air pollution fromheating and cooking with

biomass in poorly ventilateddwellings

Outdoor air pollution


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Risk Factors for COPD

Nutrition

Infections

Socio-economicstatus

Aging Populations


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Burden of COPD

Risk Factors


Management



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LUNG INFLAMMATION

COPD PATHOLOGY

Oxidativestress Proteinases

Repairmechanisms

Anti-proteinasesAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeBiomass particles

Particulates

Source: Peter J. Barnes, MD

Pathogenesis ofCOPD


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Alveolar wall destruction

Loss of elasticity

Destruction of pulmonary

capillary bed

Inflammatory cellsmacrophages, CD8+ lymphocytes


Changes in Lung Parenchyma in COPD


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Chronic hypoxia

Pulmonary vasoconstriction

Muscularization

Intimalhyperplasia

Fibrosis

Obliteration

Pulmonary hypertension

Cor pulmonale

Death

Edema

Pulmonary Hypertension in COPD



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Mast cell

CD4+ cell(Th2)

Eosinophil

Allergens

Ep cells

ASTHMA

BronchoconstrictionAHR

Alv macrophageEp cells

CD8+ cell(Tc1)

Neutrophil

Cigarette smoke

Small airway narrowingAlveolar destruction

COPD

Reversible IrreversibleAirflow Limitation



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Burden of COPD

Risk Factors


Management



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Four Components of COPDManagement

1.Assess and monitordisease

2. Reduce risk factors

3. Manage stable COPD

Education

Pharmacologic

Non-pharmacologic

4. Manage exacerbations

f COPD MANAGEMENT


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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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1. Assess and monitordisease



Education

Pharmacologic

Non-pharmacologic


Management of Stable COPD


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Assess and Monitor COPD: Key Points

A clinical diagnosis of COPD should be consideredin any patient who has dyspnea, chronic cough orsputum 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 fullyreversible.

Comorbidities are common in COPD and should be

actively identified.


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SYMPTOMS

cough

sputumshortness of breath

EXPOSURE TO RISKFACTORS

tobaccooccupation

indoor/outdoor pollution

SPIROMETRY

Diagnosis of COPD



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Assess and Monitor COPD: Spirometry

Spirometry should be performed after theadministration of an adequate dose of a short-acting inhaled bronchodilator to minimize

variability.

A post-bronchodilator FEV1/FVC < 0.70 confirmsthe presence of airflow limitation that is not fully

reversible.

Where possible, values should be compared toage-related normal values to avoid overdiagnosis

of COPD in the elderly.

S i t N l d


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Spirometry: Normal and

Patients with COPD

Differential Diagnosis:


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Differential Diagnosis:COPD 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

F C f COPD


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Education

Pharmacologic

Non-pharmacologic




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Reduce Risk Factors: Key Points

Reduction of total personal exposure to tobaccosmoke, occupational dusts and chemicals, andindoor and outdoor air pollutants are importantgoals to prevent the onset and progression ofCOPD.

Smoking cessation is the single most effective and cost effective intervention in mostpeople to reduce the risk of developing COPDand stop its progression (Evidence A).

Brief Strategies to Help the


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Brief Strategies to Help thePatient Willing to Quit Smoking

ASK Systematically identify alltobacco users at every visit.

ADVISE Strongly urge all tobaccousers to quit.

ASSESS Determine willingness tomake 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 otherhealth professionals significantly increases quitrates over self-initiated strategies. Even a brief

(3-minute) period of counseling to urge a smokerto quit results in smoking cessation rates of 5-10%.

Numerous effective pharmacotherapies forsmoking cessation are available andpharmacotherapy is recommended when

counseling is not sufficient to help patients quit

smoking.



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g

Reduce Risk Factors: Indoor/Outdoor AirPollution

Reducing the risk from indoor and outdoor airpollution is feasible and requires a combination of

public policy and protective steps taken byindividual patients.

Reduction of exposure to smoke from biomass fuel,

particularly among women and children, is acrucial goal to reduce the prevalence of COPDworldwide.

Four Components of COPD


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Education

Pharmacologic

Non-pharmacologic




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Manage Stable COPD: Key Points

The overall approach to managing stable COPD should beindividualized to address symptoms and improve quality oflife.

For patients with COPD, health education plays an importantrole in smoking cessation (Evidence A) and can also play arole in improving skills, ability to cope with illness and healthstatus.

None of the existing medications for COPD have been shownto modify the long-term decline in lung function that is thehallmark 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 thesymptomatic management of COPD (Evidence A).They are given on an as-needed basis or on a regular

basis to prevent or reduce symptoms andexacerbations.

The principal bronchodilator treatments are 2- agonists,anticholinergics, and methylxanthines used singly or in

combination (Evidence A).

Regular treatment with long-acting bronchodilators ismore effective and convenient than treatment withshort-acting bronchodilators (Evidence A).



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Pharmacotherapy: Glucocorticosteroids

The addition of regular treatment with inhaledglucocorticosteroids to bronchodilator treatment isappropriate for symptomatic COPD patients with

an FEV1 < 50% predicted (Stage III: Severe COPDand Stage IV: Very Severe COPD) and repeatedexacerbations (Evidence A).

An inhaled glucocorticosteroid combined with along-acting 2-agonist is more effective than theindividual 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 systemicglucocorticosteroids should be avoided

because of an unfavorable benefit-to-riskratio (Evidence A).



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Pharmacotherapy: Vaccines

In COPD patients influenza vaccines canreduce serious illness (Evidence A).

Pneumococcal polysaccharide vaccine isrecommended for COPD patients 65 years

and older and for COPD patients youngerthan 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

Therapy at Each Stage of COPD


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IV: Very SevereIII: SevereII: ModerateI: 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 15 hours per day) to patients withchronic respiratory failure has been shown toincrease survival (Evidence A).

Four Components of COPD


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Education

Pharmacologic

Non-pharmacologic


Revised 2006

Management COPD Exacerbations


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g

Key Points

An exacerbation of COPD is defined as:

An event in the natural course of thedisease characterized by a change in thepatients baseline dyspnea, cough, and/orsputum that is beyond normal day-to-day

variations, is acute in onset, and maywarrant a change in regular medication ina patient with underlying COPD.



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g

Key Points

The most common causes of an exacerbationare infection of the tracheobronchial tree andair 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., increasedsputum purulence) may benefit from antibiotictreatment (Evidence B).

Manage COPD Exacerbations


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g

Key Points

Inhaled bronchodilators (particularly

inhaled 2-agonists with or without

anticholinergics) and oral glucocortico-

steroids are effective treatments for

exacerbations of COPD (Evidence A).



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g

Key Points

Noninvasive mechanical ventilation inexacerbations improves respiratory acidosis,increases pH, decreases the need for endotrachealintubation, and reduces PaCO2, respiratory rate,severity of breathlessness, the length of hospitalstay, and mortality (Evidence A).

Medications and education to help prevent futureexacerbations should be considered as part offollow-up, as exacerbations affect the quality of lifeand prognosis of patients with COPD.

Global Strategy for Diagnosis


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Burden of COPD

Risk Factors


Management


Translating COPD Guidelines into Primary Care


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KEY POINTS

Better dissemination of COPD guidelines andtheir 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 healthcampaigns and in bringing messages aboutreducing exposure to risk factors to bothpatients and the public.



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KEY POINTS

Spirometric confirmation is a keycomponent of the diagnosis of COPD andprimary care practitioners should haveaccess to high quality spirometry.

Older patients frequently have multiple

chronic health conditions. Comorbiditiescan magnify the impact of COPD on apatients health status, and can complicatethe management of COPD.

Global Strategy for Diagnosis,


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SUMMARY


Burden of COPD Risk Factors

Pathogenesis, Pathology,

Pathophysiology Management


Global Strategy for Diagnosis, Management


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Global Strategy for Diagnosis, Managementand Prevention of COPD: Summary

COPD is increasing in prevalence inmany countries of the world.

COPD is treatable and preventable.

The GOLD program offers a

strategy to identify patients and totreat them according to the bestmedications available.

Global Strategy for Diagnosis, Management


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COPD can be prevented by avoidance ofrisk factors, the most notable beingtobacco smoke.

Patients with COPD have multiple otherconditions (comorbidities) that must betaken into consideration.

GOLD has developed a global network toraise awareness of COPD and disseminate

information on diagnosis and treatment.

Global Strategy for Diagnosis, Managementand Prevention of COPD: Summary

BrazilGermany

Ireland

Slovenia Saudi Arabia

Bangladesh


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United States

United Kingdom

Argentina

Australia

z

AustriaCanada

Chile

Belgium

China

Denmark

Columbia

Croatia

Egypt

Greece

Italy

Syria

Hong Kong ROC

Japan

Iceland

India

Korea

KyrgyzstanUruguay

Moldova

Nepal

Macedonia

Malta

Netherlands

New Zealand

Poland

Norway

Portugal

Georgia

Romania

Russia

SingaporeSlovakia

South Africa

Spain

Sweden

Thailand

Switzerland

Ukraine

United Arab Emirates

Taiwan ROC

Venezuela

Vietnam

Peru

Yugoslavia

Albania

France

Mexico

Turkey CzechRepublic

PakistanIsrael

GOLD National Leaders

Philippines


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WORLD COPD DAY

November 14, 2007

Raising COPD Awareness Worldwide

GO b dd


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GOLD Website Address

http://www.goldcopd.org


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ADDITIONAL SLIDES WITH NOTESPREPARED BY:

PROFESSOR PETER J. BARNES, MD

NATIONAL HEART AND LUNG INSTITUTE

LONDON, ENGLAND


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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 inairway smooth muscle

CD8+ lymphocytes

Changes in Large Airways of COPD Patients


Changes in Small Airways in COPD Patients


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Disrupted alveolar attachments

Inflammatory exudate in lumen

Peribronchial fibrosisLymphoid follicle

Thickened wall with inflammatory cellsmacrophages, CD8+ cells, fibroblasts

g y


Changes in the Lung Parenchyma in COPD Patients


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Alveolar wall destruction

Loss of elasticity

Destruction of pulmonary

capillary bed

Inflammatory cellsmacrophages, 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


Pathogenesis of COPD


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LUNG INFLAMMATION

COPD PATHOLOGY

Oxidativestress Proteinases

Repairmechanisms

Anti-proteinasesAnti-oxidants

Host factorsAmplifying mechanisms

Cigarette smokeBiomass particles

Particulates


Inflammatory Cells Involved in COPD


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Cigarette smoke(and other irritants)

PROTEASESNeutrophil elastase

CathepsinsMMPs

Alveolar wall destruction(Emphysema)

Mucus hypersecretion

CD8+lymphocyte

Alveolar macrophageEpithelialcells

Fibrosis(Obstructivebronchiolitis)

Fibroblast

MonocyteNeutrophil

Chemotactic factors


Macrophage NeutrophilOxidative Stress in COPD


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Anti-proteases

SLPI 1-AT

Proteolysis

O2-

, H202OH., ONOO-

Mucus secretion

Plasma leak Bronchoconstriction

NF- B

IL-8

Neutrophilrecruitment

TNF-

Isoprostanes

HDAC2

InflammationSteroid

resistance


Differences in Inflammation and its Consequences: Asthma and COPD

COPD


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Mast cell

CD4+ cell(Th2)

Eosinophil

Allergens

Ep cells

ASTHMA

Bronchoconstriction

AHR

Alv macrophageEp cells

CD8+ cell(Tc1)

Neutrophil

Cigarette smoke

Small airway narrowing

Alveolar destruction

COPD

Reversible IrreversibleAirflow Limitation


Normal

Mild/moderate SevereAir Trapping in COPD


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NormalInspiration

Expiration

alveolar attachments

d/ ode ateCOPD

loss of elasticity

SevereCOPD

loss of alveolar attachments

closure

smallairway

Dyspnea Exercise capacity

Air trappingHyperinflation

Healthstatus


Pulmonary Hypertension in COPD


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Chronic hypoxia

Pulmonary vasoconstriction

Muscularization

Intimalhyperplasia

Fibrosis

Obliteration

Pulmonary hypertension

Cor pulmonale

Death

Edema


Inflammation in COPD Exacerbations


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Macrophages

TNF- IL-8 IL-6

Bacteria Viruses Non-infectivePollutants

Epithelialcells

Oxidative stress

Neutrophils



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Documents

Gold Slides 07