COPD BLOK 12 2011.pptx

PowerPoint Presentation

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2AIRFLOWLIMITATIONIN SMALL AIRWAYSPROGRESSIVEIRREVERSIBLEPARTIALREVERSIBLE CHRONIC BRONCHITISEMPHYSEMATOUS LUNGCHRONICINFLAMMATION12ALVEOLER STRUCTURE DAMAGED DECREASED ELASTIC RECOILDEFINITION COPD23

pathophysiology

DEFINITON COPDGlobal Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2006. Available from http://www.goldcopd.com/

Percent change in age-adjusted Death rates, U.S, 1965-1998

Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970Source: Jemal A. et al. JAMA 20057

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PATOGENESA COPD

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Asap rokok dan zat iritan lain mengaktifkan macrophag dan epitel sal. napas , melepaskan neutrophil chemotactic factors, IL-8, LB4. Neutrophils dan macrophag kemudian melepaskan protease yang merusak connective tissue parenkim paru, menimbulkan emphysema, dan merangsang hipersekresi mucus . Secara normal Protease akan dihambat oleh protease inhibitor, yaitu (alpha)1-antitrypsin, secretory leukoprotease inhibitor, and tissue inhibitors of matrix metalloproteinases. Cytotoxic T cells (CD8) ikut juga berperan dalam rangkaian proses inflamasi sel Inflammasi dan Mediator

Protease inhib.

COPD : Proses poteolitik tidak terkendali oleh mekanisme tubuh

protease

Stres oksidatif

pathophysiology

Asthma : COPD

Inflammatory cascade in COPD and Asthma

15normalBronkitis kronisasmaemfisema

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Bronchus

Wall thickening inflammation -- mucus gland hypertrophy Secretions

Alveoli

Wall thinning - inflammation - elastolysisCoalescence Elasticity

BronchioleWall thickening inflammation repair -- remodelingLoss of alveolar attachments

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19Risk for COPDGenes Exposure to particle Tobacco smoke Occupational dust, organic and inorganic indoor air pollution from heating and cooking with bio-mass In poorly vented dwellings Outdoor air pollutionLung growth and developmentOxidative stressGender Age Respiratory infectionSocioeconomic statusNutrition Comorbidities Risk factors for COPD

20EstablishedProbablePossibleCigarette smokingExposure to primary and secondary smokeLow birth weightOccupational exposure Hyperactive airwaysChildhood respiratory infection 1 antitrypsin deficiency (genetic abnormality)alcoholFamily historyAir pollutanpovertyatopyIgA deficiencyBlood type ARisk factors for COPD

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NutritionInfectionsSocio-economic statusAging Populations

COPD risk is related to thetotal burden of inhaled particles

Reversibility in COPD

Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2006. Available from http://www.goldcopd.com/





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Future COPD caseFuture asthmaticFuture COPD if smokerBiomass Fuel and COPD26

Lama sebagai perokokJumlah rokok sehariJenis rokokCara merokok

OhnoTOBACO SMOKE

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Smoking causes 80-90% of COPD.50% of smokers develop chronic bronchitis15-20% of smokers develop clinical airflow obstructionNon-SmokerSmoker281Barcelona April 1997 - Afternoon Day 102-Apr-9774877 - Rick FullerBarcelona

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SYMPTOMScoughsputumshortness of breathtobaccooccupationindoor/outdoor pollutionSPIROMETRY

Diagnosis of COPD EXPOSURE TO RISKFACTORS 12331A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry. To help identify individuals earlier in the course of disease, spirometry should be performed for patients who have chronic cough and sputum production even if they do not have dyspnea. Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to 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.SPIROMETRY 32

33SPIROMETRI

34Spirometry: Normal and COPD

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Clinical Features of COPDTypically smokers - mean 20 cigs/day for 20 yearsUsually present in 5th decade of life with productive cough or acute chest illness when the disease is far advancedDOE not usual until 6th or 7th decadePatients who are dyspnea give up activities wheezing accompanying dyspnea may lead to erroneous dx of asthma

Sputum production initially only in AMdaily volume rarely exceeds 60 mlusually mucoidAcute exacerbations characterized by increased cough, purulent sputum, wheezing, dyspnea, sometimes feverInterval between exacerbations grows shorter with disease progressionClinical Features of COPD

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EMFISEMA

BRONKHITIS KRONIS12

38EMFISEMABRONKHITIS KRONIS

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2The Blue BloaterThe Pink Puffer

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Emphysema(The Pink Puffer Phenotype)A condition of the lung characterized by abnormal, permanent enlargement of airspaces distal to the terminal bronchiole, accompanied by the destruction of their walls, and without obvious fibrosis

Chronic Bronchitis(The Blue Bloater Phenotype)Cough productive of sputum on most days during at least three consecutive months for more than two successive years

More profound hypoxemia at restElevated PaCO2 with chronic respiratory acidosisCor pulmonale with right heart failure

Sutherland, E. R. et al. N Engl J Med 2004;350:2689-2697Deterioration in Lung Function in Patients with COPD

42Figure 1. Deterioration in Lung Function in Patients with COPD.

Symptoms generally develop only after a significant decline in forced expiratory volume in one second (FEV1) has occurred; they progress as lung function deteriorates further.

DyspnoeaCOPDThe cycle of physical, social and psychososial consequenses of COPDImmobilityLack of Fitnesspathophysiology

Social isolationDepression

COPD patients are at increased risk for: Myocardial infarction.Osteoporosis.Respiratory infection.Diabetes.Lung cancer.COPD and co -morbidities

COPD has significant extrapulmonary(systemic) effects including: Weight lossNutritional abnormalitiesSkeletal muscle dysfunctionCOPD and Co-Morbidities

Differential DiagnosisA major differential diagnosis is asthmaIn some patients with chronic asthma, a clear distinction from COPD is not possibleIn these cases, current management is similar to that of asthmaOther potential diagnoses are usually easier to distinguish from COPDCOPDOnset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation

Asthma

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

Clinical features of Asthma vs. COPD

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STAGE of COPD

STAGE I :STAGE II :

52STAGE of COPD

STAGE III :STAGE IV :53

TIME COURSE OF COPD

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The definition of COPD exacerbation is an acute change in a patients baseline dyspnoea, cough and/or sputum beyond day-to-day variability sufficient to warrant a change in therapy.Causes of exacerbation can be both infectious and non-infectious. Medical therapy includes bronchodilators, corticosteroids, antibiotics and supplemental oxygen therapy.Acute Exacerbation of COPD54

INFEKSI VIRUSPOLUSI UDARAHAEMOPHILUS INLUENZASTREPTOCOCCUS PNEUMONIAMORAXELLA CATARRHALISPRODUKSI SPUTUMSESAK NAPAS

KAUSA DEMAM

KEADAAN MEMBURUKDALAM WAKTU SINGKATSPUTUM PURULEN1234KAUSAACUTE EXACERBATION OF COPD 55BronchodilatorsEitherAct as agonists at beta receptorsorAct as antagonists at muscarinic receptors

. Chest 2003;124:459467; 5. Soler-Cataluna JJ, et al. Thorax 2005;60:925931.Exacerbations drive morbidity and mortality

COPD exacerbations lead to:Increased symptoms (breathlessness)Increased risk of hospitalisationIncreased risk of mortality4,5Decline in lung functionWorsening health status

Date of preparation Sept 2007. Prescribing Information can be found at the end of this presentation and is available on request.Symbicort and Turbuhaler are trademarks owned by the AstraZeneca Group.

56Exacerbations drive morbidity and mortalityExacerbations are an important outcome measure in COPD.Exacerbations of COPD are of major importance in terms of their prolonged detrimental effects on patients well being, the acceleration in disease progression and high healthcare costsCOPD patients are prone to severe exacerbations, which increase in frequency with the severity of disease. Furthermore, the impact of exacerbations may increase over time. COPD exacerbations can lead to a decline in lung function,1 increased symptoms (e.g. breathlessness),2 worsening health status,3 an increased risk of hospitalisation4 and may culminate in an increased risk of mortality.4,5

1. Donaldson GC, et al. Thorax 2002;57:847852. 2. Donaldson GC, et al. Eur Respir J 2003;22:931936. 3. Seemungal TA, et al. Am J Respir Crit Care Med 1998;157:14181422. 4. Groenewegen KH, et al. Chest 2003;124:459467.5. Soler-Cataluna JJ, et al. Thorax 2005;60:925931.

Frequent exacerbations lead to declining lung function

Frequent exacerbations impair health status COPD

Prolonged recovery period following a COPD exacerbation health status

Increased frequency of exacerbations increases the risk of mortality in COPD

ACUTE EXACERBASI OF COPD PENURUNAN KWALITAS HIDUPPENURUNAN FUNGSI PARUPENINGKATAN ANGKA RAWAT INAPPENINGKATAN ANGKA KEMATIAN1234MENGAKIBATKAN61BronchodilatorsEitherAct as agonists at beta receptorsorAct as antagonists at muscarinic receptors

Four Components of COPD ManagementAssess and monitor disease Reduce risk factorsManage stable COPDEducationPharmacologicNon-pharmacologicManage exacerbations

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 SEVERITYAdapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2006. Available from http://www.goldcopd.com/63

Goals of COPD managementAdapted from Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines, 2006. Available from http://www.goldcopd.com/Relieve symptomsImprove exercise tolerance Prevent and treat exacerbationsPrevent and treat complications

Improve health status

Slow disease progression Prevent mortality

Reduce future risk

Help patients achieve greater daily control of symptoms and avoid fearful exacerbations

Enable patients to enjoy as good a quality of life as possible

Date of preparation Sept 2007. Prescribing Information can be found at the end of this presentation and is available on request.Symbicort and Turbuhaler are trademarks owned by the AstraZeneca Group.

64Management of COPD The GOLD guidelines recommend several goals for the effective management of COPD. These goals aim to enable patients to achieve daily control of symptoms and to avoid exacerbations, allowing them to enjoy a good quality of life and to reduce the risk of future exacerbations. Pharmacological treatments can control symptoms, improve exercise tolerance and reduce exacerbations, thus leading to improvements in health status. These goals should be reached with minimal side effects from treatment. The best pharmacological treatment is one that achieves most of these COPD management goals with the least side effects. Frequently, as the disease progresses, more than one treatment approach is often required to achieve these goals.


Management of Stable COPDReduce 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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66 SMOKING CESSATION SMOKINGCESSATIONCig. smoking is the single most important risk factor.80 % patiens with COPD are current or former smokers.Smoking accounts for 80% of the mortality attributable to COPD.SMOKINGCESSATIONHigest priority for COPD patiens

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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 & exacerbations. The principal bronchodilator treatments are 2-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).Management of Stable COPDFarmacotherapy : bronchodilators68

The addition of regular treatment with inhaled steroid to bronchodilator treatment is appropriate for symptomatic severe COPD, very severe COPD and repeated exacerbations (Evidence A).

An inhaled steroid combined with a long-acting 2-agonist is more effective than the individual components (Evidence A).Management of Stable COPDFarmacotherapy : bronchodilators69

THERAPY OF STABLE COPDN Engl J Med 2004; 350: 2689-97

Cellular effects of corticosteroids

72BRONCHODILATORSFOR COPDIPRATROPIUM BROMIDEOXITROPIUM BROMIDETIOTROPIUM BROMIDEINHALEDANTICHOLINERGICSIPRATOPRIUM BROMIDE&SHORT ACTING INHALEDBETA 2 AGONISTSHORT /LONG ACTING INHALED BETA 2 AGONISTBETA 2AGONISTCOMBINATIONTHERAPY13THEOPHYLLIN4272

73BRONCHODILATORSIN COPDRELAXAIRWAY SMOOTHMUSCLEDECREASEDPLASMAEXUDATION DECREASEDINFLAMMATORYMEDIATORRELEASE IMPROVERESPIRATORYMUSCLEFATIGUE DECREASEDNEUROTRANSMITTERRELEASE 1234573

74BRONCHODILATORSEFFECT IN COPDINCREASEDFEV1, FVC,PEF[ < 10 % ]DECREASEDHYPERINFLATIONDECREASEDDYSPNOEAIMPROVEDEXERCISETOLERANCEIMPROVED RESPIRATORY MUSCLE STRENGTH 12374

75NONPHARMACOLOGICALMANAGEMENTPULMONARY REHABILITATIONAVOIDANCE OF POLLUTANTSURGERYBULLECTOMYVOLUME REDUCTIONTRANSPLANTATIONEDUCATIONNUTRITIONALVACCINATIONPSYSCOTHERAPYANXIETAS&DEPRESSION123456EXERCISEINFLUENZAPNEUMOCOCCUS75

76OTHER TREATMENTIN COPDIMMUNOMODULATORPROPHYLACTICANTIBIOTICSANTI TUSIVESDUGSCARBOCYSTINEBROMHEXOLAMBROXOLMUCOLYTICS1453RESPIRATORYSTIMULANDOXAPRAM

VASODILATORSNITRIC OXID INHALASI67NO EVIDENCEN-ACETYLCYSTEIN( EVIDENCE B )ANTIOXIDANTS2 KONTRA INDIKASI NO RECOMMEND. KONTRA INDIKASI7677

78SEKIAN .

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0
5
1
4
2
3
Liter
1
6
5
4
3
2
FVC
FVC
FEV1
FEV1
Normal
COPD
3.500
3.500
2.100
2.800
Normal
COPD
FVC
FEV1
FVC
FEV1/
Seconds

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COPD BLOK 12 2011.pptx