2019年-Global Initiative for Chronic Obstructive课件-PPT精选文档
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NHLBI/WHO WORKSHOP REPORT
NATIONAL INSTITUTES OF HEALTH National Heart, Lung, and Blood Institute
CHAPTER 1 DEFINITION
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.
Cells
COPD
▪ Neutrophils ▪ Large increase in ▪ macrophages
Increase in CD+8 T lymphocytes
Asthma
▪ Eosinophils ▪ Small increase in macrophages ▪ Increase in CD+4 Th2 lymphocytes ▪ Activation of mast cells
Central Airways
changes includes:
•macrophages and CD+8 T lymphocytes infiltrating •increasing epithelial goblet and squamous cells •dysfunction, damage , and/or loss in cilia •enlarged mucus-secreting glands •increasing smooth muscle and connective tissue in the airway wall •degeneration of the airway cartilage •mucus hypersecretion
The focus of this Report is primarily on COPD caused by inhaled particles and gases, the most common of which worldwide is tobacco smoke. Poorly reversible airflow limitation associated with bronchiectasis, cystic fibrosis, tuberculosis, or asthma is not included except insofar as these conditions overlap with COPD.
(cough, sputum production, dyspnea) FFEErVVe11s/<pF3iVr0a%Cto<rp7yr0ef%adiilcutreedoorrcFliEnVic1a<l5s0ig%nsporferdiigchtetdhpealurst
failure
CHAPTER 2 BURDEN OF COPD
Many previous definitions of COPD have emphasized the terms “emphysema” and “chronic bronchitis”, which are no longer included in the definition in this report. Because emphysema describes only one of several structural abnormalities present in COPD and chronic bronchitis does not reflect the major impact of airflow limitation on morbidity and mortality in COPD patients.
▪ Airway
Chemicals
Hyperresponsiveness ▪ Indoor and Outdoor Air
▪ Lung Growth
Pollution
▪ Infections
▪ Socioeconomic Status
CHAPTER 4: PATHOGENESIS, PATHOLOGY,
destruction
▪ Mucus metaplasia ▪ Glandular enlargemet
▪ Mucus metaplasia ▪ Glandular enlargement
▪ Response to Glucocorticosteroids
Treatment
have little or no effect
Mediators Consequences
▪▪▪
LTB4 IL-8 TNF-α
▪ LTD4 ▪ IL-4,IL-5 ▪ (Plus many others)
▪ ▪ Squamous metaplasia of Fragile epithelium
▪ epithelium Parenchymal
▪ Thickening of basement membrane
EPIDEMIOLOGY
▪ The imprecise and variable definitions of COPD
have made it hard to quantify the morbidity and mortality of this disease in developed and developing countries.
PATHOPHYSIOLOGY
•Physiological changes include mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, and cor pulmonale. •Expiratory airflow limitation is the hallmark physiological change. •The irreversible component of airflow limitation is primarily due to remodeling –fibrosis and narrowingof the small airways.
CLASSIFICATION OF SEVERITY: STAGES OF COPD
Stage 0: At Risk Ⅰ: Mild COPD
Ⅱ: Moderate COPD
Ⅲ: Severe COPD
Characteristics Normal spirometry Chronic symptoms (cough, sputum production) FFWEEitVVh11/≥oF8rV0w%Cit<hp7or0ue%tdcichtreodnic symptoms (cough,sputum production) F3W0Ei%tV(hⅡⅡ≤1/oFFBArEV::w3V5C0i01t<%<h%78o0≤≤0u%FF%tEEchVpVrr11o<e<nd58ii00cc%%tseydmpprrpeetddoiimccttesedd),
CHAPTER 5 MANAGEMENT OF COPD
While disease prevention is the ultimate goal, once COPD has been diagnosed, effective management should be aimed at the following goals:
Global Initiative for Chronic Obstructive Lung Disease
GLOBAL STRATEGY FOR THE DIAGNOSIS, MANAGEMENT, AND PREVENTION OF
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
PATHOLOGY
Pathological changes characteristic of COPD are found in the central airways, peripheral airways , lung parenchyma, and pulmonary vasculature.
▪ Most epidemiological studies have found that
COPD prevalence, morbidity, and mortality have increased over time.
▪ The prevalence of COPS is highest in countries
▪ Glucocorticosteroids
inhibit inflammation
In addition to inflammation, two other processes thought to be important in the pathogenesis of COPD are an imbalance of proteinases and antiproteinases in the lung, and oxidative stress.
Peripheral Airways
•The early lung function decline is correlated with inflammatory changes in peripheral airways, similar to those in central airways. •However, the most characteristic change in the peripheral airways of patients with COPD is airway narrowing.
AND PATHOPHYSIOLGY
PATHOGENESIS
COPD is characterized by chronic inflammation throughout the airways, parenchyma, and pulmonary vasculature.
Characteristics of Inflammation in COPD and Asthma
Lung Parenchyma
The most common type of parenchymal destruction in COPD patients is the centrilobular form of emphysema.
Pulmonary Vasculature
Pulmonary vascular changes are characterized by a thickening of the vessel wall. Thickening of the intima is the first structural change, following by an increase in smooth muscle and the infiltration by inflammatory cells.
where cigarette smoking has been, or still is, very common.
CHAPTER 3 RISK FACTORS
Host Factors
Exposures
▪ Genes (e.g., alpha-1 ▪ Tobacco Smoke
antitrypsin deficiency) ▪ Occupational Dusts and
NATIONAL INSTITUTES OF HEALTH National Heart, Lung, and Blood Institute
CHAPTER 1 DEFINITION
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.
Cells
COPD
▪ Neutrophils ▪ Large increase in ▪ macrophages
Increase in CD+8 T lymphocytes
Asthma
▪ Eosinophils ▪ Small increase in macrophages ▪ Increase in CD+4 Th2 lymphocytes ▪ Activation of mast cells
Central Airways
changes includes:
•macrophages and CD+8 T lymphocytes infiltrating •increasing epithelial goblet and squamous cells •dysfunction, damage , and/or loss in cilia •enlarged mucus-secreting glands •increasing smooth muscle and connective tissue in the airway wall •degeneration of the airway cartilage •mucus hypersecretion
The focus of this Report is primarily on COPD caused by inhaled particles and gases, the most common of which worldwide is tobacco smoke. Poorly reversible airflow limitation associated with bronchiectasis, cystic fibrosis, tuberculosis, or asthma is not included except insofar as these conditions overlap with COPD.
(cough, sputum production, dyspnea) FFEErVVe11s/<pF3iVr0a%Cto<rp7yr0ef%adiilcutreedoorrcFliEnVic1a<l5s0ig%nsporferdiigchtetdhpealurst
failure
CHAPTER 2 BURDEN OF COPD
Many previous definitions of COPD have emphasized the terms “emphysema” and “chronic bronchitis”, which are no longer included in the definition in this report. Because emphysema describes only one of several structural abnormalities present in COPD and chronic bronchitis does not reflect the major impact of airflow limitation on morbidity and mortality in COPD patients.
▪ Airway
Chemicals
Hyperresponsiveness ▪ Indoor and Outdoor Air
▪ Lung Growth
Pollution
▪ Infections
▪ Socioeconomic Status
CHAPTER 4: PATHOGENESIS, PATHOLOGY,
destruction
▪ Mucus metaplasia ▪ Glandular enlargemet
▪ Mucus metaplasia ▪ Glandular enlargement
▪ Response to Glucocorticosteroids
Treatment
have little or no effect
Mediators Consequences
▪▪▪
LTB4 IL-8 TNF-α
▪ LTD4 ▪ IL-4,IL-5 ▪ (Plus many others)
▪ ▪ Squamous metaplasia of Fragile epithelium
▪ epithelium Parenchymal
▪ Thickening of basement membrane
EPIDEMIOLOGY
▪ The imprecise and variable definitions of COPD
have made it hard to quantify the morbidity and mortality of this disease in developed and developing countries.
PATHOPHYSIOLOGY
•Physiological changes include mucus hypersecretion, ciliary dysfunction, airflow limitation, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, and cor pulmonale. •Expiratory airflow limitation is the hallmark physiological change. •The irreversible component of airflow limitation is primarily due to remodeling –fibrosis and narrowingof the small airways.
CLASSIFICATION OF SEVERITY: STAGES OF COPD
Stage 0: At Risk Ⅰ: Mild COPD
Ⅱ: Moderate COPD
Ⅲ: Severe COPD
Characteristics Normal spirometry Chronic symptoms (cough, sputum production) FFWEEitVVh11/≥oF8rV0w%Cit<hp7or0ue%tdcichtreodnic symptoms (cough,sputum production) F3W0Ei%tV(hⅡⅡ≤1/oFFBArEV::w3V5C0i01t<%<h%78o0≤≤0u%FF%tEEchVpVrr11o<e<nd58ii00cc%%tseydmpprrpeetddoiimccttesedd),
CHAPTER 5 MANAGEMENT OF COPD
While disease prevention is the ultimate goal, once COPD has been diagnosed, effective management should be aimed at the following goals:
Global Initiative for Chronic Obstructive Lung Disease
GLOBAL STRATEGY FOR THE DIAGNOSIS, MANAGEMENT, AND PREVENTION OF
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
PATHOLOGY
Pathological changes characteristic of COPD are found in the central airways, peripheral airways , lung parenchyma, and pulmonary vasculature.
▪ Most epidemiological studies have found that
COPD prevalence, morbidity, and mortality have increased over time.
▪ The prevalence of COPS is highest in countries
▪ Glucocorticosteroids
inhibit inflammation
In addition to inflammation, two other processes thought to be important in the pathogenesis of COPD are an imbalance of proteinases and antiproteinases in the lung, and oxidative stress.
Peripheral Airways
•The early lung function decline is correlated with inflammatory changes in peripheral airways, similar to those in central airways. •However, the most characteristic change in the peripheral airways of patients with COPD is airway narrowing.
AND PATHOPHYSIOLGY
PATHOGENESIS
COPD is characterized by chronic inflammation throughout the airways, parenchyma, and pulmonary vasculature.
Characteristics of Inflammation in COPD and Asthma
Lung Parenchyma
The most common type of parenchymal destruction in COPD patients is the centrilobular form of emphysema.
Pulmonary Vasculature
Pulmonary vascular changes are characterized by a thickening of the vessel wall. Thickening of the intima is the first structural change, following by an increase in smooth muscle and the infiltration by inflammatory cells.
where cigarette smoking has been, or still is, very common.
CHAPTER 3 RISK FACTORS
Host Factors
Exposures
▪ Genes (e.g., alpha-1 ▪ Tobacco Smoke
antitrypsin deficiency) ▪ Occupational Dusts and