英文PPT课件ChronicobstructivepulmonarydiseaseCOPD
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【COPD英文精品课件】Chronic Obstructive Pulmonary Disease (COPD)
Oxidative stress
Proteinases
2020/6/28
Repair mechanisms
COPD PATHOLOGY
Source: GOLD 2007
Changes in Small Airways in COPD Patients
Lymphoid follicle
Sou20rc20e/:6/2C8OLD 2007
Number Deaths x 1000
70
60
50
Men
40 Women
30
20
10
0 1980
1985
1990
1995
2000
2020/S6/o2u8rce: US Centers for Disease Control and Prevention, 2002 – cited in GOLD 2007
➢ Increase in proteinases compared to antiproteinases and in free radicals leading to parenchymal destruction
➢ Changes in pulmonary vasculature leading to ventilation-perfusion mismatching, pulmonary hypertension, cor pulmonale
Chronic Obstructive Pulmonary Disease (COPD)
PGY-1 Seminar
David Thom, MD, PhD
2020/6/28
Definition of COPD*
➢COPD is a preventable and treatable chronic lung disease characterized by airflow limitation that is not fully reversible.
英文精品课件ChronicObstructivepulmonaryDisease33p
Hypertrophy and hyperplasia of mucus secreting glands secretions
Chemoattractant, upregulation of adhesion molecules neutrophil sequestration in lungs
expression of pro-inflammatory mediators: IL-8, NF-B recruitment of N, B, E and T lymphocytes
hyperreactivity.
Def: Emphysema
Permanent abnormal distention of air spaces distal to the terminal bronchiole with destruction of alveolar septa (containing alveolar capillaries) and attachments to the bronchial walls.
the p53 gene locus epithelial dysplasia and lung cancer
ciliary function retained secretions; airway resistance vagal-mediated smooth muscle contraction
Effects of smoking -2
levels of myeloperoxidase and eosinophilic cationic
protein bronchoconstriction
levels of TGF- (transforming growth factor)
Chemoattractant, upregulation of adhesion molecules neutrophil sequestration in lungs
expression of pro-inflammatory mediators: IL-8, NF-B recruitment of N, B, E and T lymphocytes
hyperreactivity.
Def: Emphysema
Permanent abnormal distention of air spaces distal to the terminal bronchiole with destruction of alveolar septa (containing alveolar capillaries) and attachments to the bronchial walls.
the p53 gene locus epithelial dysplasia and lung cancer
ciliary function retained secretions; airway resistance vagal-mediated smooth muscle contraction
Effects of smoking -2
levels of myeloperoxidase and eosinophilic cationic
protein bronchoconstriction
levels of TGF- (transforming growth factor)
慢性阻塞性肺疾病ChronicObstructivePulmonaryDisease,COPDPPT课件
1．第一秒用力呼气容积占用力肺活量百分比（FEV1/FVC）是评价 气流受限的一项敏感指标。第一秒用力呼气容积占预计值百分比 （FEV1％预计值），是评估COPD严重程度的良好指标，其变 异性小，易于操作。吸入支气管舒张药后FEV1/FVC<70％及 FEV1<80％预计值者，可确定为持续的气流受限。
慢性阻塞性肺疾病
Chronic Obstructive Pulmonary Disease，COPD
1
❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖
内容提要
预治并鉴稳诊辅临病病发病现定 防疗发别定断助床理理病因状义
症诊期 检表生 机 断程 查现理 制 度 评 估
2
定义
❖ 慢性阻塞性肺疾病：简称慢阻肺，是一种常见的、 可以预防及治疗的疾病，其特征是持续存在的呼吸 系统症状和气流受限，通常与显著暴露于有害颗粒 或气体引起的气道和（或）肺泡异常有关。肺功能 检查对确定气流受限有重要意义，在吸入支气管扩 张剂后，第一秒用力呼气容积（FEV1）占用力肺活 量（FVC）之比值（FEV1/FVC）＜70%表明存在 持续性气流受限。
4
5
现状——认识情况
❖ 我国慢阻肺知晓率及肺功能检查普及率极低。研究 的受访者中，仅约 10% 知道慢阻肺这一疾病；不 足 10% 的受访者曾接受过肺功能检查。在所有慢 阻肺患者中，不足 3% 知道自己患有慢阻肺；近 90% 此前从未得到明确诊断。特别需要引起关注的 是，60% 的慢阻肺患者没有明显的咳嗽、咳痰、喘 息等症状，说明普及肺功能检查对实现慢阻肺早诊 早治的重要性。
6
病因
❖ 慢性阻塞性肺病的确切病因不清楚，一般认 为与慢支和阻塞性肺气肿发生有关的因素都 可能参与慢性阻塞性肺病的发病。已经发现 的危险因素大致可以分为外因（即环境因素） 与内因（即个体易患因素）两类。
慢性阻塞性肺疾病
Chronic Obstructive Pulmonary Disease，COPD
1
❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖ ❖
内容提要
预治并鉴稳诊辅临病病发病现定 防疗发别定断助床理理病因状义
症诊期 检表生 机 断程 查现理 制 度 评 估
2
定义
❖ 慢性阻塞性肺疾病：简称慢阻肺，是一种常见的、 可以预防及治疗的疾病，其特征是持续存在的呼吸 系统症状和气流受限，通常与显著暴露于有害颗粒 或气体引起的气道和（或）肺泡异常有关。肺功能 检查对确定气流受限有重要意义，在吸入支气管扩 张剂后，第一秒用力呼气容积（FEV1）占用力肺活 量（FVC）之比值（FEV1/FVC）＜70%表明存在 持续性气流受限。
4
5
现状——认识情况
❖ 我国慢阻肺知晓率及肺功能检查普及率极低。研究 的受访者中，仅约 10% 知道慢阻肺这一疾病；不 足 10% 的受访者曾接受过肺功能检查。在所有慢 阻肺患者中，不足 3% 知道自己患有慢阻肺；近 90% 此前从未得到明确诊断。特别需要引起关注的 是，60% 的慢阻肺患者没有明显的咳嗽、咳痰、喘 息等症状，说明普及肺功能检查对实现慢阻肺早诊 早治的重要性。
6
病因
❖ 慢性阻塞性肺病的确切病因不清楚，一般认 为与慢支和阻塞性肺气肿发生有关的因素都 可能参与慢性阻塞性肺病的发病。已经发现 的危险因素大致可以分为外因（即环境因素） 与内因（即个体易患因素）两类。
【COPD英文PPT课件】Chronic Obstructive Pulmonary Disease (32p)
More on Diagnosis
• Physical examination findings are not sensitive for the initial diagnosis of COPD
– Many patients have normal examination findings
• 10 million adults in the United States have been diagnosed with COPD
• National Health and Nutrition Examination Survey (NHANES) suggests that roughly 10 percent of the adult U.S. population has evidence of impaired lung function consistent with COPD
• Although the diagnosis of COPD is often overlooked in both populations, it is diagnosed even less in women than in men
How is it Diagnosed?
• Clinical suspicion in patients presenting with any of the hallmark symptoms which is then confirmed by spirometry. – Cough, ↑’ed sputum production, and dyspnea – Especially in patients with a smoking history
--英文精品课件ChronicObstructive Pulmonary Disease and
How Respiratory function during sleepduced intercostal muscle activity also affects breathing during sleep in those with impaired diaphragmatic contraction secondary to hyperinflation who may be more dependent on accessory muscle function in order to maintain ventilation. Hypoxemia and hypercapnia during sleep are probably related to hypoventilation in patients with reduced respiratory function
Chronic Obstructive Pulmonary Disease and Sleep
AWAKE Meeting Anstella Robinson, MD FCCP FAASM
Introduction
Respiratory changes during sleep exacerbate gas exchange abnormalities present in those with COPD. Subsequent hypoxemia may predispose to secondary pulmonary hypertension, heart arrhythmias and premature death. More than 40% of COPD patients complain of sleep disturbances including reduced sleep time and increased arousals.
【COPD英文精品课件】Chronic Obstructive pulmonary Disease (33p)
Epidemiology of COPD
30% of smokers develop COPD 20% of adult males have COPD 15% of COPD patients are severely symptomatic 4 th leading cause of death (USA) Mortality rate still rising prevalence in low birth weight and low
COPD
SS Visser, Pulmonology Internal Medicine UP
Def: Emphysema
Permanent abnormal distention of air spaces distal to the terminal bronchiole with destruction of alveolar septa (containing alveolar capillaries) and attachments to the bronchial walls.
Hypertrophy and hyperplasia of mucus secreting glands secretions
Pathogenesis-3
Air pollution exacerbations of CB related to heavy pollution with SO2 and NO2
the p53 gene locus epithelial dysplasia and lung cancer
ciliary function retained secretions; airway resistance vagal-mediated smooth muscle coБайду номын сангаасtraction
COPD英文课件Chronic Obstructive Pulmonary Disease 32p
What's the Physiology?
? Related to chronic airway irritation, mucus production, and pulmonary scarring.
? Irritation from environmental pollutants (most commonly cigarette smoke) or a genetic predisposition leads to airway inflammation, which causes increased mucus production and decreased mucociliary function
– Emphysema: pathologic term used to describe destruction of the alveolar capillary membrane
– Chronic Bronchitis: clinical term used to describe the presence of cough or sputum production for at least a three month duration during two consecutive years
? Without symptoms many patients will not seek medical attention and therefore disease can progress before diagnosis or treatment
Epidemiologically Speaking
Who gets COPD?
? Smokers ? Smokers ? Smokers ? More than 80 percent of deaths from the disease
英文PPT课件ChronicObstructivePulmonaryDisease32p
• The pathological hallmarks of chronic bronchitis are congestion of the bronchial mucosa and a prominent increase in the number and size of the bronchial mucus glands. Copious mucus may be seen within airway lumens. The terminal airways are most susceptible to obstruction by mucus.
MECHANISMS II
Increases in RBC, Blood viscosity, BP Ventilation / Perfusion imbalances Hypoxemia Carbon dioxide retention Bronchial hyperreactivity Hyperinflation
Bronchial glands / cells inflame Increased secretions
Inflammation spreads to smooth muscle (bronchiole) Airway obstruction, decreased ciliary action Air trapping / Collapse of small airways Further air trapping Hyperventilation Increased pressure in airways Weakened airway walls / wall destruction Alveolar destruction Overstressed right ventricle
MECHANISMS II
Increases in RBC, Blood viscosity, BP Ventilation / Perfusion imbalances Hypoxemia Carbon dioxide retention Bronchial hyperreactivity Hyperinflation
Bronchial glands / cells inflame Increased secretions
Inflammation spreads to smooth muscle (bronchiole) Airway obstruction, decreased ciliary action Air trapping / Collapse of small airways Further air trapping Hyperventilation Increased pressure in airways Weakened airway walls / wall destruction Alveolar destruction Overstressed right ventricle
--英文PPT课件ChronicObstructive Pulmonary Disease (32p)
• Without symptoms many patients will not seek medical attention and therefore disease can progress before diagnosis or treatment
Epidemiologically Speaking
Who else is at risk for getting COPD?
• People of advancing age • Those exposed to
secondhand smoke • Chronic exposure to
environmental or occupational pollutants • Alpha1-antitrypsin deficiency (typically early) • Childhood history of recurrent respiratory infections • Family history of COPD
Who gets COPD?
• Smokers • Smokers • Smokers • More than 80 percent of deaths from the disease
are directly attributable to smoking, and persons who smoke are 12 to 13 times more likely to die from COPD than nonsmokers. • The absolute risk of COPD among active, continuous smokers is at least 25 percent
– Emphysema: pathologic term used to describe destruction of the alveolar capillary membrane
Epidemiologically Speaking
Who else is at risk for getting COPD?
• People of advancing age • Those exposed to
secondhand smoke • Chronic exposure to
environmental or occupational pollutants • Alpha1-antitrypsin deficiency (typically early) • Childhood history of recurrent respiratory infections • Family history of COPD
Who gets COPD?
• Smokers • Smokers • Smokers • More than 80 percent of deaths from the disease
are directly attributable to smoking, and persons who smoke are 12 to 13 times more likely to die from COPD than nonsmokers. • The absolute risk of COPD among active, continuous smokers is at least 25 percent
– Emphysema: pathologic term used to describe destruction of the alveolar capillary membrane
【COPD英文PPT课件】Chronic obstructive pulmonary disease (COPD)_
Evidence guiding health care
Methodology:
• Fiscal year 2006/07 • Cohort = Ontarians (derived from the Registered Persons
Database [RPDB]) • EDC algorithm applied to Canadian Institute for Health
• Prevalence rates for other chronic conditions (diabetes, asthma, cancer, congestive heart failure and hypertension) not reported using the ACG System already being measured, or will be measured in the near future, using validated algorithms developed by ICES and Cancer Care Ontario.
• Exclusions: Persons less than 20 years of age (less than 35 years of age for calculation of COPD rates) Out-of-province residents Records with missing/invalid age, sex, and/or LHIN information Individuals who died or whose date of last contact with the health care system was greater than 5 years
Methodology:
• Fiscal year 2006/07 • Cohort = Ontarians (derived from the Registered Persons
Database [RPDB]) • EDC algorithm applied to Canadian Institute for Health
• Prevalence rates for other chronic conditions (diabetes, asthma, cancer, congestive heart failure and hypertension) not reported using the ACG System already being measured, or will be measured in the near future, using validated algorithms developed by ICES and Cancer Care Ontario.
• Exclusions: Persons less than 20 years of age (less than 35 years of age for calculation of COPD rates) Out-of-province residents Records with missing/invalid age, sex, and/or LHIN information Individuals who died or whose date of last contact with the health care system was greater than 5 years
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Background:
• Chronic diseases affect a significant number of Canadians; account for a large proportion of health care service utilization and associated direct and indirect health care costs; are more common with increasing age and lower socioeconomic status; are often associated with modifiable risk factors such as tobacco use, unhealthy diet and lack of physical activity; are subject to delayed onset; and are often considered to be preventable.
• Johns Hopkins Bloomberg School of Public Health. The Johns Hopkins Adjusted Clinical Groups (ACG) Case-Mix System Reference Manual. Version 7.0. Baltimore: The Johns Hopkins University; 2005.
• Johns Hopkins Bloomberg School of Public Health. The Johns Hopkins Adjusted Clinical Groups (ACG) Case-Mix System Technical User Guide. Version 7.0. Baltimore: The Johns Hopkins University; 2005.
6–7
8–19 20–31 32–43 44–56 57–68
Interpretative Cautions ......................................................... 69–70
Sources
• Breezing AM, Watson DE, Black C. Chronic conditions and comorbidity among residents of British Columbia. Vancouver: Centre for Health Services and Policy Research; 2005.
Methodology .......................................................................... Key Findings • Degenerative joint disease (osteoarthritis)..................... • Ischemic heart disease (IHD) ........................................... • Arrhythmia ......................................................................... • Chronic obstructive pulmonary disease (COPD) .......... • Cerebrovascular disease ..................................................
• Estimated “treated” prevalence in Ontario for 2006/07 for 5 of the 11 high-impact and/or high-prevalence chronic diseases, including: Degenerative joint disease (osteoarthritis) Ischemic heart disease (IHD) Cardiac arrhythmia Chronic obstructive pulmonary disease (COPD) Cerebrovascular disease
Table of Contents
Slides
Sources ................................................................................... 3
Background ........................................................................... 4–5
• Centre for Health Services and Policy Research (CHSPR) at the University of British Columbia identified eleven “high-impact and/or high-prevalence” chronic conditions.
• Combination—prevalence and impact—has important implications for the planning and allocation of health care resources.
Background (cont’d):
• Used the Expandedபைடு நூலகம்Diagnosis Clusters (EDCs) Johns Hopkins ACG Case-Mix System (version 7.0) tool