COPD英文ppt课件留学生授课内科学

COPD英文课件留学生授课内科学COPD英文课件留学生授课内科学COPD英文课件留学生授课内1COPD英文ppt课件留学生授课内科学2Chronic BronchitisDefinition:Chronic and unspecific inflammation of bronchi and the surrounding tissue.A clinical syndrome defined -chronic sputum production -Persistent cough -for at least 3 months -in at least 2 consecutive years Anatomic site -Bronchus 3Chronic BronchitisDefinition:PathogenesisChronic irritation of airwaysSmokingDust Air pollutants The major risk factor for the development of chronic bronchitis is cigarette smokingInfective agents-secondary factorPathogenesisChronic irritation4nChronic inflammation nHypertrophy&hyperplasia of bronchial glands that secrete mucusnIncrease number of goblet cellsnCilia are destroyedChronic Bronchitis PathophysiologyCilia DamagedChronic inflammation Chronic B5Inflammatory Cells Studies show that smokers with symptoms of chronic bronchitis have an increased number of inflammatory cells in their bronchial glands when compared with asymptomatic smokers.This inflammatory process consists predominantly of neutrophils and macrophages,and of an increased proportion of CD8+T-lymphocytes.Inflammatory Cells Studies6MacrophagesNeutrophilsMast cellsLymphocytes7MacrophagesNeutrophilsMast celChronic Bronchitis-pathological sectionChronic Bronchitis-pathologica8Narrowing of airway airflow resistancework of breathChronic Bronchitis Pathophysiology9Narrowing of airway Chronic BrChronic Bronchitis PathophysiologyBronchospasm often occursEnd resultHypoxemiaHypercapneaPolycythemia(increase RBCs)Chronic Bronchitis Pathophysio10COPD英文ppt课件留学生授课内科学11Clinical manifestation Main symptoms:cough:chronic,long term,repeatedly expectoration:mucoid sputum,purulent sputum when infection wheezing:seen in some patientsClinical manifestation Main sy12Clinical manifestation Sign:1.no obvious sign in early stage2.sometimes moist rales and rhonchi Clinical manifestation 13Diagnosis Chronic cough and sputum production for 3 consecutive months in at least 2 successive years（3m/y2y）excluding other chronic lung diseasesDiagnosis Chronic cough and s14Emphysema15Emphysema15Definition Pulmonary emphysema is described in clinical,radiological and physiologic terms,but the condition is best defined morphologically.It means abnormal enlargement of airspaces distal to the terminal bronchioles with destruction of their wall.It is characterized by destruction and enlargement of alveoli.Definition Pulmonary emph16Etiology Environment FactorsCigarette smoking(In industrialized countries,cigarette smoking accounts for most cases of COPD)environmental pollutantsOccupational dusts and chemicalsHost FactorsGenes:Alpha1-antitrypsin deficiencyLow birth weight is also a risk of COPDIn old person,the ability of the immune system is decrease,therefore bronchitis is more common in old people.Etiology Environment Factors17Emphysema:PathophysiologyStructural changesHyperinflation of alveoliDestruction of alveolar&alveolar-capillary wallsLung elasticity decreases18Emphysema:PathophysiologyStruLoss of Lung Surface Area for Gas Exchange and Oxygen TransportLoss of Lung Surface area is due to death of Lung Endothelial CellsCigarette Smoke and Environmental Pollution may cause endothelial cell deathEmphysema:Pathophysiology19Loss of Lung Surface Area for Pathology feature Alveolar walls become thinnerAlveolar sacs enlargementRupture of alveoli and formation of bleb20Pathology feature Alveolar wa Severe destruction of small airways can lead to the formation of large air pockets-known as bullae-that replace lung tissue.This form of disease is called bullous emphysemamicroscope21 Severe destruction of smDissection22Dissection22A lateral chest x-ray of a person with emphysema.Note the barrel chest and flat diaphragm23A lateral chest x-ray of a perCT image of the lung of a person with bullous emphysema.24CT image of the lung of a persTypes of Emphysemacentrilobular emphysema panacinar emphysemaTypes of Emphysemacentrilobula25In centrilobular emphysema,respiratory bronchioles are selectively and dominantly involved.26In centrilobular emphysema,26Inpanacinaremphysema,theenlargementanddestructionofairspaceinvolvetheacinusmoreorlessuniformly.27In panacinar emphysema,27emphysemaisonlyadescriptionoflungchangesratherthanadiseaseitself28emphysema is only a descriptioChronic Obstructive Pulmonary Disease(COPD)Chronic Obstructive Pulmonary 29What is COPD?What is COPD?30Global Strategy for Diagnosis,Management and Prevention of COPDnnDefinitionDefinitionnnDiagnosis and AssessmentDiagnosis and AssessmentnnTherapeutic OptionsTherapeutic OptionsnnManage Stable COPDManage Stable COPDnnManage ExacerbationsManage ExacerbationsnnManage ComorbiditiesManage ComorbiditiesREVISED 2011Global Strategy for Diagnosis,31What is COPD?COPD,a common preventable and treatable disease,is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response to noxious particles or gases.What is COPD?COPD,a comm32COPDisatypeofobstructivelungdiseaseinwhichchronicincompletelyreversiblepoorairflow(airflowlimitation)andinabilitytobreatheoutfully(airtrapping)exist.Thepoorairflowistheresultofbreakdownoflungtissue(knownasemphysema)andsmallairwaysdisease(knownasobstructivebronchiolitis).Therelativecontributionsofthesetwofactorsvarybetweenpeople.33 COPD is a type of obstrRelationship of COPD and Chronic bronchitis,Asthma or Emphysema34Relationship of COPD and ChronWhy COPD is Important?COPD is the chronic disease that is showing progressive upward trend in both mortality and morbidityWHO predicts that COPD will become the third leading cause of death worldwide by 2030.Why COPD is Important?COPD is35Worldwide,COPD affects 329 million people or nearly 5 percent of the population.In 2013,it resulted in 2.9 million deaths,up from 2.4 million deaths in 1990.The number of deaths is projected to increase because of higher smoking rates and an aging population in many country.Worldwide,COPD affects 329 mi36EconomicsGlobally,as of 2010,COPD is estimated to result in economic costs of$2.1 trillion,half of which occurring in the developing world.Of this total an estimated$1.9 trillion are direct costs such as medical care,while$0.2 trillion are indirect costs such as missed workEconomicsGlobally,as of 2010,37Global Strategy for Diagnosis,Management and Prevention of COPDRisk Factors for COPDLung growth and development肺的生物自然过程 Gender性别Age 年龄Respiratory infections呼吸系统感染Socioeconomic status社会经济地位Asthma/Bronchial hyperreactivity哮喘/气道高反应性Chronic Bronchitis慢性支气管炎Genes遗传因素Exposure to particles粉尘暴露Tobacco smoke吸烟Occupational dusts,organic and inorganic有机、无机职业粉尘Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings室内空气污染（尤其是在通风不良的室内燃烧生物燃料做饭）Outdoor air pollution室外空气污染Global Strategy for Diagnosis,38Risk Factors for COPDGenesGenesInfectionsInfectionsSocio-economic Socio-economic statusstatusAgingAgingRisk Factors for COPDGenesInfe39PathogenesisTobacco smoking is the most common cause of COPD,with a number of other factors such as air pollution and genetics playing a smaller role.In the developing world,one of the common sources of air pollution is poorly vented cooking and heating fires.Long-term exposure to these irritants causes an inflammatory response in the lungs resulting in narrowing of the small airways and breakdown of lung tissue,known as emphysema.PathogenesisTobacco smoking is404141PathogenesisInflammationsImbalance of proteinases and antiproteinases in the lungsOxidative stress are also important in the pathogenesis of COPD.PathogenesisInflammations424343Mechanisms Underlying Airflow Limitation in COPDSmall Airways Disease小气道病变Airway inflammation气道炎症Airway fibrosis纤维化Increased airway resistance气道阻力增大Parenchymal Destruction肺实质的破坏Loss of alveolar attachments肺泡减少Decrease of elastic recoil弹力下降AIRFLOW LIMITATION44Mechanisms Underlying Airflow On the left is a diagram of the lungs and airways of normal bronchioles and alveoli.On the right is lungs damaged by COPD,bronchiole loose their shape and clogged by mucus.The walls of alveoli are destroyed forming larger alveoli.Pathological changeOn the left is a diagram of th454646Airway in COPDNon-smokerCOPDSaetta.199847Airway in COPDNon-smokerCOPDSaCOPD PathophysiologyHypoventialtion-PaCO2 -Airflow obstruction/airway narrowingHyperinflation:air trappingGas exchange defects-PaO2 Destruction of alveolar wall/alveolar-capillary membraneV/Q mismatch COPD PathophysiologyHypoventia484949COPD PathophysiologySystemic effects of COPD Muscular weakness Impaired salt&water excretion leading to peripheral oedema.Altered fat metabolism contributing to weight lossIncreased prevalence of osteoporosis.Increased circulating inflammatory markers.COPD PathophysiologySystemic 50【医生】COPD的病理_标清.mp4【医生】COPD的病理_标清.mp451The most common symptoms of COPD are sputum production,dyspnea,and a productive cough.These symptoms are present for a prolonged period of time and typically worsen over time.Clinical manifestationSigns and symptomsThe most common symptoms of CO52Clinical manifestationSymptom1.Cough and Expectoration A chronic cough is often the first symptom to develop.It is characteristically accompanied by mucoid sputum.Some people with COPD attribute the symptoms to a smokers cough.Those with COPD often have a history of common colds that last a long time.Clinical manifestationSymptom53Clinical manifestationSymptom2.Dyspnea:Progressive,persistent and characteristically worse with exercise.Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.Clinical manifestationSymptom54Symptom3.Other featuresProlonged expiratory phase.In COPD,it may take longer to breathe out than to breathe in.Chest tightness may occur.Systemic wastingSignificant weight lossanxiety disorder and depression Symptom55Clinical manifestationSign:1.not obvious in early stage2.typical sign:barrel chestdecreased chest movementdiminished tactile fremitusprolong expiration WheezeClinical manifestationSign:56fingernail clubbing is not specific to COPDfingernail clubbing is not spe57barrel chestthoracic antero-posteral-diameter/transverse-diameterbarrel chest58ExaminationPulmonary function test (SpirometrySpirometry)DiagnosisAssessing Monitoring progressionIncompletely reversible airflow limitation is the necessary criteria to diagnose COPD(after inhaled bronchodilator FEV1/FVC 70%59ExaminationPulmonary function Spirometry:Normal and COPD forced expiratory volume in 1 second(FEV1)forced vital capacity(FVC)60Spirometry:Normal and COPD fChest X-rayBlood gas：to detect respiratory failureBlood routine and sputum examination ExaminationChest X-rayExamination61Chest X-rayIntercostal space wideningDiaphragm are low and flatShadow of the heart narrowing62Chest X-rayIntercostal space wComplications of COPD1.Chronic respiratory failure Type 2 2.Spontanous pneumothorax 3.Cor pulmonale Complications of COPD63Global Strategy for Diagnosis,Management and Prevention of COPD nnDefinitionDefinitionnnDiagnosis and Diagnosis and Therapeutic Therapeutic OptionsOptionsnnManage Stable COPDManage Stable COPDnnManage ExacerbationsManage ExacerbationsnnManage ComorbiditiesManage ComorbiditiesREVISED 2011Global Strategy for Diagnosis,64Diagnosis 1、Smoking history2、Symptom:cough,sputum production,gradually progressive dyspnea3、Sign：emphysema4、PFT:airway flow limitationDiagnosis 1、Smoking history65Diagnosis: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.Spirometry is required to make the diagnosis;the presence of a post-bronchodilator FEV1/FVC 0.780I:Mild COPD80II:Moderate COPD0.750-80III:Severe COPD0.730-50IV:Very severe COPD0.730Assessment of COPDSeverityPos76Clinical Features of COPD Patients of different severityMild COPD:no abnormal signs,smokers cough,little or no breathlessnessModerate COPD:breathlessness with/without wheezing,cough with/without sputumSevere COPD:breathlessness on any exertion/at rest,wheeze and cough prominent,lung inflation usual,cyanosis,peripheral edema,and polycythemia in advanced diseaseClinical Features of COPD Pati77Stage of diseaseAcute ExacerbationsStableStage of diseaseAcute Exacerba78Acute exacerbations of COPDAcuteexacerbationsofCOPDarecharacterisedbyanincreaseinsymptomsanddeteriorationinlungfunction.Theybecomemorecommonasthediseaseprogressesandmaybecausedbybacteria,virusesorachangeinairquality.Theymaybeaccompaniedbythedevelopmentofrespiratoryfailureand/orfluidretentionandrepresentanimportantcauseofdeath79Acute exacerbations of COPDAcuThis may present with signs of increased work of breathing such as fast breathing,a fast heart rate,sweating,active use of muscles in the neck and even a bluish tinge to the skin in very severe exacerbations.Crackles may also be heard.This may present with signs of80 During exacerbations,airway inflammation is also increased,resulting in increased hyperinflation,reduced expiratory airflow and worsening of gas transfer.This can also lead to insufficient ventilation and,eventually,low blood oxygen levels During exacerbations,ai81Causes:75%infectiousVirusBacteria20%environmental5%Other:MI/CHFSurgeryAspiration.Pulmonary embolism(20%in one study!)caution-select patient populationCOPD ExacerbationsCauses:COPD Exacerbations82Global Strategy for Diagnosis,Management and Prevention of COPD nnDefinitionDefinitionnnDiagnosis and AssessmentDiagnosis and AssessmentnnTherapeutic OptionsTherapeutic OptionsnnManage Stable COPDManage Stable COPDnnManage ExacerbationsManage ExacerbationsnnManage ComorbiditiesManage ComorbiditiesREVISED 2011Global Strategy for Diagnosis,83Global Strategy for Diagnosis,Management and Prevention of COPDTherapeutic Options:Key PointsSmoking cessation has the greatest capacity to influence the natural history of COPD.Health care providers should encourage all patients who smoke to quit.Pharmacotherapy and nicotine replacement reliably increase long-term smoking abstinence rates.All COPD patients benefit from regular physical activity and should repeatedly be encouraged to remain active.Global Strategy for Diagnosis,84Appropriate pharmacologic therapy can reduce COPD symptoms,reduce the frequency and severity of exacerbations,and improve health status and exercise tolerance.None of the existing medications for COPD has been shown conclusively to modify the long-term decline in lung function.Influenza and pneumococcal vaccination should be offered depending on local guidelines.Global Strategy for Diagnosis,Management and Prevention of COPDTherapeutic Options:Key PointsAppropriate pharmacologic ther85COPD:TherapySmoking cessationMedicationsLong term oxygen therapyRehabilitationManagement of COPDCOPD:Therapy86Therapeutic Options:Smoking CessationKeeping people from starting smoking is a key aspect of preventing COPD.Counseling delivered by physicians and other health professionals significantly increases quit rates over self-initiated strategies.Smoking bans in public areas and places of work are important measures to decrease exposure to secondhand smoke.Therapeutic Options:Smoking C87Therapeutic Options:Risk ReductionTherapeutic Options:Risk Red88Therapeutic Options:COPD MedicationsBeta2-agonists Short-acting beta2-agonists Long-acting beta2-agonistsAnticholinergicsCombination beta2-agonists+anticholinergic in one inhaler TheophyllineInhaled corticosteroids Combination beta2-agonists+corticosteroids in one inhalerSystemic corticosteroidsBronchodilatorsTherapeutic Options:COPD Medi89Therapeutic Options:BronchodilatorsTherapeutic Options:Bronchod90Therapeutic Options:BronchodilatorsTherapeutic Options:Bronchod91 The principal action of 2-agonists is to relax airway smooth muscle by stimulating 2-adrenergic receptors,which increases cyclic AMP and produces functional antagonism to bronchoconstriction.Inhaled 2-agonists have a relatively rapid onset of bronchodilator effect although this is probably slower in COPD than in asthmaBronchodilators：2-agonist bronchodilators The principal action of 92Rapid-acting 2-agonists(SABA)Agents such as salbutamol(ventolin 万托林)terbutalineThe bronchodilator effects of shoracting 2-agonists usually wear off within 4 to 6 hours.Use this prnminimal risk of side effectsBronchodilators：2-agonist bronchodilatorsRapid-acting 2-agonists(SABA93-Long acting 2-agonists(LABA)Agents such as salmeterol,formoterolshow a duration of effect of 12 hours or more with no loss of effectiveness overnight or with regular use in COPD patientsThe benefit for longtime usingpatients activity and QOL-Long acting 2-agonists 94 The most important effect of anticholinergic medications,in COPD patients appears to be blockage of acetylcholines effect on M3 receptors.Current short-acting drugs also block M2 receptors and modify transmission at the pre-ganglionic junction,although these effects appear less important in COPD.Therapy-Bronchodilators The most important effect o95Anticholinergic bronchodilatorsAgents such as Ipratropium,Tiotropium:Ipratropium is a short-acting agent while tiotropium is long-acting.Regular therapyTherapy-BronchodilatorsAnticholinergic bronchodilator96AnticholinergicSymptomatic benefits,decrease in exacerbations and improved quality of lifeSide effects:dry mouth,urinary retention,also associated with increased risk of heart disease and stroke.Anticholinergic97Inhaled bronchodilators are the primary medications used and result in a small overall benefit.They reduce shortness of breath,wheeze and exercise limitation,resulting in an improved quality of life.It is unclear if they change the progression of the underlying disease.Therapy-BronchodilatorsInhaled bronchodilators are th98Theophylline-Agents such as aminophylline,doxofylline-Usage:intravenous or oral Multiple but less effectsBronchodilationrespiratory stimulant improved cardiovascular functionimproved diaphragm functionTherapy-TheophyllineTheophyllineTherapy-Theophylli99TheophyllineTheophylline100The effects of oral and inhaled glucocorticosteroids in COPD are much less dramatic than in asthma,and theirrole in the management of stable COPD is limited tospecific indications.Corticosteroids are usually used in inhaled form but may also be used as tablets even intravenous to treat and prevent acute exacerbations.Inhaled corticosteroids(ICS):decrease acute exacerbations in those with either moderate or severe diseaseTherapy-CorticosteroidsThe effects of oral and inhale101Regular treatment with inhaled corticosteroids(ICS)improves symptoms,lung function and quality of life and reduces frequency of exacerbations for COPD patients with an FEV1 60%predicted.When used in combination with a LABA they decrease mortality more than either ICS or LABA alone Inhaled corticosteroid therapy is associated with an increased risk of pneumonia.Inhaled CorticosteroidsRegular treatment with inhaled102Chronic treatment with systemic corticosteroids should be avoided because of an unfavorable benefit-to-risk ratio.Systemic CorticosteroidsChronic treatment with systemi103Supplemental oxygen is recommended in those with low oxygen levels at rest(a partial pressure of oxygen of less than 5055 mmHg or oxygen saturations of less than 88%).During acute exacerbations,many require oxygen therapyTherapy-OxygenSupplemental oxygen is recomme104AllCOPDpatientsbenefitfromexercise training programs withimprovementsinexercisetoleranceandsymptomsofdyspneaandfatigue.Thelongerthepulmonaryrehabilitationprogramcontinues,themoreeffectivetheresults.Ifexercisetrainingismaintainedathomethepatientshealthstatusremainsaboveprerehabilitationlevels.Therapeutic Options:RehabilitationAll COPD patients benefit from105Respiratoryrehabilitationmayimproveprognosisandthispossibilityviameta-analysisofpublishedresults.Pulmonary RehabilitationRespiratory rehabilitation may106Influenza vaccines can reduce serious illness.Pneumococcal polysaccharide vaccine is recommended for COPD pa