1、Chronic and unspecific inflammation of bronchi and the surrounding tissue.Feature:chronic mucus hypersecretion and cough.Morbidity:3.2%in population over 15 y,up to 15%in elderly over 50 y.Etiology and mechanism Environment FactorsCigarette smokingOccupational dusts and chemicalsInfectionsHost Facto
2、rsGenes Lung growth and defense mechanismChronic BronchitisClinical manifestation Character:chronic onset,recurrent attack and long course of diseaseMain symptoms:cough:chronic,long term,repeatedly expectoration:mucoid sputum,purulent sputum when infection wheezing:seen in some patientsClinical mani
3、festation Sign:1.no obvious sign in early stage2.sometimes moist rales and rhonchi Examination Chest x-ray imagingExamination Pulmonary function test:maybe normal in early stage.Gradually obstructive airway function appeared.Blood routine:elevated neutrophil or eosinophil Sputum examination:bacteria
4、l culture guide antibiotic treatmentDiagnosis Chronic cough and sputum production for 3 consecutive months in at least 2 successive years(3m/y2y),excluding other chronic lung diseases(TB,Bronchiectasis)Definite chest imaging or lung functionTyping Typing:1、simple:cough,sputum2、wheezing:with wheezing
5、(actually Chronic bronchitis plus asthma)Emphysema DefinitionEmphysema is characterized by enlargement and destruction of respiratory bronchioles and/or alveoli in the lungs.Etiology Environment FactorsCigarette smokingOccupational dusts and chemicalsInfectionsHost FactorsGenes:Alpha1-antitrypsin de
6、ficiencyContributing factorAirway obstruction due to chronic inflammationDamaged bronchial cartilage and lead to the loss of supporting functionIncreased activity of proteinase due to chronic airway inflammation or smokingAlpha1-antitrypsin deficiencyOthers:Poor nutrition of alveoli or respiratory b
7、ronchiole due to decreased blood supply because of oppression of high airway pressureCigarette smokeAlveolar macrophageNeutrophil PROTEASES Alveolar wall destruction(Emphysema)Mucus hypersecretion(Chronic bronchitis)PROTEASEINHIBITORSNeutrophil chemotactic factors CELLULAR MECHANISMS OF COPD Neutrop
8、hil elastaseCathepsinsMatrix metalloproteinasesCytokines(IL-8)Mediators(LTB4)?CD8+lymphocyte-MCP-1 1-Antitrypsin TIMPs SLPI Elafin Neutrophil elastase Cathepsins MMP-1,MMP-9,MMP12 Granzymes,perforins Others.PROTEASE-ANTIPROTEASE IMBALANCE IN COPDPathology feature Alveolar walls become thinnerAlveola
9、r sacs enlargementRupture of alveoli and formation of blebPathological CategoryPanacinar(panlobular)emphysemaGross section of lung.Dilated,saccular airspaces.In cases of disease dueto a1-antitrypsin deficiency,lower part of lung tendsto be more affectedMagnifiedsection.Diffuseinvolvementof allportio
10、nsof acini NovartisPanacinar(panlobular)emphysemaGross section of lung.Dilated,saccular airspaces.In cases of disease dueto a1-antitrypsin deficiency,lower part of lung tendsto be more affectedMagnifiedsection.Diffuseinvolvementof allportionsof acini NovartisIn panlobular emphysema,the enlargement a
11、nd destruction of air space involve the acinus more or less uniformly.Centriacinar(centrilobular)emphysemaMagnified section.Distended,inter-communicating,sac-like spacesin central areaof aciniMicroscopic section.Distention of airspaceswith rupture ofalveolar wallsGross specimen.Involvement tends tob
12、e most marked inupper part of lung NovartisCentriacinar(centrilobular)emphysemaMagnified section.Distended,inter-communicating,sac-like spacesin central areaof aciniMicroscopic section.Distention of airspaceswith rupture ofalveolar wallsGross specimen.Involvement tends tobe most marked inupper part
13、of lung NovartisIn centrilobular emphysema,respiratory bronchioles are selectively and dominantly involved.COPD-chronic bronchitis-emphysemaCOPD PathophysiologyHypoventialtion-PaO2,PaCO2 Airflow obstruction/airway narrowing mucus plugging airway inflammation,edema,fibrosis airway collapse due to alveolar wall destruction Hyperinflation:air trappingGas exchange defects-PaO2 Destruction of alveolar wall/alveolar-capillary membrane V/Q mismat
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