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COPD Review. Progressive Syndrome Expiratory airflow obstruction Chronic airway and lung parenchyma inflammation.

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Presentation on theme: "COPD Review. Progressive Syndrome Expiratory airflow obstruction Chronic airway and lung parenchyma inflammation."— Presentation transcript:

1 COPD Review


3 Progressive Syndrome Expiratory airflow obstruction Chronic airway and lung parenchyma inflammation


5 Preventable, treatable 24 million adults in US 4th leading cause of death in US: –Heart disease –Cancer –Stroke –COPD –Accidents –Diabetes

6 GOLD: global initiative for chronic obstructive lung diseasae –Expiratory airflow not fully reversible –Progressive, association with an “abnormal” lung response to noxious gases and particles

7 Two major clinical types –Chronic bronchitis: inflammation of small and medium sized airways –Leads to expiratory defect, chronic cough, sputum production and dyspnea

8 Emphysema –Inflammation of lung parenchyma –Loss of elastic recoil of lungs –Airflow limitation –Hypoxemia –dyspnea





13 COPD Irreversible airflow (as measured by FEV1 or FEV1/FVC) caused by: –Increased airway resistance in the conducting airways, or, –Increased lung compliance due to destruction of lung parenchyma/elasticity Or a combination of both the above

14 Chronic Bronchitis Inflammation of the central airways (airways >4mm diameter and peripheral airways < 2 mm) Extends to gland ducts and into the mucus producing glands –This produces increase mucus –Defective mucociliary clearance –Disruption (destruction) of epithelial barrier

15 Airflow obstruction occurs primarily in the small airways which are <2mm diameter

16 Emphysema Decrease in elastic recoil force needed to drive air out of lung (“paper sack”) Centrilobular or centriacinar form is associated with cigarette smoking –Major destruction of the acinus at the respiratory bronchiole level

17 Panlobular or panacinar form is associated with alpha-1 antitrypsin disease –Destruction of the entire acinus –Occurs as a result of an imbalance of proteolytic enzymes in lung tissue

18 In both forms of the disease, the cause of COPD is inflammation, both in the airways and in lung tissue

19 Inflammation Smoking, in Chronic Bronchitis –Neutrophils and macrophages, lymphocytes Emphysema –Cellular changes in terminal bronchioles –Destruction (protease enzymes) extracellular matrix of aleveoli –Ineffective repair mechanism

20 COPD vs Asthma Asthma –Anatomical location of inflammation –With bronchodilators and steroids, lung function returns to normal or near-normal with occasional transient inflammation COPD –Anatomical (airways and lung parenchyma) –Some degree of irreversible deterioration

21 Cellular differences Asthma –Eosinophils –Mast cells –Lymphocytes –CD4 T cells

22 Same cells: CB & Emphysema COPD –Neturophils –Macrophages –No mast cells –CD8 T cells

23 COPDAsthma Age5th decadeAll ages Smoking Hx>10 pack yearsNone, minimal SputumCB frequentFrequent, clear AllergiesInfrequentFrequent Course of disease Progressive worsening Nonprogressive SymptomsPersistentIntermittent

24 A 20 pack year smoking history indicates that the subject’s lungs have received 20 of these short cyclic exposures per day for a cumulative total of 7300 exposures per year and 146,000 exposures over the lifetime of their smoking habit.

25 GOLD Stages COPD StageAirflow Limitation 1 Mild FEV1/FVC <70%FEV1 >80% predicted 2 Moderate FEV1/FVC <70%FEV1 <50%- <80% 3 Severe FEV1/FVC <70%FEV1 <30% - <50% 4 Very severe FEV1/FVC <70%FEV1 <30% or FEV1 <50% with chronic respiratory failure


27 In Sum Toxic gases and particles generated in tobacco smoke come into contact with lung tissues each time a puff of smoke is inhaled Tissue injury recurs in a cyclic fashion as each cigarette is smoked

28 Chronic Bronchitis Inflammation: mucociliary clearance disrupted epithelial barrier/defense lost increased sputum production (goblet cells) irreversible airway remodeling airflow obstruction

29 Emphysema In lung tissue, the chronic inhalation also causes inflammation, destroys elastic recoil, disrupts balance of protective, anti- protease enzymes proteinase-antiproteniase theory elastase-antielastase “extracellular matrix”

30 Toxins/free radicalsCigarette smokeToxins/free radicals Stimulation of alveolar macrophages & other inflammatory cells chemotactic factors Airway inflammation Lung (pulmonary) inflammation & Injury to parenchymal cells Airflow obstructionProteinase inhibitors (alpha1-antitrypsin) Injury to extracellular matrix Repair of extracellular matrix Chronic Bronchitis Emphysema Coughexcessive sputum productiondyspnea at rest


32 Alpha1-antitrypsin Neutrophil elastase linked to alpha-1 antitrypsin deficiency Other cells producing proteinase enzymes: macrophages, lymphocytes—still not determined












44 Decreased airflow resistance (airways) and decreased elastic recoil lead to: Hyperinflation V/Q mismatching, which further leads to decreases in Pa02, increases in PaC02 with decreased ventilation

45 In end-stage COPD –Cor pulmonale –Pulmonary vasoconstriction (in presence of chronic low Pa02) –Increased pulmonary vascular resistance –Increased pressure, leading eventually to right heart enlargement

46 CXR

47 COR Pulmonale




51 Emphysema


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