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COPD.pptx

Mazin Al Zo'ubi
Mazin Al Zo'ubi

Chronic Obstructive Pulmonary Disease (COPD) is an irreversible lung disease characterized by limited airflow and an abnormal inflammatory response in the lungs caused by long-term exposure to harmful particles like cigarette smoke. The main symptoms are breathlessness, cough, and wheezing. Diagnosis is based on a history of symptoms and cigarette smoking, and confirmed with lung function tests showing reduced airflow. Treatment focuses on smoking cessation and drug therapy with bronchodilators and corticosteroids to manage symptoms and reduce exacerbations.

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Chronic Obstructive Pulmonary Disease Dr. Mazen Al Zoubi Rheumatology and Internal Medicine Senior Specialist
Definition COPD is an irreversible lung disease characterized by limited airflow It is progressive and accompanied by an abnormally inflammatory response of the lungs to toxic substances or gases Emphysema, small airways disease, and chronic bronchitis are grouped under the umbrella diagnosis of COPD Lung hyperinflation, ventilation/perfusion mismatch, increased work of breathing, and dyspnea follow as a result The presence of several comorbidities, including cancer, ischemic heart disease, hypertension, diabetes, and heart failure, suggests that the condition could be a result of a broad systemic inflammatory response.
Epidemiology and Aetiology Long-term exposure to harmful chemicals and particles results in COPD Over 90% of cases in developed nations involve smoking cigarettes Biomass heating fuels and cooking smoke in poorly ventilated locations, play a role in developing nations Only 1020% of smokers experience the development of COPD, indicating a possible underlying individual predisposition
Pathophysiology Structurally, there may be evidence of emphysema and small airways disease, with increased mucus-producing goblet cells in the bronchial mucosa, which may lead to chronic bronchitis Pathologically, there is evidence of both acute and chronic inflammation This chronic inflammation results in scarring and fibrosis of the small airways. In addition, there is destruction of the alveolar walls, which results in emphysema.
Emphysema It is an abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, accompanied by destruction of their walls. Distension and damage of lung tissue are concentrated around the respiratory bronchioles Distension and destruction affect the whole acinus, and in severe cases the lung is just a collection of bullae There is scarring and damage that affect the lung parenchyma patchily, independent of acinar structure
Pathogenesis Cigarette smoking 1) Imbalance between protease and antiprotease activity 2) Mucous gland hypertrophy Infections precipitating cause of acute exacerbations 留-1 antitrypsin Deficiency 1) It is a proteinase inhibitor. 2) Inhibits proteolytic enzymes such as neutrophil elastase, which can destroy alveolar wall connective tissue.
Symptoms Breathlessness Productive cough Wheeze
Signs Early disease Asymptomatic Quit wheeze Severe disease Tachypnoea Prolonged expiration Accessory muscle use Lips purse Reduced cricosternal distance Poor chest expansion Advanced disease Signs of right heart failure
Signs
Diagnosis This is usually clinical and based on a history of breathlessness and sputum production in a chronic smoker. In the absence of a history of cigarette smoking, asthma is a more likely explanation, unless there is a family history suggesting 留1- antitrypsin deficiency.
Investigations Show evidence of airflow limitation (FEV1:FVC ratio is reduced) Often normal Over-inflation Flattened diaphragms Sometimes the presence of large bullae Useful, particularly when the CXR is normal helpful to determine if there is any evidence of respiratory failure worth measuring in premature disease or lifelong non-smokers
Classification of airflow limitation severity in COPD (based on post-bronchodilator FEV1) Global Initiative for Chronic Obstructive Lung Disease (GOLD)
Management Healthcare The single most useful measure Smoke from burning biomass fuels in poorly ventilated homes should also be reduced Smoking cessation single dose of the polyvalent pneumococcal polysaccharide vaccine Yearly influenza vaccinations Vaccines
Management Drug therapy Mild COPD: short-acting 硫2 agonist Moderate and severe COPD: long-acting 硫2 agonist 硫-Adrenoceptor agonists Regular use of a LAMA (such as inhaled tiotropium) improves lung function, symptoms of dyspnea and quality of life Use of a LAMA does not prevent the decline in FEV1 Antimuscarinic drugs It is used as an adjunct to bronchodilators for maintenance treatment in those patients with an FEV1 of less than 50% and chronic bronchitis Phosphodiesterase type 4 inhibitors Inhaled corticosteroids are recommended in patients with frequent exacerbations or a FEV1 of less than 50% predicted Demonstration of a blood eosinophilia may identify patients who are more likely to have a beneficial response to inhaled corticosteroid therapy Corticosteroids Long-acting preparations of theophylline are of little benefit Theophyllines
Management Oxygen therapy PaO2 of <7.3 kPa (55 mmHg) when breathing air; measurements should be taken on two occasions at least 3 weeks apart after appropriate bronchodilator therapy PaO2 of <8 kPa with secondary polycythemia, nocturnal hypoxemia, peripheral oedema or evidence of pulmonary hypertension Carboxyhemoglobin of <3% (i.e., patients who have stopped smoking). Domiciliary oxygen is best provided via an oxygen concentrator
Algorithm for the treatment of chronic obstructive pulmonary disease
COPD.pptx

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COPD.pptx

  • 1. Chronic Obstructive Pulmonary Disease Dr. Mazen Al Zoubi Rheumatology and Internal Medicine Senior Specialist
  • 2. Definition COPD is an irreversible lung disease characterized by limited airflow It is progressive and accompanied by an abnormally inflammatory response of the lungs to toxic substances or gases Emphysema, small airways disease, and chronic bronchitis are grouped under the umbrella diagnosis of COPD Lung hyperinflation, ventilation/perfusion mismatch, increased work of breathing, and dyspnea follow as a result The presence of several comorbidities, including cancer, ischemic heart disease, hypertension, diabetes, and heart failure, suggests that the condition could be a result of a broad systemic inflammatory response.
  • 3. Epidemiology and Aetiology Long-term exposure to harmful chemicals and particles results in COPD Over 90% of cases in developed nations involve smoking cigarettes Biomass heating fuels and cooking smoke in poorly ventilated locations, play a role in developing nations Only 1020% of smokers experience the development of COPD, indicating a possible underlying individual predisposition
  • 4. Pathophysiology Structurally, there may be evidence of emphysema and small airways disease, with increased mucus-producing goblet cells in the bronchial mucosa, which may lead to chronic bronchitis Pathologically, there is evidence of both acute and chronic inflammation This chronic inflammation results in scarring and fibrosis of the small airways. In addition, there is destruction of the alveolar walls, which results in emphysema.
  • 5. Emphysema It is an abnormal and permanent enlargement of air spaces distal to the terminal bronchiole, accompanied by destruction of their walls. Distension and damage of lung tissue are concentrated around the respiratory bronchioles Distension and destruction affect the whole acinus, and in severe cases the lung is just a collection of bullae There is scarring and damage that affect the lung parenchyma patchily, independent of acinar structure
  • 6. Pathogenesis Cigarette smoking 1) Imbalance between protease and antiprotease activity 2) Mucous gland hypertrophy Infections precipitating cause of acute exacerbations 留-1 antitrypsin Deficiency 1) It is a proteinase inhibitor. 2) Inhibits proteolytic enzymes such as neutrophil elastase, which can destroy alveolar wall connective tissue.
  • 8. Signs Early disease Asymptomatic Quit wheeze Severe disease Tachypnoea Prolonged expiration Accessory muscle use Lips purse Reduced cricosternal distance Poor chest expansion Advanced disease Signs of right heart failure
  • 10. Diagnosis This is usually clinical and based on a history of breathlessness and sputum production in a chronic smoker. In the absence of a history of cigarette smoking, asthma is a more likely explanation, unless there is a family history suggesting 留1- antitrypsin deficiency.
  • 11. Investigations Show evidence of airflow limitation (FEV1:FVC ratio is reduced) Often normal Over-inflation Flattened diaphragms Sometimes the presence of large bullae Useful, particularly when the CXR is normal helpful to determine if there is any evidence of respiratory failure worth measuring in premature disease or lifelong non-smokers
  • 12. Classification of airflow limitation severity in COPD (based on post-bronchodilator FEV1) Global Initiative for Chronic Obstructive Lung Disease (GOLD)
  • 13. Management Healthcare The single most useful measure Smoke from burning biomass fuels in poorly ventilated homes should also be reduced Smoking cessation single dose of the polyvalent pneumococcal polysaccharide vaccine Yearly influenza vaccinations Vaccines
  • 14. Management Drug therapy Mild COPD: short-acting 硫2 agonist Moderate and severe COPD: long-acting 硫2 agonist 硫-Adrenoceptor agonists Regular use of a LAMA (such as inhaled tiotropium) improves lung function, symptoms of dyspnea and quality of life Use of a LAMA does not prevent the decline in FEV1 Antimuscarinic drugs It is used as an adjunct to bronchodilators for maintenance treatment in those patients with an FEV1 of less than 50% and chronic bronchitis Phosphodiesterase type 4 inhibitors Inhaled corticosteroids are recommended in patients with frequent exacerbations or a FEV1 of less than 50% predicted Demonstration of a blood eosinophilia may identify patients who are more likely to have a beneficial response to inhaled corticosteroid therapy Corticosteroids Long-acting preparations of theophylline are of little benefit Theophyllines
  • 15. Management Oxygen therapy PaO2 of <7.3 kPa (55 mmHg) when breathing air; measurements should be taken on two occasions at least 3 weeks apart after appropriate bronchodilator therapy PaO2 of <8 kPa with secondary polycythemia, nocturnal hypoxemia, peripheral oedema or evidence of pulmonary hypertension Carboxyhemoglobin of <3% (i.e., patients who have stopped smoking). Domiciliary oxygen is best provided via an oxygen concentrator
  • 16. Algorithm for the treatment of chronic obstructive pulmonary disease