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Basics on Chronic obstructive Pulmonary disease
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- 2. NAMES OF GROUPMEMBERS AND ID NUMBERS 1. Fatima Zainab Kamara 22044 2. Isata Kattie Koroma 22058 3. Mohamed Saidu Mansaray 22064 4. Patricia King Conteh 22016 5. Mariama M. Bendu 22011 6. Precious Faith Kanu 22048 7. Isatu N. Turay 22081
- 3. OUTLINE • Introduction (Definition) •Etiology & Risk factors • Pathophysiology • Common presentations of COPD • Emphysema • Chronic Bronchitis • Bronchiectasis • Investigations • management • Questions • Summary
- 4. Introduction • Chronic obstructive pulmonarydisease (COPD) is a chronic lung condition characterized by air flow obstruction and breathing difficulties • It typically present with a combination of symptoms, which can vary in severity among individuals
- 5. Etiology & Riskfactors • Smoking • Genetic factors • Occupational exposures • Air pollution • Respiratory infections • Asthma • Aging
- 6. Pathophysiology • The pathophysiologyof COPD involves a complex interplay of various factors, which includes: Genetic predisposition ands Environmental pollutants
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- 8. Common features –signs & symptoms • Progressive breathlessness • Chronic cough • Increased sputum production • Wheezing • Chest tightness • Fatigue • Recurrent respiratory infections
- 9. Emphysema • Emphysema ischaracterized by permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without significant fibrosis. N.B. the acinus is the structure distal to terminal bronchioles, and a cluster of three to five acini is called a lobule
- 10. Emphysema • There arefour major types of emphysema: • (1) centriacinar, (2) panacinar, (3) distal acinar, and (4) irregular. • Only the first two types cause significant airway obstruction, with centriacinar emphysema being about 20 times more common than panacinar disease.
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- 12. Centriacinar (Centrilobular) Emphysema •The distinctive feature of centriacinar emphysema is that the central or proximal parts of the acini, formed by respiratory bronchioles, are affected, while distal alveoli are spared. • Thus, both emphysematous and normal air spaces exist within the same acinus and lobule • The lesions are more common and severe in the upper lobes • This type of emphysema is most common in cigarette smokers, often in association with chronic bronchitis.
- 13. Panacinar (Panlobular) emphysema •In panacinar (Panlobular) emphysema, the acini are uniformly enlarged, from the level of the respiratory bronchiole to the terminal blind alveoli • In contrast to centriacinar emphysema, panacinar emphysema occurs more commonly in the lower lung zones and is associated with α1-anti-trypsin deficiency.
- 14. Distal acinar (Paraseptal)emphysema • In this form of emphysema, the proximal portion of the acinus is normal but the distal part is primarily involved. • The cause of this type of emphysema is unknown; it comes to attention most often in young adults who present with spontaneous pneumothorax.
- 15. Irregular emphysema • Irregularemphysema, so named because the acinus is irregularly involved, is almost invariably associated with scarring, such as that resulting from healed inflammatory diseases. • Although clinically asymptomatic, this may be the most common form of emphysema.
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- 17. Clinical Features ofEmphysema • Dyspnea usually is the first symptom • Weight loss is common and may be severe enough to suggest an occult malignant tumor • Barrel-chested • Pulmonary hypertension • Cardiac failure • Recurrent infections • Respiratory failure
- 18. Chronic Bronchitis • Chronicbronchitis is diagnosed on clinical grounds: it is defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. • It is common among cigarette smokers and urban dwellers in smog-ridden cities
- 19. Pathogenesis of Chronicbronchitis • The distinctive feature of chronic bronchitis is hypersecretion of mucus, beginning in the large airways. • Although the most important cause is cigarette smoking, other air pollutants, such as sulfur dioxide and nitrogen dioxide, may contribute.
- 20. Pathogenesis of Chronicbronchitis cont… • These environmental irritants induce hypertrophy of mucous glands in the trachea and bronchi as well as an increase in mucin- secreting goblet cells in the epithelial surfaces of smaller bronchi and bronchioles. • These irritants also cause inflammation marked by the infiltration of macrophages, neutrophils, and lymphocytes
- 21. Pathogenesis of Chronicbronchitis • The airflow obstruction in chronic bronchitis results from: 1. Small airway disease, induced by mucous plugging of the bronchiolar lumen, inflammation, and bronchiolar wall fibrosis, and 2. Coexistent emphysema.
- 22. Clinical Features ofChronic bronchitis • Productive cough • Hypercapnia • Hypoxemia • Cyanosis • Pulmonary hypertension • Cardiac failure • Recurrent infections • Respiratory failure
- 23. Bronchiectasis • Bronchiectasis isthe permanent dilation of bronchi and bronchioles caused by destruction of smooth muscle and the supporting elastic tissue; it typically results from or is associated with chronic necrotizing infections. • It is not a primary disorder, as it always occurs secondary to persistent infection or obstruction caused by a variety of conditions.
- 24. Predisposing factors ofBronchiectasis • Bronchial obstruction • Congenital or hereditary conditions Cystic fibrosis Immunodeficiency states Primary ciliary dyskinesia (also called the immotile cilia syndrome). • Necrotizing, or suppurative, pneumonia, particularly with virulent organisms such as Staphylococcus aureus or Klebsiella spp., predispose affected patients to development of bronchiectasis. • Post-tuberculosis bronchiectasis continues to be a significant cause of morbidity in endemic areas.
- 25. Pathogenesis of Bronchiectasis •Two intertwined processes contribute to bronchiectasis: obstruction and chronic infection. • Either may be the initiator. • For example, obstruction caused by a foreign body impairs clearance of secretions, providing a favorable substrate for superimposed infection.
- 26. Pathogenesis of Bronchiectasiscont… • The resultant inflammatory damage to the bronchial wall and the accumulating exudate further distend the airways, leading to irreversible dilation. • Conversely, a persistent necrotizing infection in the bronchi or bronchioles may lead to poor clearance of secretions, obstruction, and inflammation with peribronchial fibrosis and traction on the bronchi, culminating again in full-blown bronchiectasis.
- 27. Clinical Features ofBronchiectasis • Bronchiectasis is characterized by severe, persistent cough associated with expectoration of mucopurulent, sometimes fetid, sputum. • Dyspnea • Rhinosinusitis and • Hemoptysis • Hypoxemia, hypercapnia, pulmonary hypertension, and cor pulmonale.
- 28. Investigations • History taking •Clinical examination • Spirometry • Chest x-ray • Alpha -1 testing • CT scan • Oximetry or arterial blood gas • Others ( lung volume test, diffusion capacity test, exercise testing e.t.c)
- 29. Managements • There iscurrently no cure for COPD, but treatments can help slow the progression of the condition and control the symptoms • The various treatments include: Stopping smoking Inhalers and tablets Pulmonary rehabilitation Surgery or a lung transplant
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- 31. Summary • Emphysema ischaracterized by permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without significant fibrosis • There are four major types of emphysema: centriacinar, panacinar, distal acinar, and irregular • Chronic bronchitis is diagnosed on clinical grounds: it is defined by the presence of a persistent productive cough for at least 3 consecutive months in at least 2 consecutive years. • It is common among cigarette smokers and urban dwellers in smog-ridden cities
- 32. Summary • Bronchiectasis isthe permanent dilation of bronchi and bronchioles caused by destruction of smooth muscle and the supporting elastic tissue • Two intertwined processes contribute to bronchiectasis: obstruction and chronic infection.
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