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Pulmonary diseases. Hana Maxová Department of Pathophysiology 2nd Faculty of Medicine Charles University in Prague. Ventilatory defect. Obstructive  FEV1/FVC n  TLC Asthma bronchiale COPD Chronic bronchitis Emphysema Cystic fibrosis. Restrictive

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Pulmonary diseases

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    1. Pulmonary diseases Hana Maxová Department of Pathophysiology 2nd Faculty of Medicine Charles University in Prague

    2. Ventilatory defect Obstructive  FEV1/FVC n TLC Asthma bronchiale COPD Chronic bronchitis Emphysema Cystic fibrosis Restrictive n FEV1/FVC  TLC Interstitial lung disease Idiopathic pulmonary fibrosis Pneumothorax Lung resection Pulmonary oedema ARDS Mixed  FEV1/FVC  TLC Coexistence of airway obstruction and parenchymal processes

    3. General symptoms  Dyspnoea - acute x chronic, at rest x during exercise  Cough - acute x chronic, productive x non-productive (wet)  Haemoptysis  Chest pain  Tachypnoea  Tachycardia  Cyanosis

    4. Pathophysiological findings  Changes in lung compliance  Changes in airway resistance  Increased work of breathing  Reduction of diffusing capacity  Changes in alveolar ventilation  Changes in ventilation/perfusion ratio  Changes in resistance of pulmonary vessels, hypertension

    5. Obstructive lung disease

    6. Asthma bronchiale Asthma is a chronic (long-lasting) inflammatory disease of the airways characterized by reversible airflow obstruction. Individual predisposition:  Genetic  Atopy (IgE)  Airways hyperreactivity Environmental factors:  Allergens  Infections  Nutrition, drugs „Triggers“:  Smoking  Allergens  Infections  Excercise  Weather  Psychic influence  Others - GER, sinusitis

    7. Allergen Mast cells Macrophage 1. Inflammation TH2 Neutrophile Eosinophile 2. Obstruction Epitelial damage Mucous plug Nerves activation subepithelial fibrosis Activation of sens. nerves Plasma leak hypersecretion hyperplasia Oedema cholinergic reflex vasodilatation angiogenesis 3. Remodeling bronchoconstriction hypertrophia/hyperplasia Astma bronchiale - pathogenesis

    8. Asthma - classification GINA 2010 - Global Initiative for Asthma Classification of asthma severity 1) diurnal symptoms frequency 2) exacerbation 3) nocturnal symptoms 4) spirometry PEF, FEV1 1. Intermitent asthma 2. Mild persistent 3. Moderate persistent 4. Severe persistent Status asthmaticus – acute exacerbation of asthma that does not respond to standard treatments. It is a life-threatening episode of airway obstruction.

    9. COPD Chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterized by airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. Syndrome with different clinical forms. Emphysema Chronic bronchitis Risks factors: Smoking, passive smoking Air pollution Infection Asthma Genetic predisposition (1- antitripsine defect)

    10. smoking, air pollution, infection Epithelial cells CD4/CD8 Tl Alveolar macrophages Fibroblasts Proteases/Antiproteases Neutrophils Tissue remodeling Alveolar destruction Mucus secretion Emphysema Bronchitis COPD - pathogenesis

    11. Emphysema Abnormal permanent enlargement of air spaces distal to the terminal bronchioles, accompanied by the destruction of alveolar walls and without obvious fibrosis Signs: Dyspnea Non productive cough Barrel chest Increased respiratory rate „pink puffers“ Prolonged expiratory phase Complications: Pneumothorax Respiratory failure Cor pulmonale

    12. Chronic bronchitis Cough that occurs every day with sputum production that lasts for at least 3 months, 2 years in a row. Signs: Productive cough Shortness of breath Complications: Cor pulmonale Respiratory insufficiency Source:

    13. Assesment of COPD GOLD 2011 (Global Initiative for Chronic Obstructive Lung Disease) 1) obstruction – spirometry FEV1, FEV1/FVC 2) exacerbation 3) severity of symptoms mMRC (Modified Medical Research Council Dyspnea Scale)

    14. CAT - COPD Assessement Test

    15. COPD - classification

    16. Cystic fibrosis AR inherited disease, CFTR (cystic fibrosis transmembrane conductance regulator) mutation Obstructive ventilatory defect with hyperinflation, in terminal state combine defect, cardiovascular failure is a major cause of death (90%) Cardiovascular signs: Dyspnoea Nonproductuive (wet) cough Cyanosis Complications: Bronchiolitis Pneumonia (bacterial colonization of distal airways) Bronchiectasis, emfysematous bullae – pneumothorax Parenchymal fibrosis Cor pulmonale, Pulmonary hypertension

    17. normal CF Sodium channel CTFR Chloride channels Sodium channel Alternative chloride channels absorption Absorption Secretion GAGs Chemokine Growth f.  Secretion  Periciliar liquid layer Periciliar liquid layer Mucus Inflammation Hyperplasia of goblet cells. Neutrophils Elastase Granulas Physiol. state Modify: Nature Medicine  10, 452 - 454 (2004) doi:10.1038/nm0504-452 Cystic fibrosis- pathogenesis

    18. Interstitial pulmonary diseases Heterogenic group of diseases that inflame or scar the lungs. Large number of insults induce exsudation, cellular infiltration and fibrotization. Etiology: known - inorganic dust (silicosis, asbestosis), organic (exogenous allergic alveolitis), toxic gases, radiation, carcinomas unknown - IPF, sarcoidosis, vasculitis, amyloidosis, collagenosis Signs: Dyspnoea – during exercise, at rest Caught Complications: Pneumonia Cor pulmonale chronicum Respiratory insufficiency

    19. TGF- Damage Alveolar epithelial cells Neutrophils Genetic predisposition TGF- Chemotactines Oxidative stress Myofibroblasts Collagen Extracellular matrix  plasma levels Pulmonary fibrosis Idiopathic pulmonary fibrosis - pathogenesis Modify: Barnes PJ (2008) A Blood Test for Lung Fibrosis. PLoS Med 5(4): e98. doi:10.1371/journal.pmed.0050098

    20. ARDS ARDS is an acute diffuse, inflammatory lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue, hypoxemia and bilateral radiographic opacities. Etiology of lung tissue damage: Direct: inhalation, aspiration drugs, chemicals infections embolia Indirect: sepsis anafylactic reaction DIC pancreatitis Signs: Dyspnoea Tachypnoea Caugh Tachycardia Cyanosis and respiratory failure Phases: Exsudative Proliferative Fibrotic

    21. Direct insult Indirect insult Epithel Alveolar macrophage Endothel IL-1, IL-6, TNF Activation/migration of neutrophils Chemokines, leucocytes recruitment, inflammation Degranulation Oxidative burst Migration Epitelial damage Permeability of alveolar barier ARDS Phases: Exsudative Proliferative Fibrotic Modify: 306 L217-L230 10.1152/ajplung.00311.2013

    22. Principles of therapy  Antiinflammatory drugs – decrease of mediators, cytokines, amount of inflammatory cells (inhalatory steroids, antileukotriens, antihistaminics)  Imunotherapy  Antibiotics  Mukolytics  Bronchodilatants (2 mimetics, anticholinergics)  Oxygenotherapy