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Premium member Presentation Transcript COPD Cor Pulmonale: COPD Cor PulmonaleCOPD: COPD Disease state characterised by airflow limitation that is not fully reversibleCOPD: COPD Emphysema Chronic Bronchitis Chronic Bronchiolitis / Small Airway DiseaseEMPHYSEMA: EMPHYSEMA Permanent and destructive enlargement of air spaces distal to terminal bronchioles with loss of architecture. Congenital or AcquiredCHRONIC BRONCHITIS: CHRONIC BRONCHITIS Productive cough on most of the days for at least three months over two consecutive years.Risk Factors: Risk Factors Tobacco smoke – 10 pack years Biomass solid fuel fire Occupation–Coal Miners / Cadmium Air Pollution Infections Lung Growth – Infection / Maternal / InuteroSlide 7: 7 Risk Factors for COPD Nutrition Infections Socio-economic status Aging PopulationsHost / Genetic factors: Host / Genetic factors 1 Antitrypsin deficiency Airway hyper-reactivityPathophysiology: Pathophysiology Enlargement of mucus secreting glands number of goblet cells Loss of elastic tissue / inflammation and fibrosis in airway wall / mucus accumulation / enhanced cholinergic tone airflow limitation Decreased pulmonary and chest wall compliancePathophysiology: Pathophysiology Ventilation perfusion mismatch Flattening of diaphragmatic muscles and horizontal alignment of intercostal muscles work of breathing Unopposed action of proteases & antioxidants Alveoli destructionEmphysema Types: Emphysema Types Centriacinar PanacinarClinical Features: Clinical Features Symptoms Cough / Sputum production Dyspnoea Hemoptysis Morning Headache OedemaClinical Features: Clinical Features General Examination Odour of smoke Nicotine staining of finger nails Accessory muscle of respiration Pursed Lip breathing CyanosisClinical Features: Clinical Features General Examination Systemic wasting Signs of RVF Clubbing Body built asthenicClinical Features: Clinical Features “Pink Puffers” – thin, breathless “Blue Blotters” – Oedema, CyanosisClinical Features: Clinical Features Inspection Shape - Barrel shaped Symmetry - Bilaterally Symmetrical Trachea - Central Apex Beat - Not visualized Movements - Decreased BilaterallyClinical Features: Clinical Features Palpation Trachea - Central Apex - Not Palpable Movements - Decreased bilaterally Measurement - AP / TD Chest ExpansionClinical Features: Clinical Features Percussion Hyper resonant Cardiac dullness obliterated Liver dullness – pushed downClinical Features: Clinical Features Auscultation Intensity of breath sounds decreased bilaterally NVBS with prolonged expiration Rhonchi / CrepitationsInvestigations: Investigations Chest X-Ray PA View Hyperlucent lung fields Wide intercostal spaces Horizontally placed ribs Low set diaphragm Tubular Heart BullaeInvestigations: Investigations Polycythemia PFT FEV 1 < 80% FEV 1 / FVC < 70% Exercise tests ABG CT ScanSlide 26: 26 A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. Confirmed by spirometry. A post-bronchodilator FEV 1 /FVC < 0.70 confirms Airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.Slide 27: SYMPTOMS Cough Sputum Shortness of breath EXPOSURE TO RISK FACTORS Tobacco Occupation Indoor / outdoor pollution SPIROMETRY Diagnosis of COPD èManagement: Management Smoking Cessation Oxygen Therapy Lung Volume reduction surgeryManagement: Management Smoking Cessation Bronchodilators 2 agonist Anticholinergic Theophylline preparationsManagement: Management Corticosteroids Inhaled Oral Parentral Oxygen TherapyOxygen Therapy: Oxygen TherapySurgical Intervention: Surgical Intervention Giant Bullous Disease Consider bullectomy if bullae compress smoking normal lung tissue Lung Volume Reduction Surgery Lung TransplantationManagement: Management Vaccination Influenzae Pneumococcal Mucolytic therapy AcetylcysteineSlide 34: COPD Exacerbation Bacterial Infection 50% Viral Infection 25% Air Pollution 5% Unknown 20% Exacerbation Acute Inflammation Pathophysiology - Current Hypothesis Chronic InflammationAcute Exacerbation of COPD: Acute Exacerbation of COPD Oxygen therapy Bronchodilators 2 agonists / Ipratropium Bromide Corticosteroids Parentral / oral Antibiotics NIVSlide 36: It is not enough for the physician to do what is necessary, but the patient and the attendants must do their part as well and circumstances must be favorable. HippocratesCor Pulmonale: Cor Pulmonale Dilation and Hypertrophy of RV in response to disease of pulmonary vasculature and or lung parenchymaCor Pulmonale: Cor Pulmonale Acute ChronicEtiology: Etiology Chronic Bronchitis COPD ILD Pneumoconiosis Sarcoidosis Bronchiectasis Hypoventilation Syndromes / Cystic FibrosisPathophysiology: Pathophysiology Pulmonary Hypertension Hypoxic Vasoconstriction Acidemia Hypercapnia Lung destruction and fibrosisSymptoms: Symptoms Underlying lung disorder Dyspnoea, Fatigue,. Angina Tussive / effort related syncope RVFSigns: Signs Pulmonary Hypertension Visible & palpable pulmonary artery pulsations Left 2 nd ICS – dull on percussion Loud P 2 Systolic pulmonary ejection click Pulmonary ESM Graham Steel Murmur Prominent a-waves in JVPSigns: Signs RVH Parasternal heave RV pulsation in epigastrium TR (Carvallo’s sign) Cyanosis - Late findingInvestigations: Investigations ECG P Pulmonale RAD RVH ECHO – RV / Pulmonary / Tricuspid valve / Pulmonary ArteryInvestigations: Investigations X-Ray Enlargement of main pulmonary artery CT scan (VP Scan)Treatment: Treatment Treat underlying condition Bronchodilators Steroids NIV Oxygen TherapyTreatment: Treatment RV Failure Diuretics DigoxinTreatment: Treatment PAH Avoid Physical stress Calcium Channel Blockers Endothelial receptor antagonists – Bosentan Phosphodiesterase – 5 inhibitors – Sildenafil ProstacyclinsSlide 49: WORLD COPD DAY November 14 Raising COPD Awareness Worldwide You do not have the permission to view this presentation. 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