COPD (3).pptx.. discussion slide.....
Download as PPTX, PDF0 likes15 views
Compiled
![Chronic obstructive pulmonary disease (COPD) severity assessment
Modified Medical Research Council Dyspnea Scale
[mMRC]
0—only with strenuous activity
1—hurrying on level ground or walking up a slight hill
2—walk slower than peers or stop walking at their own
pace
3—walking about 100 yards or after a few minutes on
level ground
4—too breathless to leave the house or when dressing.
The CAT is measure with Likert scale responses for questions
about cough, phlegm, chest tightness, dyspnea on one flight
of stairs, limitation in home activities, confidence in leaving
the home, sleep, and energy. Range of total score is 0–40](https://image.slidesharecdn.com/copd3-250527054813-bc076fbf/85/COPD-3-pptx-discussion-slide-31-320.jpg)
COPD (3).pptx.. discussion slide.....
- 1. IM 24.10 Chronic Obstructive Pulmonary Disease
- 2. Introduction Chronic obstructive pulmonary disease (COPD) is defined as a disease state characterized by persistent respiratory symptoms and airflow obstruction. emphysema, an anatomically defined condition characterized by destruction of the lung alveoli with air space enlargement chronic bronchitis, a clinically defined condition with chronic cough and phlegm small airway disease, a condition in which small bronchioles are narrowed and reduced in number.
- 3. PATHOGENESIS comprises a series of four interrelated events- (1) Chronic exposure to cigarette smoke in genetically susceptible individuals triggers inflammatory and immune cell recruitment within large and small airways and in the terminal air spaces of the lung. (2) Inflammatory cells release proteinases that damage the extracellular matrix supporting airways, vasculature, and gas exchange surfaces of the lung. (3) Structural cell death occurs through oxidant-induced damage, cellular senescence, and proteolytic loss of cellular-matrix attachments leading to extensive loss of smaller airways, vascular pruning, and alveolar destruction. (4) Disordered repair of elastin and other extracellular matrix components contributes to air space enlargement and emphysema
- 5. elastase:antielastase hypothesis the balance of elastin-degrading enzymes and their inhibitors determines the susceptibility of the lung to destruction, resulting in air space enlargement. This hypothesis was based on the clinical observation that patients with genetic deficiency in α1 antitrypsin (α1AT), the inhibitor of the serine proteinase neutrophil elastase, were at increased risk of emphysema, and that instillation of elastases, including neutrophil elastase, into experimental animals' results in emphysema
- 6. Pathology LARGE AIRWAYS • Cigarette smoking often results in mucus gland enlargement and goblet cell hyperplasia, leading to cough and mucus production. • Bronchi also undergo squamous metaplasia, predisposing to carcinogenesis and disrupting mucociliary clearance. • Neutrophil influx has been associated with purulent sputum during respiratory tract infections.
- 7. Pathology SMALL AIRWAYS • Characteristic cellular changes include goblet cell metaplasia, with these mucus-secreting cells replacing surfactant-secreting Club cells. • Luminal narrowing can occur by fibrosis, excess mucus, edema, and cellular infiltration. • Reduced surfactant may increase surface tension at the air-tissue interface, predisposing to airway narrowing or collapse. • Respiratory bronchiolitis with mononuclear inflammatory cells collecting in distal airway tissues may cause proteolytic destruction of elastic fibers in the respiratory bronchioles and alveolar ducts.
- 8. Pathology LUNG PARENCHYMA • Emphysema is characterized by destruction of gas-exchanging air spaces, i.e., the respiratory bronchioles, alveolar ducts, and alveoli. • Large numbers of macrophages accumulate in respiratory bronchioles of essentially all smokers. • Neutrophils, B lymphocytes, and T lymphocytes, mainly CD8+ cells, are also increased in the alveolar space of smokers. • Alveolar walls become perforated and later obliterated with coalescence of the delicate alveolar structure into large emphysematous air spaces.
- 10. PATHOPHYSIOLOGY Persistent reduction in forced expiratory flow rates. Hyperinflation with increases in the residual volume Increase in residual volume/total lung capacity ratio Nonuniform distribution of ventilation, and Ventilation-perfusion mismatching.
- 11. PATHOPHYSIOLOGY AIRFLOW OBSTRUCTION • Patients with airflow obstruction related to COPD have a chronically reduced ratio of FEV1 /FVC. • In contrast to asthma, the reduced FEV1 in COPD seldom shows large improvements to inhaled bronchodilators, although improvements up to 15% are common. HYPERINFLATION • In COPD, there is often “air trapping” (increased residual volume and increased ratio of residual volume to total lung capacity) • Progressive hyperinflation (increased total lung capacity) in more advanced disease
- 12. PATHOPHYSIOLOGY HYPERINFLATION Hyperinflation can push the diaphragm into a flattened position with a number of adverse effects- I. Decreasing the zone of apposition between diaphragm and abdominal wall, positive abdominal pressure during inspiration is not applied as effectively to the chest wall. II. Muscle fibers of the flattened diaphragm are shorter than those of a more normally curved diaphragm and are less capable of generating inspiratory pressures than normal. III. Flattened diaphragm must generate greater tension to develop the transpulmonary pressure required to produce tidal breathing. IV. The thoracic cage is distended and during tidal breathing, the inspiratory muscles must do extra work to overcome the resistance of the thoracic cage.
- 13. PATHOPHYSIOLOGY GAS EXCHANGE The partial pressure of oxygen in arterial blood PaO2 usually remains near normal until the FEV1 is decreased to below 50% of predicted An elevation of arterial level of carbon dioxide (PaCO2 ) is not expected until the FEV1 is <25% of predicted. Pulmonary arterial hypertension severe enough to cause cor pulmonale and right ventricular failure due to COPD typically occurs in individuals who have marked decreases in FEV1 (<25% of predicted) and chronic hypoxemia (PaO2 <55 mmHg)
- 14. RISK FACTORS CIGARETTE SMOKING AIRWAY RESPONSIVENESS RESPIRATORY INFECTIONS OCCUPATIONAL EXPOSURES AMBIENT AIR POLLUTION PASSIVE OR SECOND-HAND SMOKING EXPOSURE GENETIC CONSIDERATIONS
- 15. CLINICAL PRESENTATION The three most common symptoms in COPD are- cough, sputum production, and exertional dyspnea. PHYSICAL FINDINGS • In the early stages may have normal physical examination. • Current smokers may have signs of active smoking, including an odour of smoke or nicotine staining of fingernails.
- 16. CLINICAL PRESENTATION In severe disease • Prolonged expiratory phase with expiratory wheezing • Hyperinflation include a barrel chest • Enlarged lung volumes with poor diaphragmatic excursion by percussion • Use of accessory muscles of respiration • Sitting in the characteristic “tripod” position • Purse-lip breathing • hoover’s chest sign • Inspiratory recession of supraclavicular fossa and intercostal spaces • Abdominal paradox or respiratory paradox • The laryngeal height is shorter in copd • Absent apical impulse and an impaired cardiac dullness • Chest hyperresonance • Early inspiratory crackles appear at the beginning of inspiration and end before mid-inspiration. • Pulsus paradoxus • Right-sided heart failure or cor pulmonale • Cyanosis
- 17. Grade Level of dyspnea 1 Not bothered by dyspnea, except during strenuous activity 2 Shortness of breath when walking up a short hill 3 Walks more slowly than others because of breathlessness; stops to catch breath when walking at own pace 4 Stops to catch breath after walking 100 m (328 ft) on level ground 5 Too short of breath to leave the house; breathless with activities of daily living, such as dressing and undressing Medical Research Council Dyspnea Index
- 18. CLINICAL PRESENTATION • Predominant emphysema, termed “pink puffers,” are thin, noncyanotic at rest, and have prominent use of accessory muscles • Predominant chronic bronchitis are heavy and cyanotic “blue bloaters”. • Advanced disease is accompanied by cachexia, with significant weight loss and diffuse loss of subcutaneous adipose tissue.
- 19. LABORATORY FINDINGS Pulmonary function testing shows- • Airflow obstruction with a reduced FEV1 and FEV1 /FVC • Increase in total lung capacity, functional residual capacity, and residual volume • The diffusing capacity may be reduced. Arterial blood gases and oximetry shows hypoxemia, arterial PCO2 and pH. CXR shows increased lung volumes and flattening of the diaphragm suggest hyperinflation, Obvious bullae, paucity of parenchymal markings, or hyperlucency. Chest CT scan shows the pattern of emphysema, coexisting interstitial lung disease and bronchiectasis. In advanced COPD, CT scans can help determine the possible value of surgical therapy. Testing for α1AT deficiency in all subjects with COPD or asthma with chronic airflow obstruction.
- 20. GOLD Criteria for Severity of Airflow Obstruction in COPD
- 21. Treatment The two main goals of therapy are- • to provide symptomatic relief (reduce respiratory symptoms, improve exercise tolerance, and improve health status) and • reduce future risk (prevent disease progression, prevent and treat exacerbations, and reduce mortality). Three interventions- smoking cessation, oxygen therapy in chronically hypoxemic patients, and lung volume reduction surgery (LVRS) in selected patients with emphysema—have improve survival. Recent studies indicate that triple inhaled therapy (long-acting beta agonist bronchodilator, long- acting muscarinic antagonist bronchodilator and inhaled corticosteroid) reduces mortality.
- 22. Smoking Cessation nicotine replacement therapy available as gum, transdermal patch, lozenge, inhaler, and nasal spray; bupropion; and varenicline, a nicotinic acid receptor agonist/antagonist.
- 23. Bronchodilators Muscarinic Antagonists Short-acting muscarinic antagonists like ipratropium bromide improves symptoms with acute improvement in FEV1 Long-acting muscarinic antagonists including aclidinium, glycopyrrolate, glycopyrronium, revefenacin, tiotropium, and umeclidinium) improve symptoms and reduce exacerbations.
- 24. Bronchodilators Beta Agonists • Short-acting beta agonists ease symptoms with acute improvements in lung function. • Long-acting beta agonists (LABAs) provide symptomatic benefit and reduce exacerbations, though to a lesser extent than an LAMA. Currently available long acting inhaled beta agonists are formoterol, indacaterol, olodaterol, salmeterol, and vilanterol. • The main side effects are tremor and tachycardia.
- 25. Inhaled Corticosteroids • The main role of ICS is to reduce exacerbations. • ICS are never used alone in COPD due to little symptomatic benefit but are combined with a LABA or used with a LABA and LAMA. • Side effects are increased rates of oropharyngeal candidiasis and pneumonia and in some studies an increased rate of loss of bone density and development of cataracts.
- 26. Bronchodilators Theophylline Theophylline produces modest improvements in airflow and vital capacity. It is not first-line therapy due to side effects and drug interactions. Nausea is a common side effect; tachycardia and tremor have also been reported. Monitoring of blood theophylline levels is required to minimize toxicity.
- 27. PDE4 Inhibitors The selective phosphodiesterase 4 (PDE4) inhibitor roflumilast has been demonstrated to reduce exacerbation frequency in patients with severe COPD, chronic bronchitis, and a prior history of exacerbations Its effects on airflow obstruction and symptoms are modest Side effects (including nausea, diarrhea, and weight loss) are common.
- 28. Antibiotics • There are strong data implicating bacterial infection as a precipitant. • Azithromycin is chosen for both its anti-inflammatory and antimicrobial properties, • Azithromycin was most effective in older patients and milder GOLD stages and exacerbations.
- 29. Oxygen • O2 is the only pharmacologic therapy demonstrated to unequivocally decrease mortality in patients with COPD. • Patients with resting hypoxemia (resting O2 saturation 88% in any patient or 89% ≤ ≤ with signs of pulmonary arterial hypertension, right heart failure or erythrocytosis), O2 has been demonstrated to have a significant impact on mortality. • Patients meeting these criteria should be on continuous oxygen supplementation because the mortality benefit is proportional to the number of hours per day oxygen is used.
- 30. α1AT Augmentation Therapy • Specific treatment in the form of IV α1AT augmentation therapy is available for individuals with severe α1AT deficiency. • Although biochemical efficacy of α1AT augmentation therapy has been shown, the benefits of α1AT augmentation therapy are controversial. • Eligibility for α1AT augmentation therapy requires a serum α1AT level <11 μM (∼50 mg/dL).
- 31. Chronic obstructive pulmonary disease (COPD) severity assessment Modified Medical Research Council Dyspnea Scale [mMRC] 0—only with strenuous activity 1—hurrying on level ground or walking up a slight hill 2—walk slower than peers or stop walking at their own pace 3—walking about 100 yards or after a few minutes on level ground 4—too breathless to leave the house or when dressing. The CAT is measure with Likert scale responses for questions about cough, phlegm, chest tightness, dyspnea on one flight of stairs, limitation in home activities, confidence in leaving the home, sleep, and energy. Range of total score is 0–40
- 34. NONPHARMACOLOGIC THERAPIES • Patients with COPD should receive the influenza vaccine annually. • Pneumococcal vaccines and vaccination for Bordetella pertussis are also recommended. • Pulmonary Rehabilitation refers to a comprehensive treatment program that incorporates exercise, education, and psychosocial and nutritional counselling. • Lung Volume Reduction Surgery In carefully selected patients with emphysema, surgery to remove the most emphysematous portions of lung improves exercise capacity, lung function, and survival. Patients with upper lobe–predominant emphysema and a low post rehabilitation exercise capacity are most likely to benefit from LVRS.
- 35. Lung Transplantation • COPD is currently the second leading indication for lung transplantation. • Current recommendations are that candidates for lung transplantation should have very severe airflow obstruction, severe disability despite maximal medical therapy, and be free of significant comorbid conditions such as liver, renal, or cardiac disease.
- 36. EXACERBATIONS OF COPD • Exacerbations are episodic acute worsening of respiratory symptoms, including increased dyspnea, cough, wheezing, and/or change in the amount and character of sputum. • The strongest single predictor of exacerbations is a history of a previous exacerbation. • Precipitating Causes a new strain of bacteria is involved in >50% of exacerbations. Viral respiratory infections are present in approximately one-third of COPD exacerbations.
- 37. EXACERBATIONS OF COPD • The physical examination includes assessment of the degree of distress of the patient. • Specific attention should be focused on tachycardia, tachypnea, use of accessory muscles, signs of perioral or peripheral cyanosis, the ability to speak in complete sentences, and the patient’s mental status. • The chest examination should establish the presence or absence of focal findings, degree of air movement, presence or absence of wheezing, asymmetry in the chest examination (suggesting large airway obstruction or pneumothorax mimicking an exacerbation), and the presence or absence of paradoxical motion of the abdominal wall.
- 38. TREATMENT OF ACUTE EXACERBATIONS • Bronchodilators Typically, patients are treated with inhaled beta agonists and muscarinic antagonists. The addition of methylxanthines (theophylline) to this regimen can be considered • Antibiotics Patients with COPD are frequently colonized with potential respiratory pathogens, and it is often difficult to identify conclusively a specific species of bacteria responsible for a particular clinical event. • Bacteria frequently implicated in COPD exacerbations include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Chlamydia pneumoniae; viral pathogens are also common etiologies of exacerbations.
- 39. TREATMENT OF ACUTE EXACERBATIONS • In patients admitted to the hospital, the use of systemic glucocorticoids reduces the length of stay, hastens recovery, and reduces the chance of subsequent exacerbation or relapse. • Oxygen Supplemental O2 should be supplied to maintain oxygen saturation 90%. ≥ • Mechanical Ventilatory Support The initiation of non-invasive positive-pressure ventilation (NIPPV) in patients with respiratory failure results in a significant reduction in mortality rate, need for intubation, complications of therapy, and hospital length of stay.
- 40. TREATMENT OF ACUTE EXACERBATIONS Mechanical Ventilatory Support Invasive (conventional) mechanical ventilation via an endotracheal tube is indicated for patients with severe respiratory distress despite initial therapy, life-threatening hypoxemia, severe hypercarbia and/or acidosis, markedly impaired mental status, respiratory arrest, hemodynamic instability, or other complications.