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COPD

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01.copd

  1. 1. Chronic Obstructive Lung Disease: GOLD Guidelines
  2. 2. COPD - Definition Global Obstructive Lung Disease Guidelines (GOLD) : 2013 • “A common preventable and treatable disease state characterized by persistent airflow limitation that is usually progressive and associated with enhanced chronic inflammatory response in the airways and the lung to noxious particles or gasses. “ • GOLD guidelines were recently updated in 2013
  3. 3. Extrapulmonary effects : skeletal muscle wasting, cachexia Comorbidities: cardiovascular (ischemic heart disease and heart failure), osteoporosis , normocytic anemia, diabetes, metabolic syndrome and depression, musculoskeletal and psychological conditions Chronic obstructive pulmonary disease (COPD) encompasses several diffuse pulmonary diseases, including chronic bronchitis, emphysema, chronic asthma, bronchiectasis, and: The result is irreversible airflow obstruction.
  4. 4. Chronic bronchitis (definition): — Chronic bronchitis is defined as a chronic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough (eg, bronchiectasis) have been excluded. It may precede or follow development of airflow limitation. This definition has been used in many studies, despite the arbitrarily selected symptom duration.
  5. 5. Chronic bronchitis can be categorized as: 1.Non-obstructive chronic bronchitis: a) simple chronic bronchitis - (mucoid sputum production characterizes simple chronic bronchitis), b) chronic mucopurulent bronchitis - (persistent or recurrent purulent sputum production in the absence of localized suppurative disease, such as bronchiectasis, characterizes chronic mucopurulent bronchitis). 2. Obstructive chronic bronchitis (chronic bronchitis with obstruction). Chronic bronchitis with obstruction must be distinguished from chronic infective asthma. The differentiation is based mainly on the history of the clinical illness: • patients who have chronic bronchitis with obstruction present with a long history of productive cough and a late onset of wheezing, whereas •patients who have asthma with chronic obstruction have a long history of wheezing with a late onset of productive cough.
  6. 6. Emphysema — Emphysema is defined by abnormal and permanent enlargement of the airspaces distal to the terminal bronchioles that is accompanied by destruction of the airspace walls, without obvious fibrosis (ie, there is no fibrosis visible to the naked eye). Exclusion of obvious fibrosis was intended to distinguish the alveolar destruction due to emphysema from that due to the interstitial pneumonias, etc. However, many studies have found increased collagen in the lungs of patients with mild COPD, indicating that fibrosis can be a component of emphysema. While emphysema can exist in individuals who do not have airflow obstruction, it is more common among patients who have moderate or severe airflow obstruction. The various subtypes of emphysema (eg, centriacinar, panacinar, distal acinar (paraseptal) are described below.
  7. 7. Asthma — The Global Initiative for Asthma gives the following definition of asthma. “Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. The chronic inflammation is associated with airway responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are usually associated with widespread, but variable, airflow obstruction within the lung that is often reversible either spontaneously or with treatment.”
  8. 8. Interrelationships of COPD subtypes
  9. 9. Chronic obstruction as an element, (but not an essence) of other nosological entities: •Patients with airflow obstruction due to diseases that have a known etiology or a specific pathology (eg, cystic fibrosis, bronchiectasis, obliterative bronchiolitis, tuberculosis) are not considered to have COPD. However, these exclusions are loosely defined.
  10. 10. PATHOLOGY — The predominant pathologic changes of COPD are found in the airways, but changes are also seen in the lung parenchyma and pulmonary vasculature. In an individual, the pattern of pathologic changes depends on the underlying disease (eg, chronic bronchitis, emphysema, alpha-1 antitrypsin deficiency), possibly individual susceptibility, and disease severity.
  11. 11. Airways — Airways abnormalities in COPD include chronic inflammation, increased numbers of goblet cells, mucus gland hyperplasia, fibrosis, narrowing and reduction in the number of small airways, and airway collapse due to the loss of tethering caused by alveolar wall destruction in emphysema. •Chronic inflammation in chronic bronchitis and emphysema is characterized by the presence of CD8+ T-lymphocytes, neutrophils, and CD68+ monocytes/macrophages in the airways. Among patients with chronic bronchitis who have mucus hypersecretion, an increased number of goblet cells and enlarged submucosal glands are typically seen. •In comparison, the bronchial inflammation of asthma is characterized by the presence of CD4+ T-lymphocytes, eosinophils, and increased interleukin (IL)-4 and IL-5.
  12. 12. Lung parenchyma — Emphysema affects the structures distal to the terminal bronchiole, consisting of the respiratory bronchiole, alveolar ducts, alveolar sacs, and alveoli, known collectively as the acinus. These structures in combination with their associated capillaries and interstitium form the lung parenchyma. The part of the acinus that is affected by permanent dilation or destruction determines the subtype of emphysema. •Proximal acinar (also known as centrilobular) emphysema refers to abnormal dilation or destruction of the respiratory bronchiole, the central portion of the acinus. It is commonly associated with cigarette smoking, but can also be seen in coal workers’ pneumoconiosis. •Panacinar emphysema refers to enlargement or destruction of all parts of the acinus. Diffuse panacinar emphysema is most commonly associated with alpha-1 antitrypsin deficiency, although it can be seen in combination with proximal emphysema in smokers. •In distal acinar (also known as paraseptal) emphysema, the alveolar ducts are predominantly affected. Distal acinar emphysema may occur alone or in combination with proximal acinar and panacinar emphysema. When it occurs alone, the usual association is spontaneous pneumothorax in a young adult.
  13. 13. Pulmonary vasculature — Changes in the pulmonary vasculature include •intimal hyperplasia and •smooth muscle hypertrophy/hyperplasia thought to be due to chronic hypoxic vasoconstriction of the small pulmonary arteries. •Destruction of alveoli due to emphysema can lead to loss of the associated areas of the pulmonary capillary bed.
  14. 14. COPD - Risk FactorsCOPD - Risk Factors • Hereditary - Alpha-1 Antitrypsin Deficiency • Environmental • Cigarette Smoking • 15-20% of smokers will develop COPD • (~1 in 5) - this implies a genetic predisposition to developing COPD; tends to cluster in families • Occupational exposures to dust, chemicals • Hereditary - Alpha-1 Antitrypsin Deficiency • Environmental • Cigarette Smoking • 15-20% of smokers will develop COPD • (~1 in 5) - this implies a genetic predisposition to developing COPD; tends to cluster in families • Occupational exposures to dust, chemicals
  15. 15. CLINICAL FEATURES Smoking and inhalational exposure history — The most important risk factor for COPD is cigarette smoking and the amount and duration of smoking contribute to disease severity. Thus, a key step in the evaluation of patients with suspected COPD is to ascertain the number of pack years smoked (packs of cigarettes per day multiplied by the number of years), as the majority (80 percent) of patients with COPD have a history of cigarette smoking. It is useful to ask the age of starting and the age of quitting, as patients may underestimate the number of years they smoked. With enough smoking, almost all smokers will develop measurably reduced lung function. In the absence of agenetic/environmental/occupational predisposition, smoking less than 10 to 15 pack years of cigarettes is unlikely to result in COPD. Best variable for predicting which adults will have airflow obstruction on spirometry is a history of more than 40 pack years of smoking
  16. 16. The chronologically taken environmental/occupational history may disclose other important risk factors for COPD, such as exposure to fumes or organic or inorganic dusts. These exposures help to explain the 20 percent of patients with COPD (defined by lung function alone) and the 20 percent of patients who die from COPD who never smoked
  17. 17. Symptoms and pattern of onset — The three cardinal symptoms of COPD are: •dyspnea, •chronic cough and sputum production and the most common early symptom is •exertional dyspnea. •Less common symptoms include •wheezing and •chest tightness. •However, any of these symptoms may develop independently and with variable intensity. •There are three typical ways in which patients with COPD present:
  18. 18. 1. Patients who have an extremely sedentary lifestyle but few complaints require careful questioning to elicit a history that is suggestive of COPD. Some patients unknowingly avoid exertional dyspnea by shifting their expectations and limiting their activity. They may be unaware of the extent of their limitations or that their limitations are due to respiratory symptoms, although they may complain of fatigue.
  19. 19. 2. Patients who present with respiratory symptoms generally complain of dyspnea and chronic cough. The dyspnea may initially be noticed only during exertion. However, it eventually becomes noticeable with progressively less exertion or even at rest. The chronic cough is characterized by the insidious onset of sputum production, which occurs in the morning initially, but may progress to occur throughout the day. The daily volume rarely exceeds 60 mL. The sputum is usually mucoid, but becomes purulent during exacerbations.
  20. 20. •3. Patients who present with episodes of increased cough, purulent sputum, wheezing, and dyspnea that occur intermittently, with or without fever. • Diagnosis can be problematic in such patients. The combination of wheezing plus dyspnea may lead to an incorrect diagnosis of asthma. • Conversely, other illnesses with similar manifestations are often incorrectly diagnosed as a COPD exacerbation (eg, heart failure, bronchiectasis, bronchiolitis). The interval between exacerbations decreases as the severity of the COPD increases
  21. 21. Approximately 62 percent of patients with moderate to severe COPD report variability in symptoms (eg, dyspnea, cough, sputum, wheezing, or chest tightness) over the course of the day or week-to-week; morning is typically the worst time of day.
  22. 22. SYSTEMIC SYMPTOMS, etc. Patients with COPD may experience weight gain (due to activity limitations), weight loss (possibly due to dyspnea while eating), muscle weakness, limitation of activity (including sexual), cough syncope, or feelings of depression or anxiety. Weight loss, even cachexia (PP-emphysema) generally reflects more advanced disease and is associated with a worse prognosis. However, the majority of COPD patients are overweight or obese (BB-bronchitis).
  23. 23. Comorbid diseases that may accompany COPD include lung cancer, coronary heart disease, osteoporosis, metabolic syndrome, skeletal muscle weakness, depression, and cognitive dysfunction. Patients may also report a family history of COPD or other chronic respiratory illness.
  24. 24. Physical examination — 1 The findings on physical examination of the chest vary with the severity of the COPD. •Early in the disease, the physical examination may be normal, or may show only prolonged expiration or wheezes on forced exhalation. •As the severity of the airway obstruction increases, physical examination may reveal hyperinflation (eg, increased resonance to percussion), decreased breath sounds, wheezes, crackles at the lung bases, and/or distant heart sounds. •Features of severe disease include an increased anteroposterior diameter of the chest (“barrel-shaped” chest) and a depressed diaphragm with limited movement based on chest percussion. Yellow nicotine stains on the fingers are a clue to ongoing and heavy cigarette smoking. Clubbing of the digits is not typical in COPD (even with associated hypoxemia) and suggests comorbidities such as lung cancer, interstitial lung disease, or bronchiectasis.
  25. 25. •Patients with end-stage COPD may adopt positions that relieve dyspnea, such as leaning forward with arms outstretched and weight supported on the palms or elbows. This posture may be evident during the examination or may be suggested by the presence of callouses or swollen bursae on the extensor surfaces of forearms. Other physical examination findings include use of the accessory respiratory muscles of the neck and shoulder girdle, expiration through pursed lips, paradoxical retraction of the lower interspaces during inspiration (ie, Hoover's sign), cyanosis, asterixis due to severe hypercapnia, and an enlarged, tender liver due to right heart failure. Neck vein distention may also be observed because of increased intrathoracic pressure, especially during expiration. Physical examination — 2
  26. 26. EVALUATION — Evaluation for COPD is appropriate in adults who report dyspnea, chronic cough, chronic sputum production or have had a gradual decline in level of peak activity, particularly if they have a history of exposure to risk factors for the disease (eg, cigarette smoking, indoor biomass smoke). All patients are evaluated with spirometry and selected patients have laboratory testing and imaging studies.
  27. 27. COPD - Prevalence • Fourth leading cause of mortality (100,000/year) • Only major health problem for which mortality has been increasing for past 20 years • Results in 500,000 hospitalizations/year • Second leading cause of missed work days
  28. 28. COPD - Diagnosis • Symptoms • chronic cough - intermittent, nonproductive • cough with sputum production, ‘smoker’s cough’ • dyspnea on exertion, usually progressive and indolent (slow advancing) • Spirometry • Should spirometry screening be performed on the general population? • No, but in those with higher risk - i.e. all current and former smokers over the age of 40 years with any of the above symptoms of disease
  29. 29. The Importance of Screening for COPD • The Rule of 50s • 50% of COPD patients are undiagnosed (or approximately 12 million patients in U.S.) • COPD is evident by age 50 • At time of diagnosis, FEV1 is <50% predicted • 50% 5-year survival rate
  30. 30. COPD Staging • Based upon the GOLD Guidelines • Classified into 4 stages • Staging is based primarily upon FEV1: • FEV1 < 80% • FEV1:FVC < 70% more severe the disease • The lower the FEV1 the classification.
  31. 31. GOLD Guidelines for Therapy
  32. 32. COPD Management and Therapies • Vaccination - pneumococcal (i.m.) and influenza (s.c.) • Regular Assessment of lung function - annually • Cessation of tobacco use • Drug Therapy: • short acting (SABA) vs. long acting bronchodilators (LABA) • inhaled (ICS) vs. oral corticosteroids (systemic steroids)
  33. 33. COPD - Management of Stable Disease • Smoking cessation: rate of FEV1 deterioration will slow to near normal (20 ml /yr vs. 65 ml /yr for active smokers) if patient stops smoking
  34. 34. COPD - Drug Therapy • Therapy recommendations based on their effect on FEV1. • First Line therapy: • Beta agonists - short (SABA) and long acting (LABA) • Anticholinergics - short (SAMA) and long acting (LAMA) • Second Line therapy: • Steroids - inhaled (ICS) vs. oral (systemic steroids) • Supplemental therapies
  35. 35. Beta agonists • Mechanism of Action - bronchodilate by stimulating Beta-2 receptors • Studies show that COPD patients do not develop tolerance to short acting or long acting beta agonists • Asthmatics tend to develop tolerance to short acting agonists • Can Salmeterol be used as monotherapy? Drug Albuterol Salmeterol Onset 1 to 3 min 20 min Duration 4 to 6 hrs 12+ hrs YES, salmeterol monotherapy had adverse outcomes in asthma study, note COPD.
  36. 36. Anticholinergics • Mechanism of action- bronchodilation by decreasing airway smooth muscle tone • Also reduces sputum production • Combination of an anticholinergic + β2-agonist produces greater and more sustained rise in FEV1 than either drug alone. Drug Ipratropiu m Tiotropium Onset 20 min ? Duration 4 to 8 hrs 24 hrs Selectivity All Muscarinic M1 and M3> M2
  37. 37. Tiotropium (Spiriva) • Studies show that once daily tiotropium has resulted in a lasting increase in FEV1 out to one year. • 174 ml above baseline in good short-term responders • 56 ml increase in poor short-term responders Special delivery device.
  38. 38. Inhaled Corticosteroids (ICS) • Have not been shown to slow the progression of disease or provide long term benefit • ISOLDE trial - patients with FEV1 of 50% predicted value had a 25% reduction of exacerbations • Combination with salmeterol more effective in reducing exacerbations than either drug alone • Unfortunately, recently published trial failed to demonstrate statistically significant reduction in mortality with salmeterol/fluticasone combo.
  39. 39. New COPD Treatment Data • compared salmeterol/fluticasone head to head with tiotropium • No difference in exacerbation rate although more in tiotropium group had higher drop out rate. • More patients in salmeterol/fluticasone developed pneumonia.
  40. 40. Oral Corticosteroids • They have no proven benefit in stable COPD • Oral steroids are useful for acute exacerbations • What is the recommended duration of therapy? • Maximum benefit obtained during first 2 weeks of therapy.
  41. 41. Supplemental Therapies • Supplemental oxygen for hypoxemia (worn for more than 15 hrs/day) has been shown to reduce moratality • What are the qualification parameters for oxygen therapy? • PaO2 of 55mmHg or less, or pulse oximetry of 88% or less • Pulmonary Rehabilitation • Lung reduction and lung transplantation surgeries
  42. 42. GOLD Guidelines for Therapy
  43. 43. Summary • Early diagnosis, disease prevention, smoking cessation and vaccination are important. • Initiate bronchodilator therapy early in disease course, combination of albuterol with ipratropium most effective • Inhaled corticosteroids may be useful in patients with severe disease or with objective responses on spirometry. • Will likely see inflammatory modulators (TNF- α) in the future
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