COPD Flashcards
Summarise COPD
Chronic obstructive pulmonary disease (COPD) is characterised by progressive airflow limitation that is not fully reversible.
Suspected in patients with a history of smoking, occupational and environmental risk factors, or a personal or family history of chronic lung disease.
Presents with progressive shortness of breath, wheeze, cough, and sputum production, including haemoptysis.
Diagnostic tests include pulmonary function tests, chest x-ray, chest computed tomography scan, oximetry, and arterial blood gas analysis.
Patients should be encouraged to stop smoking or occupational exposure and be vaccinated against viral influenza and Streptococcus pneumoniae.
Treatment options include bronchodilators, inhaled corticosteroids, and systemic corticosteroids.
Long-term oxygen therapy improves survival in severe COPD
Define COPD
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterised by airflow limitation that is not fully reversible. It encompasses both emphysema and chronic bronchitis. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases. It is primarily caused by cigarette smoking. Although COPD affects the lungs, it also has significant systemic consequences. Exacerbations and comorbidities are important contributors to the overall condition and prognosis in individual patients.
Describe the epidemiology of COPD
COPD is more common in older people, especially those aged 65 years and older. The Burden of Obstructive Lung Disease (BOLD) Initiative estimates a worldwide population prevalence of COPD for stages II or higher as equivalent to 10.1 ± 4.8% overall with 11.8 ± 7.9% for men and 8.5 ± 5.8% for women.[5] Its associated mortality in women has more than doubled over the past 20 years and now matches that in men. The number of COPD cases in the US has increased by 41% since 1982, and COPD affects 1% to 3% of white women and 4% to 6% of white men. COPD is now projected to be the third leading cause of death in the world by 2020.[1][6] This is because of the expanding epidemic of smoking and ageing of the world population and reduced mortality from other causes of death such as cardiovascular disease.[1][7] A systematic review and meta-analysis has shown that the prevalence of COPD in adult offspring of people with COPD is greater than population-based estimates.[8] A retrospective study conducted in the UK between 1990 and 1997 estimated COPD prevalence to be 2% in men and 1% in women
Describe the aetiology of COPD
Tobacco smoking is by far the main risk factor for COPD. It is responsible for 40% to 70% of COPD cases and exerts its effect by causing an inflammatory response, cilia dysfunction, and oxidative injury. Air pollution and occupational exposure are other common aetiologies. Oxidative stress and an imbalance in proteinases and antiproteinases are also important factors in the pathogenesis of COPD, especially in patients with alpha-1 antitrypsin deficiency, who have panacinar emphysema that usually presents at an early age
What is the hallmark feature of COPD
The hallmark of COPD is chronic inflammation that affects central airways, peripheral airways, lung parenchyma and alveoli, and pulmonary vasculature. The main components of these changes are narrowing and remodelling of airways, increased number of goblet cells, enlargement of mucus-secreting glands of the central airways, and, finally, subsequent vascular bed changes leading to pulmonary hypertension. This is thought to lead to the pathological changes that define the clinical presentation.
Describe the host response in COPD
Evidence suggests that the host response to inhaled stimuli generates the inflammatory reaction responsible for the changes in the airways, alveoli, and pulmonary blood vessels. Activated macrophages, neutrophils, and leukocytes are the core cells in this process. In contrast to asthma, eosinophils play no role in COPD, except for occasional acute exacerbations. However, a patient-level meta-analysis found that patients with COPD with lower blood eosinophil counts have more pneumonia events than do those with higher counts.[
Describe the two subtypes of COPD
In emphysema, which is a subtype of COPD, the final outcome of the inflammatory responses is elastin breakdown and subsequent loss of alveolar integrity.[11] In chronic bronchitis, another phenotype of COPD, these inflammatory changes lead to ciliary dysfunction and increased goblet cell size and number, which leads to the excessive mucus secretion. These changes are responsible for decreased airflow, hypersecretion, and chronic cough. In both conditions, changes are progressive and usually not reversible.
What is the physiological definition of COPD
Increased airway resistance is the physiological definition of COPD. Decreased elastic recoil, fibrotic changes in lung parenchyma, and luminal obstruction of airways by secretions all contribute to increased airways resistance. Expiratory flow limitation promotes hyperinflation. This finding, in addition to destruction of lung parenchyma, predisposes COPD patients to hypoxia, particularly during activity. Progressive hypoxia causes vascular smooth muscle thickening with subsequent pulmonary hypertension, which is a late development conveying a poor prognosis.
Describe one typical case history for COPD
A 66-year-old man with a smoking history of one pack per day for the past 47 years presents with progressive shortness of breath and chronic cough, productive of yellowish sputum, for the past 2 years. On examination he appears cachectic and in moderate respiratory distress, especially after walking to the examination room, and has pursed-lip breathing. His neck veins are mildly distended. Lung examination reveals a barrel chest and poor air entry bilaterally, with moderate inspiratory and expiratory wheezing. Heart and abdominal examination are within normal limits. Lower extremities exhibit scant pitting oedema.
Describe a second typical case history for COPD
A 56-year-old woman with a history of smoking presents to her primary care physician with shortness of breath and cough for several days. Her symptoms began 3 days ago with rhinorrhoea. She reports a chronic morning cough productive of white sputum, which has increased over the past 2 days. She has had similar episodes each winter for the past 4 years. She has smoked 1 to 2 packs of cigarettes per day for 40 years and continues to smoke. She denies haemoptysis, chills, or weight loss and has not received any relief from over-the-counter cough preparations.
Describe some other typical presentations for COPD
Other presentations include weight loss, haemoptysis, cyanosis, and morning headaches secondary to hypercapnia. Physical examination may demonstrate hypoxia, use of accessory muscles, paradoxical rib movements, distant heart sounds, lower-extremity oedema and hepatomegaly secondary to cor pulmonale, and asterixis secondary to hypercapnia. Patients may also present with signs and symptoms of COPD complications. These include severe shortness of breath, severely decreased air entry, and chest pain secondary to an acute COPD exacerbation or spontaneous pneumothorax.[2][3] Patients with COPD often have other comorbidities, including cardiovascular disease,[4] skeletal muscle dysfunction, metabolic syndrome and diabetes, osteoporosis, depression, lung cancer, gastro-oesophageal reflux disease, bronchiectasis, and obstructive sleep apnoea
Describe an approach to the history in patients with COPD
COPD has an insidious onset and usually presents in older people. A history of productive cough, wheezing, and shortness of breath, particularly with exercise, is typical. Patients may complain of fatigue as a result of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia and hypercapnia. The patient’s smoking history, occupational exposures, and any family history of lung disease should be determined.
Patients with COPD may also present with acute, severe shortness of breath, fever, and chest pain during acute infectious exacerbation. See our topic on Acute exacerbation of chronic obstructive pulmonary disease for further information.
Describe the physical examination in COPD
Examination may show tachypnoea, respiratory distress, use of accessory muscles, and intercostal retraction. Barrel chest is a common observation. There may be hyper-resonance on percussion, and distant breath sounds and poor air movement on auscultation. Wheezing, coarse crackles, clubbing, and cyanosis, as well as signs of right-sided heart failure (distended neck veins, loud P2, hepatomegaly, hepatojugular reflux, and lower-extremity oedema), may be present. Occasionally patients may exhibit asterixis - loss of postural control in the outstretched arms (commonly known as a flap) caused by hypercapnia. This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of respiratory failure.
Describe the initial tests in COPD
Spirometry is the first test for diagnosis of COPD and for monitoring disease progress. Patients with COPD have a distinctive pattern seen on spirometry, with a reduced FEV1 and FEV1/FVC ratio. The presence of airflow limitation is defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria as a post-bronchodilator FEV1/FVC <0.70.[1] In cases where FVC may be hard to measure, forced expiratory volume at 6 seconds (FEV6) can be used.[21] Chest x-ray (CXR) is rarely diagnostic but can help to exclude other diagnoses. Pulse oximetry screens for hypoxia.
In addition to airflow limitation, the GOLD guidelines recognise the importance of exacerbations in affecting the natural course of COPD, and place emphasis on assessment of symptoms, risk factors for exacerbations, and comorbidities.
Describe how acute exacerbation of COPD are monitored according to the GOLD guidelines
In addition to airflow limitation, the GOLD guidelines recognise the importance of exacerbations in affecting the natural course of COPD, and place emphasis on assessment of symptoms, risk factors for exacerbations, and comorbidities.[1]
The Modified British Medical Research Council (mMRC) questionnaire or the COPD Assessment Test (CAT) are recommended to assess symptoms. These can be found in the GOLD guidelines.[1]
The number of previously treated exacerbations (2 or more per year) is the best predictor of having another exacerbation. In addition to previous exacerbations, airflow limitation <50% is predictive of exacerbations.
The GOLD guideline uses a combined COPD assessment approach to group patients according to symptoms and previous history of exacerbations. Symptoms are assessed using the mMRC or CAT scale.
Group A: low risk (0-1 exacerbation per year, not requiring hospitalisation) and fewer symptoms (mMRC 0-1 or CAT <10)
Group B: low risk (0-1 exacerbation per year, not requiring hospitalisation) and more symptoms (mMRC≥ 2 or CAT≥ 10)
Group C: high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and fewer symptoms (mMRC 0-1 or CAT <10)
Group D: high risk (≥2 exacerbations per year, or one or more requiring hospitalisation) and more symptoms (mMRC≥ 2 or CAT≥ 10).
Describe some other important tests in COPD
Detailed pulmonary function tests performed in specialist pulmonary function laboratories can measure diffusing capacity of the lung for carbon monoxide (DLCO), flow volume loops, and inspiratory capacity. They are not used routinely but can be helpful in resolving diagnostic uncertainties and for preoperative assessment.[1]
In young patients (<45 years) with a family history or with rapidly progressing disease and lower lobe changes on imaging tests, alpha-1 antitrypsin level should be checked. The World Health Organization recommends that all patients with a diagnosis of COPD should be screened once, especially in areas with high prevalence of alpha-1 antitrypsin deficiency.[22] This may aid in family screening and counselling.
Computed tomography scans show anatomical changes, but their usefulness in diagnosis is confined to patients considered for surgery and for ruling out other pathologies.[1]
Pulse oximetry should be used to assess all patients with clinical signs of respiratory failure or right heart failure. If peripheral arterial oxygen saturation is less than 92%, then arterial or capillary blood gases should be measured.
What is associated with an increased risk of death in patients with COPD
Obstructive sleep apnoea is associated with increased risk of death and hospitalisation in patients with COPD
Describe how exercise testing may also be useful in COPD
Exercise testing can be useful in patients with a disproportional degree of dyspnoea.[24] It can be performed on a cycle or treadmill ergometer, or by a simple timed walking test (e.g., 6 minutes, or duration <6 minutes).[25] Exercise testing is also of use in selecting patients for rehabilitation. Respiratory muscle function may also be tested if dyspnoea or hypercapnia are disproportionately increased with respect to FEV1, as well as in patients with poor nutrition and those with corticosteroid myopathy.[26]
In patients with frequent exacerbations, severe airflow limitation, and/or exacerbations requiring mechanical ventilation, sputum should be sent for culture
