Chronic Obstructive Pulmonary Disease (COPD)
Introduction and Facts
The Global Initiative for Chronic Obstructive Pulmonary Disease (GOLD) in 2014 defined Chronic Obstructive Pulmonary Disease (COPD) is a preventable and treatable chronic respiratory disease characterized by persistent airflow obstruction and usually progressive and associated with an increased chronic inflammatory response. Certain irritating gases or particles cause airways. Exacerbations and comorbidities contribute to the overall severity of disease in a patient.
Pathophysiology
The airflow limitation is the main physiological change in COPD caused by characteristic changes in the proximal, peripheral, parenchymal, and pulmonary vasculature airways due to chronic inflammation and structural changes in the lung. The occurrence of increased thickening of the small airways with increased formation of lymphoid follicles and deposition of collagen in the outer walls of the airways results in restriction of airway opening. The lumen of the small airways is reduced by thickening the mucosa containing an inflammatory exudate, which increases with the severity of the disease.
The effect of pollutant gas can cause oxidative stress, which in turn will cause lipid peroxidation. Lipid peroxidation will further cause cell damage and inflammation. The inflammatory process will activate alveolar macrophage cells. The activation of these cells will cause the release of neutrophil chemotactic factors such as interleukin-8 and leukotriene B4, tumor necrosis factor (TNF), monocyte chemotactic peptide (MCP)-1, and reactive oxygen species (ROS). These factors will stimulate neutrophils to release proteases that will damage the connective tissue of the lung parenchyma, resulting in alveolar wall damage and mucus hypersecretion. Stimulation of epithelial cells will cause the release of CD8 lymphocytes, then damage occurs, such as an inflammatory process. Under normal circumstances, there is a balance between oxidants and antioxidants. NADPH enzymes present on the surface of macrophages and neutrophils
Clinical Symptoms and Complications
The most common symptom in COPD patients is shortness of breath. Shortness of breath is usually a complaint when the FEV1 is <60% predicted. Patients usually define shortness of breath as increased effort to breathe, heaviness on breathing, gasping, and "air hunger."
Cough can come and go, but a chronic cough is an early symptom of COPD development. This symptom is also usually the first clinical symptom that the patient notices. Chronic cough in COPD can also occur without sputum.
Risk factors for COPD include smoking, genetics, exposure to harmful particles, age, bronchial hyper-reactivity, socioeconomic status, and infection.
Diagnosis
Physical examination
At the beginning of its development, COPD patients did not show any abnormalities on physical examination. Patients with severe COPD usually have wheezing and prolonged expiration on physical examination. Signs of hyperinflation such as a barrel chest may also be present. Cyanosis, contraction of accessory muscles of respiration, and pursed lips breathing are typical in moderate to severe COPD patients.
Signs of chronic disease such as muscle wasting, weight loss, reduced fat tissue are signs of COPD progression. A clubbing finger is not a typical sign of COPD, but if this sign is found, the clinician must determine what the cause is.
Spirometry is a definitive supporting examination for the diagnosis of COPD as described above, where the results of the FEV1 / FVC measurement ratio < 0.7.19 In addition to spirometry, blood gas analysis can also be performed to determine the pH level in the blood, radiography can be done to help determine the diagnosis of COPD, and Computed Tomography (CT) Scan was performed to see the presence of emphysema in the alveoli. Several studies have also suggested that a-1 antitrypsin deficiency can be assessed in COPD or asthmatic patients.
Medication and Treatment
Pharmacological Therapy
A. Bronchodilators
Bronchodilators are useful medications to increase FEV1 or alter spirometry variables by affecting smooth muscle tone in the airways.
• 2-Agonist (short-acting and long-acting) The working principle of 2-agonist is relaxation of airway smooth muscle by stimulating two adrenergic receptors by increasing C-AMP and producing functional antagonism bronchoconstriction. The bronchodilator effect of a short-acting two agonist usually lasts 4-6 hours. Regular use of 2 agonists will improve FEV1 and symptoms (Evidence B). The use of high-dose short-acting two agonists pro renata in patients already being treated with long-acting bronchodilators is not supported by evidence and is not recommended. Long-acting 2 inhaled agonists have a duration of action of 12 hours or more. Formoterol and salmeterol significantly improved FEV1 and lung volume, shortness of breath, health-related quality of life and frequency of exacerbations (Evidence A). Still, they did not affect reducing mortality and lung function. Salmeterol minimizes the likelihood of hospitalization (Evidence B). Indacaterol is a new long-acting 2 agonist with a duration of 24 hours, and it works significantly to improve FEV1, shortness of breath, and quality of life of patients (Evidence A). Side effects of 2-adrenergic receptor stimulation can cause sinus tachycardia at rest and can trigger arrhythmias. Somatic tremor is a problem in elderly patients treated with this class of drugs.
• Anticholinergic Drugs belonging to this group are ipratropium, oxitropium and tiotropium bromide. Its main effect is to block the effects of acetylcholine on muscarinic receptors. The bronchodilator effect of short-acting inhaled anticholinergics is longer than that of short-acting 2 agonists. Tiotropium has a working time of more than 24 hours. Its action can reduce exacerbations and hospitalizations, improve symptoms and health status (Evidence A), and improve the effectiveness of pulmonary rehabilitation (Evidence B). The side effect that can arise from the use of anticholinergics is dry mouth. Although it can cause prostate symptoms, no data can prove a causative relationship between prostate symptoms and the use of these drugs.
B. Methylxanthine
An example of a drug belonging to methylxanthine is theophylline. This drug is reported to play a role in changes in inspiratory muscles. However, this drug is not recommended if other medications are available.
C. Corticosteroids
Inhaled corticosteroids given regularly can improve symptoms, lung function, quality of life and reduce the frequency of exacerbations in patients with FEV1 <60% predicted.
D. Phosphodiesterase-4 inhibitor
The mechanism of this drug is to reduce inflammation by inhibiting the intracellular breakdown of C-AMP. However, the use of this drug has side effects such as nausea, decreased appetite, stomach pain, diarrhea, sleep disturbances, and headaches.
Other Pharmacological Therapy
• Vaccine: the pneumococcal vaccine is recommended for COPD patients aged > 65 years
• Alpha-1 Augmentation therapy: This therapy is intended for young patients with severe hereditary alpha-1 antitrypsin deficiency. This therapy is costly, is not available in most countries, and is not recommended for COPD patients who are not associated with alpha-1 antitrypsin deficiency.
• Antibiotics: Its use is to treat bacterial infections that trigger exacerbations
• Mucolytics (mucokinetics, mucoregulatory) and antioxidants: Ambroxol, erdosteine, carbocysteine, ionated glycerol, and N-acetylcysteine can reduce symptoms of exacerbations.
• Immunoregulators (immunostimulators, immunomodulators)
• Antitussives: This class of drugs is not recommended.
• Vasodilators
• Narcotics (morphine)
• Others: Herbal therapy and other methods such as acupuncture and hemopathies) are not effective in the treatment of COPD
Other Non-pharmacological Therapies:
1. Rehabilitation
2. Nutrition counseling
3. Other Therapeutic Education
4. Oxygen Therapy
5. Ventilatory Support
6. Surgical Treatment (Lung Volume Reduction Surgery (LVRS), Bronchoscopic Lung Volume Reduction (BLVR), Lung Transplantation, Bullectomy
Reference:
1. Soeroto AY, Suryadinata H. Chronic obstructive pulmonary disease. Ina J Chest Crit and Emerg Med. 2014; 1(2):83-8.
2. F Khairani. Chronic obstructive pulmonary disease (COPD) [Internet]. Available from: http://eprints.undip.ac.id/43859/2/FATHIA_KHAIRANI_G2A009079_BAB_2_KTI.pdf
