Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) is a pathology characterized in terms of pathophysiology, by chronic airflow obstruction, which is caused by the association between chronic obstructive bronchitis and emphysema, with the predominance of one or another.
Airway obstruction has the following characters:
- It is chronic, meaning that the respiratory flow variations are not important during a period of several months;
- Is irreversible or partially reversible under the action of bronchodilator medication;
- It is progressive, with a slow natural evolution to aggravation.
COPD is the fourth leading cause of mortality worldwide, its prevalence is in constant growth. COPD is more common in men than in women, which is explained by the greater number of men who smoke.
COPD Risk Factors And Causes
Risk factors that lead to the development of COPD are divided into certain factors and possible factors.
Certain risk factors for COPD are:
Smoking is the most important causative agent of COPD, disease six times more common in smokers than in nonsmokers. 70% – 90% of patients with COPD are smokers or have smoked. Pipe and cigar smokers have a lower risk to develop COPD than cigarette smokers, risk of developing COPD increases in relation to the number of cigarettes smoked, nicotine concentration of the cigarettes and the duration in years of this habit. The main actions of smoking on the lungs are:
- Inhibition of macrophages and bronchial cilia motility, causing secretion stasis and increase the risk of developing pulmonary infection;
- Hyperplasia and hypertrophy of mucus-secreting glands;
- Bronchospasm by activating the vagal irritant receptors;
- Alteration of surfactant quality.
Not all smokers develop clinically significant COPD, which suggest that in the development of COPD genetic factors are involved, which modify the susceptibility of developing the disease, depending on the individual.
Genetic susceptibility. In certain situations may be involved a deficiency of alpha 1 antitrypsin, which inhibits the protease enzyme. Proteases are secreted mainly by neutrophils, but also by macrophages and fibroblasts and degrade proteins like elastin and collagen. A reduce concentration of alpha 1 antitrypsin will increasing the level of proteolytic enzymes, which has as consequence the appearance of emphysema.
Premature development of emphysema and decline in pulmonary function, occur in both in smokers and nonsmokers with sever deficiency of alpha 1 antitrypsin, although smoking increasing the risk of emphysema. There are considerable variations between individuals in the severity of the emphysema.
Alpha 1 antitrypsin deficiency is relevant only in a small part of world’s population, fact that illustrates that in the development of COPD exist a interaction between genetic factors and environmental exposures.
Genetic susceptibility may be based on a bronchial hyperreactivity against various stimuli and immune deficits that increase receptivity to bacterial and fungal infections.
Air pollution. Prolonged exposure in the environment, in homes and as well in work at dust, fumes, gases and vapors is considered a causative factor for COPD. Pollutants promotes mucus hypersecretion, airway inflammation and infection and pollutants with small molecules that reach the terminal and respiratory bronchi and alveoli, triggers the goblet cell metaplasia and inflammatory processes, mucus hypersecretion, bronchial edema and will reduce up to obstruction the alveolar lumen. The same particles induce secretion of proteolytic enzymes, especially elastase, which can cause destruction of alveolar walls.
Possible factors for COPD are:
- Bronchial hyperreactivity, even if not as involved as in asthma, favors the appearance of COPD.
- Lower respiratory tract infections, especially those developed in childhood, before the age of 2 years, the majority of viral nature, especially those with respiratory syncytial virus are associated with persistent pulmonary function abnormalities.
- Long-term passive smoking.
- Other factors: alcohol consumption, age, male gender.
COPD is characterized by chronic inflammation of the airways, lung parenchyma and pulmonary vessels, caused by exposure to cigarette smoke and other harmful particles. In this process, in different areas of the lung, number and activity of macrophages, T lymphocytes and neutrophils are increased. Activated inflammatory cells release inflammatory mediators like leukotriene B4, interleukin 8 and tumor necrosis factor alpha, able to destroy the lung structures and maintaining the inflammation.
Destruction of lung parenchyma is the major change of COPD, created by an imbalance between proteinases and anti-proteinases in the lung (imbalance between elastase hypersecretion an alpha 1 antitrypsin deficit) in favor of proteinase, and oxidative stress as a consequence of inflammation. Sources of oxidizing agents are phagocytes and the products of combustion of tobacco. Their action is complex: accentuate the enzymatic proteolysis, degrades cellular matrix components, inactivate the anti-proteases system and injures the cells that synthesize the matrix cell.
In terms of pathology, COPD is a combination of various degrees of chronic bronchitis with emphysema.
Morphological changes characteristic for COPD occur in the central airways in the peripheral airways, lung parenchyma and vessels in the lungs.
In central airways (trachea and bronchi with diameter greater than 2 mm), inflammatory cells infiltrate the covering epithelium and hypertrophy of mucus-secreting glands and increased number of goblet cells are associated with hypersecretion of mucus.
In peripheral airway (small bronchi and bronchi with diameter less than 2 mm), chronic inflammation cause repeated cycles of aggression and bronchial wall repair. Repair process result is the airway wall remodeling, with increased content of collagen and formation of ciactriceal tissue, leading to lumen narrowing and the occurrence of irreversible airway obstruction.
So, in COPD, airflow obstruction is the result of narrowing of the airways, especially those with diameter less than 2 mm. To these chronic inflammatory narrowing are added viscous mucus hypersecretion, mucosal and submucosal edema and hypertrophy and spasm of bronchial smooth muscles.
COPD diagnosis is palced on symptoms, clinical examination and paraclinical examination.
- Chronic cough, usually the first symptom that occurs in COPD, may initially be intermittent, then become daily and often whole day and only rarely at night. In some cases, airflow limitation may occur before the cough.
- Chronic expectoration, mucous, viscous, is in small quantity.
- Dyspnea is the symptom for which patients with COPD seek medical advice. It is persistent, daily, progressive over time, exacerbated by exercise and respiratory infections.
The most important signs for diagnosis of COPD are: cyanosis, prolonged expiration (more than 5 seconds), wheezing, hypersonority at percussion, decreased vesicular murmur on auscultation and signs of chronic pulmonary cord: edema, hepatomegaly and jugular turgor.
The following will confirm the diagnosis of COPD, estimated severity, evolution and prognosis of COPD.
- Respiratory function tests: diagnosis of COPD requires to confirm
- Flow obstruction: showed by decreased FEV1 and FEV1/FVC report before and after administration of bronchodilator medication. Patients with COPD typically have a decrease in FEV1, and the FVC. Presence of a FEV1 <80% after administration of bronchodilator medication, associated with a report FEV1/FVC <70%, confirm the existence of the airflow limitation that is not fully reversible.
- Changes in blood gases values: when the FEV1 is less than 40% or if are any obvious clinical signs for respiratory failure or heart failure. Reduced PaO2 (partial pressure of oxygen) with more than 8 mmHg from the normal, shows hypoxia, and increased PaCO2 (partial pressure of carbon dioxide) over 45 mmHg, shows hypercapnia.
- Chest X-ray: has a relatively limited role in the diagnosis of COPD. This may reveal pulmonary hyperinflation, signs of pulmonary hypertension or exclude the presence of a lung disease that produces coughing and dyspnea: lung cancer, pleurisy, pneumothorax or may reveal causes of exacerbations (pneumonia).
- CT: this is not a routine examination for COPD, its main role in highlighting the pulmonary emphysema and emphysema bubbles.
- Screening for alpha 1 antitrypsin deficiency.
Classification of COPD according to its severity:
Staging of COPD has practical importance and is an orientation for the treatment of disease.
Assessment of COPD severity is based on the intensity of symptoms, spirometry abnormalities and the presence of complications. Global Initiative for Chronic Obstructive Lung Disease (GOLD) proposes the following classification of COPD:
- Stage I: Mild COPD – characterized by mild airflow limitation ( FEV1> 80%, FEV1/FVC < 70%). Symptoms of chronic cough and sputum production may be present, but not always. At this stage, the patient is usually unaware that the lung function is abnormal.
- Stage II: Moderate COPD - characterized by worsening air flow limitation ( 50% < FEV1 < 80%; FEV1/FVC <70%), with shortness of breath, typically developing on effort, cough and sputum production are also present. This is the stage at which patients typically seek medical attention, because of chronic respiratory symptoms or an exacerbation of their disease.
- Stage III: Severe COPD – characterized by further worsening air flow limitation ( 30% < FEV1 < 50%; FEV1/FVC < 70% ), greater shortness of breath, reduce exercise capacity, fatigue and repeated exacerbation that almost always have an impact on patient’s quality of life.
- Stage IV: Very severe COPD – characterized by sever air flow limitation (FEV1 < 30% or FEV1 < 50% plus the presence of chronic respiratory failure; FEV1/FVC < 70%). Patient may have stage IV, very severe COPD even if the FEV1 > 30%, whenever this complications are present. At this stage, quality of life is very appreciably impaired and exacerbation may be life threatening.
COPD Clinical forms
In cases where there are sufficient elements to differentiate chronic bronchitis from emphysema, the diagnosis of COPD must specify the form of COPD:
- COPD predominantly bronchitis (type B);
- COPD predominantly emfizematos (type A).
In 80% of cases, COPD is mixed and in only 20% of COPD cases are relatively pure (type A or type B), making their therapy to be similar.
- Aggravation of chronic respiratory failure, which can be precipitated by respiratory infections, sedative medications, abdominal or chest surgery, the occurrence of pneumothorax.
- Chronic pulmonary cord: represents hypertrophy and dilatation of the right ventricle which is caused by pulmonary hypertension. In decompensated stages is manifested by right heart failure.
COPD Evolution And Prognosis
COPD has an evolution that is leading to deterioration in all cases, with periods of remission and exacerbations, triggered by infection.
COPD progression is translated as follows:
- Increasing the rate of decline of FEV1;
- Accentuation of the hyperinflation;
- Progressive alteration of blood gases;
- The occurrence of pulmonary hypertension in COPD patients with hypoxemia.
It is considered as an element of poor prognosis: marked tachypnea, decrease and even abolish of the vesicular murmur, tachycardia or other arrhythmias, right ventricular hypertrophy advanced changes, FEV1 <1 Liter.