Chronic obstructive pulmonary disease

chronic obstructive pulmonary disease (COPD) is a lung disorder characterized by the existence of generally progressive and irreversible airway obstruction. A higher incidence is found in people exposed to tobacco smoke and firewood/coal, producing as a main symptom a decrease in respiratory capacity, which progresses slowly over the years and causes considerable deterioration in the quality of life of the people. people affected, being able to cause a premature death.

Between 20 and 25% of smokers develop the disease, but the causes of predisposition to development are unknown, although it may be a multifactorial component that includes environmental elements (such as individual susceptibility).

The most common cause of COPD is smoking. Other risk factors include indoor and outdoor pollution, exposure to occupational irritants such as grain dust and cadmium dust or fumes, and genetics. In developing countries, common sources of air pollution indoor are the use of charcoal and biomass such as wood and dried dung as fuel for cooking and heating. Most people living in cities are exposed to harmful levels of air pollution. Diagnosis is based on poor airflow as measured by spirometry.

Most cases of COPD can be prevented by reducing exposure to risk factors such as smoking and indoor and outdoor pollutants. While treatment can slow worsening, there is no conclusive evidence that any medication can change long-term deterioration of lung function. Treatments for COPD include smoking cessation, immunizations, pulmonary rehabilitation, inhaled bronchodilators, and corticosteroids. Some people may benefit from long-term oxygen therapy, surgical reduction of lung volume, and lung transplantation. In those who have periods of acute worsening, increased use of medication, antibiotics, corticosteroids, and hospitalization may be necessary.

Definition

In 2002, the Second Mexican Consensus for the Diagnosis and Treatment of COPD defined it as:

COPD is a disease characterized by airflow limitation, which is not significantly modified and is usually progressive. This limitation is associated with an abnormal inflammatory response of the lungs and airway, whose most important risk factors are exposure to harmful particles and gases, mainly derived from tobacco use and exposure to wood smoke.

According to the 2017 GOLD initiative, in the Guideline for the management and prevention of COPD:

Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease characterized by persistent respiratory symptoms and airflow limitation due to respiratory and/or alveolar abnormalities due to significant exposure to harmful particles or gases.

Epidemiology

The worldwide prevalence of COPD ranges from 5 to 10% of the adult population between 40 and 80 years of age. If we consider the total population, the prevalence is approximately 1% at all ages. COPD has increased in prevalence in recent decades and is 3-4 times more frequent in men than in women (15% in smokers, 12.8% in ex-smokers and 4.1% in non-smokers) given the higher prevalence of smoking in men, although this is expected to change in the coming decades, since tobacco use in young women is significantly higher than that of young men. Although the prevalence depends largely on the physiological definition used, the simplest and most sensitive value is to use the FEV1/FVC ratio <0.7 (<70%). In Spain, several population-based epidemiological studies have been carried out, obtaining an overall prevalence of 9.1% (14.3% in men and 3.9% in women) of the population of adults over 40 years of age.

The Platino project, carried out by ALAT (Latin American Thoracic Association), made it possible to determine the prevalence of COPD in five Ibero-American countries (Brazil, Chile, Mexico, Uruguay and Venezuela), varying greatly from one country to country, between 7.8% in Mexico City and 17% in Montevideo.

Mortality

Global mortality from COPD was in sixth place with 2.2 million deaths in 1990, and is expected to rise to the third leading cause of death by 2020. A study conducted in the USA in the period 1971-2000 showed that the most important change during that period was the increase in mortality in women, which went from 20.1/100,000 in 1980 to 56.7/100,000 in 2000.

In 1998, in Spain, COPD represented the fifth leading cause of death in men (56.3/100,000 inhabitants) and the eighth in women (12.3/100,000 inhabitants).

Morbidity

Overall, the morbidity of COPD is high, increases with age and is currently higher in men than in women.

Etiology

COPD is fundamentally associated with smoking, especially in developed countries. In some very depressed societies, due to exposure to toxic fumes, COPD can develop. There are also cases, although less and less in developed countries, of people who cook with wood fires in small and poorly ventilated spaces.

Risk factors

In developed countries, smoking contributes to 95% of COPD cases, being the most prevalent risk factor. Other factors commonly associated with COPD are:

Distribution of the PiZZ gene in Europe.

Host factors

• Genetic factors: There are numerous reports that in COPD pathogenesis several environmental genetic factors are or should be involved. From the base that alone. 15-20 % of smokers develop the disease, it is logical to think that genetics should play an important role in individual susceptibility. However, the Framingham study suggests that, in the general population, genetic factors contribute very little to the loss of lung function, with the spiratory flow in the first second (FEV1), mainly influenced by a locus in chromosome 5 arm q. An established genetic factor of COPD is α1-antitripsin deficiency (α1-AT) or protease inhibitor (α1-PI), although α1 deficiency (alelo ZZ of gene α1-antitripsin-PiZZ) occurs in less than 1 % of cases (see image).

• Diet: A poor intake in antioxidant vitamins (A, C, E) has sometimes been associated with increased risk of COPD and more recent studies consider the importance of vitamin C and magnesium. There is some evidence that fish oil-rich diets are linked to a lower prevalence of COPD, although similar studies did not confirm these findings. Some other evidence points out that a low carbohydrate diet with a greater contribution of healthy fats in the individual's daily requirement decreases the production of CO2, and could be beneficial for COPD patients. Fruit and vegetable flavonoids do seem beneficial. Good nutrition from the early years of life is very important and low-weight newborns for their gestational age are at greater risk of developing COPD in later stages.

• Atopia and bronchial hyperreactivity: In pneumology the call Dutch hypothesis which proposed that atopia and IgE were involved in the development of COPD. COPD may have increased airway reactivity to histamine and metacoline. COPD mortality is known to increase with more severe atopia and with hyperreactivity of the airway. A longitudinal study indicated an association between eosinoflia and mortality by COPD only in groups that had suffered asthma attacks.

• Sex: Several studies have found a higher prevalence of COPD in women than in men. Although it is discussed whether women are more sensitive to the effects of tobacco, there is evidence that confirms that young adolescent smokers attain less lung function, and that for the same amount of tobacco exposure, the risk of obstruction of the respiratory tract is greater in women. In developing countries, women may be exposed to a greater degree than men because of environmental pollution by using fuel in the kitchen.

Environmental factors

• Tabaquismo
• Atmospheric pollution: Air pollution, especially sulphur dioxide and respiratory particle contamination (black smoke or matter particles ≤10 μm [PM₁₀]) is associated with simple chronic bronchitis and COPD. There may be interaction between environmental pollution and tobacco use. BOLD study data do not support the association between PM_2.5 and chronic obstruction of the respiratory tract (The prevalence of airway obstruction was not independently associated with PM 2.5), characteristic of COPD.
• Dust and chemicals in the workplace: Labour exposure to dust (carb, silex, quartz) to issociate and solvent vapors can be a factor associated with the appearance of COPD, acting with tobacco use. It has been studied that exposure to cadmium and exposure to welding vapours could be associated with the appearance of emphysema.
• Infection: Respiratory infections during the early stages of life are associated with COPD in later stages of life. It has been seen that latent viral infections (such as adenovirus) can cause amplification of the inflammatory response in emphysema and predispose to COPD development.
• Firewood and coal: people who cook or heat the home with biomass fuels have a great risk of developing COPD.

Pathophysiology

In COPD, different pathological phenomena occur in five anatomical points, resulting in various clinical manifestations:

• Chronic bronchitis: chronic airway inflammation that leads to mucous hypersecration with chronic productive cough.
• Obstructive bronchitis: small airway inflammation that causes fibrosis and remodeled leading to airway obstruction.
• Enfisema: due to protein destruction with bronchial remodeling and alveoli.
• Pulmonary vascular disease and cor pulmonale: by destruction of lung capillary bed causing pulmonary arterial hypertension and right heart failure. This pathology is known as cor pulmonale.
• Systemic disease: In case of advanced COPD there is extrapulmonary inflammation with cachexia and loss of lean mass with muscle weakness.

The exaggerated inflammatory response to the inhalation of particles or gases (mainly tobacco smoke), beyond a "normal" protective inflammatory response, is a characteristic event of COPD that causes lung damage in susceptible smokers. Bronchial epithelial cell injury and macrophage activation cause the release of chemotactic factors that recruit circulating neutrophils. Macrophages and neutrophils then release proteases that affect matrix metalloproteinases (MMP) and neutrophil elastase (NE), causing changes in the connective tissue. Once sequestered, neutrophils adhere to the endothelial cell and migrate to the tract. under the control of chemotactic factors such as leukotriene B₄ or interleukin (IL)8.

Likewise, cytotoxic CD8+ T lymphocytes play a role in the inflammatory cascade. It has been suggested that the presence of T lymphocytes could differentiate between smokers who develop COPD and those who do not, based on the relationship between the number of T cells, the amount of alveolar destruction, and the intensity of airflow obstruction. One of the causes that have been described to explain the amplified inflammatory response in COPD is the colonization of the airways by bacterial or viral pathogens. It is also possible that tobacco smoke damages the bronchial epithelial cell, generating new autoantigens that stimulate inflammatory response, even postulating that COPD was an autoimmune disease.

Proteolysis, fibrosis, and small airway remodeling are the prominent features of emphysema pathology. Vascular endothelial cells, pneumocytes, and mast cells may also contribute to the pathogenesis of COPD.

Cells and their mechanisms

• Macrophages: The amount of macrophages is very high in bronco-alveloar washing samples in COPD. Activation of these cells is done through tobacco smoke and other inhaled irritants. The number of macrophages in the airway corresponds both with the extent of the destruction of the parenchyma in emphysema and with the severity of the obstruction. The lungs of smokers without COPD also show a larger number of macrophages, however, macrophages in COPD patients are more active, free more inflammatory proteins and have greater elastolytic capacity. Bronchial biopsies have found that COPD smokers have more cells expressing the inflammatory protein of macrophages (MIP-1α).
• Lymphocytes T: In COPD patients, CD8+ lymphocytes (cytotoxic-suppressants) increase both in number and in percentage becoming the dominant T cell subgroup. It has been seen that the increase in CD8+ is associated with decreased lung function. These cells could contribute to the physiopathology of the disease through the release of grazmines, perforins and TNF-α, factors that induce apoptosis in the type1 alveolar cells. It is unknown whether CD8+ in COPD are Tc1 (interferon producers) or type Tc2 (IL-4).
• Neutrophils

Clinical picture

Drum fingers in a 51-year-old male patient with chronic heart disease and emphysema.

	Sibilances Sounds of sybilance ears with a stethoscope.
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COPD is mainly associated with two diseases:

• Pulmonary emphysema: It is the permanent enlargement of the terminal bronchioles, with destruction of the alveolar wall, which may or may not present fibrosis. This causes the collapse of the airways. It is usually shown in the clinic by polypnea and tachypnea, but with decrease of the vesicular murmur to the auscultation and, by increase of the retroesternal space in the left lateral X-ray of the chest. The profile of patients with emphysema (Perfil Pink Puffer) is: astenia, about 60 years, low expectoration, premature dyspnea, slight alteration of the diffusion of gases, radiological signs of hyperinsuflation and bullying, very low capacity of diffusion of CO and a resistance of the unchanged airway (occasionally elevated). These patients get little clinical improvement with the use of bronchodilators and usually progress unfavorably over time.

• Chronic bronchitis: It is an inflammation of the bronchus, which causes the flow of air that enters and leaves the lungs to be reduced. At the same time, there is an increase in mucous secretion that obstructs the airways. In clinical terms, it is considered as a chronicle when coughing and expectation is seen in most days for 3 months a year, at least 2 consecutive years. The profile of patients suffering from chronic bronchitis (Perfil Blue bloater) is: overweight, about 50 years, abundant expectoration, late dyspnea, severe alteration of gas exchange, chronic radiological changes, frequent appearance of cor pulmonale, mild decrease of CO diffusion.

Diagnosis

Spirometry.Static lung volumes and capabilities.VC: Current volume;VRI:Inspiratory reserve volume;VRE: Spiracy reserve volume;CV; Vital capacity; CI: Inspiring capacity;CRF: Castile residual capacity;VR: Residual volume;CPT: total lung capacity

To diagnose COPD, a test called spirometry is used to measure functional lung capacity. Subjects have a post-bronchodilator FEV1 less than 80% (except in stage 1, where FEV1 is greater than or equal to 80%) and a FEV₁/FVC ratio less than 0.70.

Classification

The Global Initiative for Chronic Obstructive Lung Disease has categorized the grades of COPD into:

Treatment

Oxygen therapy is mandatory in the event of decreased oxygen saturation concentration, whether this is measured with arterial blood gases or pulse oximetry.

Chronic disease is treated in addition to beta 2 agonists with inhaled steroids such as beclomethasone; In addition, ipratropium bromide, tiotropium or with glycopyrronium bromide are used. The use of oral steroids such as prednisone is recommended for more than fourteen days, because after this time there is no proven effect; Schemes of five days of oral treatment have been used with good results. Parenteral steroids such as hydrocortisone or methylprednisolone are indicated in the event that bronchospasm occurs during the disease, thus reducing flow obstruction. Theophylline use is not adversarial and is not considered in most settings. The use of magnesium sulfate is controversial, and some guidelines reserve its use for asthma. Respiratory physiotherapy is indicated as a central pillar in the treatment.

A systematic review of 15 studies, most conducted in Asia, particularly China, and one in South Africa, found evidence that community-based rehabilitation has a positive impact. One of the cases was focused on chronic obstructive pulmonary disease. A cost-effectiveness evaluation of the rehabilitations is necessary to evaluate the allocation of resources.

Oxygen therapy

In general, chronic oxygen administration is indicated in patients with COPD who have hypoxemia (PaO2 less than 55 mm Hg), or a PaO2 between 55 and 60 mm Hg associated with pulmonary hypertension, cor pulmonale, or polyglobulia secondary (hematocrit >55%). In these patients, continuous oxygen therapy is at least > of 15 hours a day has been shown to improve survival. Low oxygen flows may be necessary since in COPD patients, control of respiration is controlled primarily by oxygen rather than carbon dioxide levels, increases in delivery oxygen can decrease this response and cause respiratory failure with carbon retention. The clinical guidelines of the American Thoracic Society on COPD include the use of oxygen and its risks. There is a consensus that indicates a maximum goal of oxygen saturation until pulse oximetry reaches 92%, since there is a risk of induced hypercapnia afterward. by oxygen.

Non-pharmacological treatment

Venous thromboembolic disease prophylaxis is recommended, in exacerbations that require admission, and to ensure an adequate fluid balance and nutritional support.

Quality of life

Patients with COPD show a decrease in the quality of life, compared to the reference values for the general population, in two components mainly according to the SF36 questionnaire (It is a general questionnaire that can be applied to measure the quality of of life related to health in groups with different ages, illnesses or treatments) physical and mental. The impact that the disease has on all the subscales that make up this construct is ratified, especially in the physical component.