Epoc

Notas del editor

• #5: La COPD incluye el enfisema, un cuadro anatómicamente definido y que secaracteriza por destrucción y ensanchamiento de los alvéolos pulmonares; la bronquitis crónica, un cuadro definido clínicamente por tos crónica productiva y una afección de las vías respiratoriasfinas, en la que se estrechan los bronquiolos finos. Se considera que existe COPD cuando hay unaobstrucción duradera al flujo de aire; la bronquitis crónica sin obstrucción no se incluye dentro de la neumopatía obstructiva crónica.
• #8: Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma.Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction.The primary offender has been found to be human leukocyte elastase, with synergistic roles suggested for proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator.
• #9: The primary offender has been found to be human leukocyte elastase, with synergistic roles suggested for proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells. Accelerated aging and autoimmune mechanisms have also been proposed as having roles in the pathogenesis of COPD.[3, 4]Cigarette smoke causes neutrophil influx, which is required for the secretion of MMPs; this suggests, therefore, that neutrophils and macrophages are required for the development of emphysema.Studies have also shown that in addition to macrophages, T lymphocytes, particularly CD8+, play an important role in the pathogenesis of smoking-induced airflow limitation.To support the inflammation hypothesis further, a stepwise increase in alveolar inflammation has been found in surgical specimens from patients without COPD versus patients with mild or severe emphysema. Indeed, mounting evidence supports the concept that dysregulation of apoptosis and defective clearance of apoptotic cells by macrophages play a prominent role in airway inflammation, particularly in emphysema.[5] Azithromycin (Zithromax) has been shown to improve this macrophage clearance function, providing a possible future treatment modality.[6]In patients with stable COPD without known cardiovascular disease, there is a high prevalence of microalbuminuria, which is associated with hypoxemia independent of other risk factors.[7]
• #10: El humo del cigarrillo hace que el influjo de neutrófilos, lo que se requiere para la secreción de MMP, lo que sugiere, por tanto, que los neutrófilos y los macrófagos son necesarios para el desarrollo de enfisema.
• #12: Emphysema is a pathologic diagnosis defined by permanent enlargement of airspaces distal to the terminal bronchioles. This leads to a dramatic decline in the alveolar surface area available for gas exchange. Furthermore, loss of alveoli leads to airflow limitation by 2 mechanisms. First, loss of the alveolar walls results in a decrease in elastic recoil, which leads to airflow limitation. Second, loss of the alveolar supporting structure leads to airway narrowing, which further limits airflow.
• #13: First, loss of the alveolar walls results in a decrease in elastic recoil, which leads to airflow limitation. Second, loss of the alveolar supporting structure leads to airway narrowing, which further limits airflow.
• #14: Centriacinar emphysema is characterized by focal destruction limited to the respiratory bronchioles and the central portions of the acini. This form of emphysema is associated with cigarette smoking and is typically most severe in the upper lobes.Panacinar emphysema involves the entire alveolus distal to the terminal bronchiole. The panacinar type is typically most severe in the lower lung zones and generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency.Distal acinar emphysema, or paraseptal emphysema, is the least common form and involves distal airway structures, alveolar ducts, and sacs. This form of emphysema is localized to fibrous septa or to the pleura and leads to formation of bullae (as seen in the images below). The apical bullae may cause pneumothorax. Paraseptal emphysema is not associated with airflow obstruction.
• #16: The gradual destruction of alveolar septae (shown in the image below) and of the pulmonary capillary bed in emphysema leads to a decreased ability to oxygenate blood. The body compensates with lowered cardiac output and hyperventilation. This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in chronic bronchitis. Because of low cardiac output, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as
• #17: La bronquitis es una inflamación (o irritación) de las vías respiratorias en los pulmones. Las vías respiratorias son los conductos en los pulmones por los cuales pasa el aire. También se llaman bronquios. Cuando las vías respiratorias están irritadas, se forma en ellas una mucosidad espesa. La mucosidad tapa las vías respiratorias y hace que sea difícil el paso del aire a los pulmones.La bronquitis provoca una tos que produce mucosidad (que se llama, a veces, esputo), problemas para respirar y una sensación de opresión en el pecho.
• #22:  El cuerpo responde disminuyendo la ventilación y el aumento del gasto cardíaco. Este V / Q resultados desajuste en la circulación rápida en un pulmón mal ventiladas, lo que lleva a la hipoxemia y policitemia. Con el tiempo,hipercapnia y acidosis respiratoria, lo que lleva a la vasoconstricción arterial pulmonar y cor pulmonale. 
• #28: The respiratory rate increases in proportion to disease severity. Use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces is evident (known as the Hoover sign). In advanced disease, cyanosis, elevated jugular venous pulse (JVP), and peripheral edema can be observed.