COPD - Definition, Causes, Clinical Manifestation, Classification and Pathophysiology

Chronic Obstructive Pulmonary Disease

DEFINITIONS

Chronic Obstructive Pulmonary Disease (COPD) is a chronic lung disease characterized by the air flow resistance in the airway that is progressive nonreversibel or partially reversible. COPD consists of chronic bronchitis and emphysema or both. Chronic bronchitis is a respiratory disorder characterized by chronic cough with phlegm at least 3 months of the year, at least two consecutive years, is not caused by other diseases. while emphysema is an anatomical abnormality characterized by a widening lung airspaces distal to the terminal bronchioles, accompanied by destruction of the alveoli walls.


CAUSES

There are three factors that affect the incidence of COPD is cigarette, infection and pollution, but it is also associated with heredity, allergies, age and genetic predisposition, but it is not yet clear whether these factors play a role or not.

• Smoking: According to the report of the WHO expert committee on smoking control, smoking is the main cause of COPD. Physiologically cigarettes directly related to hiperflasia bronchial mucous glands and squamous metaplasia of the respiratory tract. Can also cause acute bronchoconstriction. According Crofton and Doouglas smoke cause too inhibition activity vibrating hair cells, alveolar macrophages and surfactants.
• Infections: upper respiratory tract infection in a patient with chronic bronchitis is almost always causes lower respiratory tract infection, and cause lung damage increases. Estimated exacerbation of chronic bronchitis is most often preceded by a viral infection, which then lead to secondary infection by bacteria.
• Pollution: pollution chemical substances that can also cause bronchitis is a reducing agent such as CO2, oxidising agents such as N2O, hydrocarbons, aldehydes and ozone.

CLINICAL MANIFESTATION

Common signs and symptoms appear in patients with COPD are as follows:

• Productive cough, initially intermittent and occurs almost every day over time.
• White or mucoid sputum, if there is an infection becomes purulent or mukopurulent, shortness of breath to use additional respiratory muscles to breathe, cough and expectoration, which tends to increase and the maximum in the morning.
• Shortness of breath after strenuous activity occurred along with the development of disease in the case of weight, shortness of breath occurs even with minimal exertion and even at rest due to the deterioration of gas exchange abnormalities.
• In the moderate-to-severe disease, physical examination may show a decrease in breath sounds, expiratory elongated, Ronchi, and hyperresonance on percussion.
• Anorexia.
• Weight loss and weakness.
• Tachycardia, sweating.
• Hypoxia.

All respiratory disease characterized by chronic obstruction of the airflow. The main cause of the obstruction assortment, for example:

• Airway inflammation.
• Mucosal adhesions.
• Narrowing of the airway lumen.
• Damage to the airway.
• Tachypnea.
• Orthopnea. (Doenges, 1999: 152)

CLASSIFICATION

Classification of COPD can be divided into three, namely:

• Bronchial asthma: a disease characterized by increased reaction response of the trachea and bronchi to various kinds of stimulation with manifestations such as difficulty in breathing caused by narrowing of the airways thorough.
• Chronic bronchitis: a clinical disorder characterized by the formation of excessive mucus in the bronchi and manifested in the form of chronic cough and sputum formed during 3 months of the year, a minimum of 2 years continuously.
• Emphysema: changes in the anatomy of the lung parenchyma characterized by widening the walls of the alveoli, alveolar ducts and alveolar wall destruction (Muttaqin, 2008).

PATHOPHYSIOLOGY

Inhalation of cigarette smoke or other harmful gases activates macrophages and epithelial cells to release chemotactic factors that recruit more macrophages and neutrophils. Then, macrophages and neutrophils release proteases that destroy these structural elements in the lungs. Proteases can actually be overcome by endogenous antiproteases, but the imbalance antiproteases against the dominance of protease activity that will eventually become a predisposition to the development of COPD. The formation of highly reactive oxygen species such as superoxide, hydrogen peroxide hydroxyl free radicals have been identified as factors that contribute to the pathogenesis because these substances can increase the destruction antiproteases.

Chronic inflammation result metaplasia on the walls of the bronchial epithelium, mucous hypersecretion, increased smooth muscle mass and fibrosis. There is also the epithelial ciliary dysfunction, causing disruption clearance excessive mucus production. Clinically, this process manifests as chronic bronchitis, characterized by a chronic productive cough. In the lung parenchyma, destruction of structural elements
mediated protease causes emphysema. Alveolar septum damage leads to reduced elasticity of the recoil of the lungs and airways dynamics failure due to damage to the small airways support non-cartilage. This whole process results in a patent airway obstruction and other symptoms characteristic pathophysiological for COPD.

Obstruction of the airways produce alveoli are not ventilated or less ventilated; Continuous perfusion of the alveoli will cause hypoksemia (low PaO 2) by a mismatch between ventilation and blood flow (V / Q is not appropriate). Ventilation of the alveoli are not perfused or less pefusi increase the space of the appendix (Vd), causing inefficient disposal of CO2. Hyperventilation would normally occur to compensate for this situation, which in turn will increase the work required to overcome airway resistance has increased, in the end this process fails, and there was retention of CO2 (hypercapnia) in some patients with severe COPD.