Last updated on: August 6th, 2021

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Chronic Obstructive Pulmonary Disease

Clinicals: History


Chronic obstructive pulmonary disease (COPD) is defined as persistent progressive airflow limitation due to an enhanced inflammatory response of the airways and lungs to noxious particles and gases.

Asymptomatic phase

During this phase, patients with chronic obstructive pulmonary disease (COPD) have no symptoms. However, lung function continues to decline. Symptoms are usually not apparent until the forced expiratory volume at 1 second (FEV1) is about 50% of the expected value.


Breathlessness is the main symptom of COPD, present either on performing activities of daily living or at rest. This is due to, but not limited to, airflow limitation, gas exchange abnormalities, inspiratory muscle weakness (consequent of increased mechanical loading), lung hyperinflation as well as any combination of the above.


Persistent cough, usually productive of sputum (non-productive in a subset of patients), is a common complaint in patients with COPD. Mucus hypersecretion in the lungs and small airway remodeling with narrowing are the reasons behind this symptom.

Chest tightness, wheezing

Chest tightness and wheezing are possible symptoms in a patient with COPD. This is due to the narrowing of the small airways.

Environmental risk factors

Tobacco smoke exposure is the single most important risk factor associated with the development of COPD. Maternal smoking is also an established risk factor. Other risk factors include exposure to biomass fumes (burnt wood, animal dung, crop residues or grass, especially when used as an energy source for indoor cooking), outdoor air pollutants (such as vehicle exhaust fumes, dust from mines and brick industries) as well as childhood asthma and respiratory infections. People of low socioeconomic status are more likely to develop COPD due to the previously-mentioned risks (biomass exposure in particular).

Alpha-1 antitrypsin deficiency

Alpha-1 antitrypsin (AAT) functions to prevent proteolytic damage of the airways by neutrophil elastase. In the absence of AAT, neutrophil elastase destroys the elastic tissues of the airways and lung parenchyma leading to distension of the airway and development of COPD.


Acute exacerbation of COPD is defined by the global initiative for chronic obstructive lung disease (GOLD) as a change in the patient's baseline dyspnea, cough, and sputum beyond normal day-to-day variations, is acute in onset, and warrants a change in regular medications.

Predictors of these events include previous history of exacerbations, non-adherence to medications prescribed, continued exposure to triggers of COPD such as tobacco smoke or superimposed chest infections as well as having had COPD for a long duration.

The risk of exacerbation is assessed over the previous 12 months, and classified as either low risk, if one or fewer exacerbations not resulting in hospitalization occur or high risk if at least 2 exacerbations not needing hospitalization or any exacerbation resulting in hospitalization occurs.

Systemic comorbidities

Individuals with COPD are more likely to have other conditions such as cardiovascular and cerebrovascular disorders (such as hypertension, pulmonary hypertension, cor pulmonale, heart failure, arrhythmias and stroke), osteoporosis, peptic ulcer, reflux disease, lung cancer, diabetes mellitus and depression.

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