History and exam

Key diagnostic factors

Usually the initial symptom of COPD.

Frequently a morning cough, but becomes constant as disease progresses.

Usually productive, and sputum quality may change with exacerbations or superimposed infection.

Initially with exercise but may progress to shortness of breath even at rest.

Patients may have difficulty speaking in full sentences.

Other diagnostic factors

The anteroposterior diameter of the chest is increased.

This suggests hyperinflation and air trapping secondary to incomplete expiration.

Caused by hyperinflation and air trapping secondary to incomplete expiration.

Caused by barrel chest, hyperinflation, and air trapping.

Secondary to loss of lung elasticity and lung tissue breakdown.

A common finding in exacerbations. The current accepted descriptive word for a continuous musical lung sound.

Is indicative of airway inflammation and resistance.

A common finding in exacerbations. A discontinuous sound referring to mucus or sputum in airways.

Indicative of airway inflammation and mucus oversecretion.

An increased respiratory rate occurs to compensate for hypoxia and hypoventilation.

May involve use of accessory muscles.

Loss of postural control in outstretched arms (commonly known as a flap) caused by hypercapnia.

This is due to impaired gas exchange in lung parenchyma, worsens with exercise, and is suggestive of respiratory failure.

Occurs secondary to increased intrathoracic pressure and cor pulmonale.

Suggests cor pulmonale and secondary pulmonary hypertension as a complication of advanced chronic lung disease.

Occurs because of disrupted sleep secondary to constant nocturnal cough and persistent hypoxia and hypercapnia.

May occur due to vasodilation caused by hypercapnia.

Seen in the late stages of COPD, usually with hypoxia, hypercapnia, and cor pulmonale.

Sign of advanced COPD.

Indicates secondary pulmonary hypertension as a complication of cor pulmonale.

Sign of advanced COPD complicated by cor pulmonale.

Sign of advanced COPD complicated by cor pulmonale.

COPD itself does not cause clubbing, but if tobacco exposure in COPD patients leads to lung cancer and/or bronchiectasis, then clubbing may occur in COPD. Clubbing is usually not present until significant impairment of lung function has occurred.

Risk factors

Most important risk factor. It causes 40% to 70% of cases of COPD.[11]

Elicits an inflammatory response and causes cilia dysfunction and oxidative injury.

The effect of age may be related to a longer period of cigarette smoking as well as the normal age-related loss of FEV1.

Airway responsiveness to inhaled insults depends on genetic factors. Alpha-1 antitrypsin deficiency is a genetic disorder, mostly encountered in people of northern European ancestry, which causes panacinar emphysema in lower lobes at a young age.

Despite high rates of smoking among black Americans and other racial and ethnic groups, COPD is more common in white people.

Chronic exposure to dust, traffic exhaust fumes, and sulfur dioxide increases risk of COPD.

Frequent childhood infection may cause scarring of lungs, decrease elasticity, and increase risk for COPD.

COPD is more common in men, but that is probably secondary to more smokers being male. However, there is a suggestion that women may be more susceptible than men to the effects of tobacco smoke.[12][13][14][15]

The risk for developing COPD is increased in people with lower socioeconomic status.[16] However, this may reflect exposure to cigarette smoke, pollutants, or other factors.

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