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Chronic Obstructive Pulmonary Disease: Assessment, Analysis, and Associated Dental Management Guidelines

Chronic obstructive pulmonary disease (COPD) is a disease state associated with irreversible pulmonary damage, progressive airflow limitation, partially obstructed airways, breathing difficulty, and an abnormal inflammatory response. In COPD, the alveoli lose their elasticity, which results in some areas with collapsed airways and some areas with hyperinflated airways. Alveolar damage causes poor air exchange. Additionally, excess mucus production by the mucus-producing cells causes thickening of the airways and the airway blockade. COPD is most prevalent in the elderly.

COPD is a disease state associated with emphysema and chronic bronchitis. Emphysema is associated with hyperinflated alveoli interspersed with alveoli that have been destroyed. Chronic bronchitis is associated with thickened inflamed airways. Therefore, frequent lung infections result in rapid progression toward COPD in such patients.

COPD ETIOLOGY

The etiological factors associated with COPD:

Familial COPD is often associated with α1 antitrypsin deficiency. Alpha-1 antitrypsin inactivates destructive proteins, so lack of α1 antitrypsin leads to destruction of the lungs and COPD.

Prevalence rates for COPD are directly related to tobacco smoking and indoor air pollution. COPD is characterized by progressive decline in respiratory function and health-related quality of life, with substantial risk for premature death. COPD affects the proximal and peripheral airways, lung parenchyma, and vasculature. Comorbidities, such as cardiovascular disease, diabetes mellitus, and depression, as well as associated systemic consequences including weight loss and muscle disease, increase the overall burden of disease.

The clinical course of COPD is viewed as a progressive decline in lung function over time, as assessed by forced expiratory volume in one-second (FEV1) measurement. Recently, however, it has been suggested that disease progression depends on contributing phenotypes. Acute exacerbation of COPD is what leads to deterioration in lung function, particularly when this is complicated with acute respiratory failure. The frequency of exacerbations increases with decline in lung function. The patients with the most severe disease, especially the one with many comorbidities, is at risk of more severe attacks and is more likely to need hospital admission. With COPD, a progressive decline in airflow is associated with an abnormal inflammatory response of the lung to noxious particles or gases.

COPD SYMPTOMS AND SIGNS

COPD patients frequently experience shortness of breath on exertion and at rest, in addition to persistent cough with excessive expectoration, wheezing, and chest tightness.

COPD DIAGNOSIS

Diagnosis of COPD is made with the following information:

COPD CLASSIFICATION

COPD can be classified as:

• Mild
• Moderate
• Severe
• Very Severe

Mild COPD

The patient may not yet be aware of the airway limitation, and it is detected only by spirometry, which shows mild airflow limitation. The PO2 is close to 75 mmHg and the PCO2 is normal at 35–45 mmHg.

Moderate COPD

Symptoms occur on exertion and this prompts the patient to seek help. Spirometry shows worsening of airflow. A moderate COPD patient has a PO2 close to 60mmHg and the PCO2 is normal.

Severe COPD

Symptoms and signs associated with COPD are present at rest. Spirometry shows severe airflow limitation. Heart or respiratory failure could occur in these patients. In severe COPD, the PO2 is ≤50 mmHg and the PCO2 is ≥50 mmHg.

Very Severe COPD

Very severe COPD is associated with highly significant airflow limitation associated with chronic respiratory failure, cor pulmonale, and/or eventual death. In very severe COPD the PO2 is ≤50mmHg and the PCO2 is ≥50mmHg.

COPD TREATMENT GOALS

Relief of the symptoms and signs, improvement in exercise tolerance, and slowing of the progression of the disease are the prime treatment goals. Treatment options include the following:

• Smoking cessation
• Bronchodilators: The short-acting bronchodilators are used for immediate effect that lasts for 4–6 hours. The long-acting bronchodilator effect lasts for 12 hours.
• Inhaled steroids: Steroids work by decreasing the airway inflammation.
• Oral or injectable steroids: These steroids provide additional support to decrease airway inflammation.
• Oxygen
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