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Chronic Obstructive Pulmonary Disease is a set of lung diseases that limit airflow into the lungs by causing airflow obstruction and is not fully reversible. It is usually progressive and is associated with inflammation of the lungs as they respond to noxious particles or gases.
COPD patients report they are “hungry” for air
COPD is potentially preventable with proper precautions and avoidance of precipitating factors
This condition entails two major diseases :
Emphysema and chronic bronchitis. Asthma has also been included.
Emphysema is an abnormal permanent enlargement of the air space distal to the terminal bronchioles accompanied by destruction of bronchioles.
Chronic bronchitis is the presence of chronic cough for 3 or more months in each of 2 successive years in a patient whom other causes of chronic cough have been excluded.
Features of Chronic Bronchitis and emphysema will be present such as:
How common is COPD?
About 13.9% of the U.S. adult population (25+ years) have been diagnosed with COPD. An estimated 15-19% of COPD cases are work-related. 24 million other adults have evidence of troubled breathing, indicating COPD is under-diagnosed by up to 60%.
Smoking is the primary risk factor. Long-term smoking is responsible for 80-90 % of cases. Nicotine stimulates the sympathetic nervous system resulting in increased heart rate, peripheral vasoconstriction, increases blood pressure and cardiac output.
How does cigarette smoking lead to COPD?
Cigarette smoking compounds problems in a person with CAD leading to reduced ciliary motility and possible loss of ciliated cells.
It also leads to abnormal dilation of the distal air spaces and alveolar wall destruction. This destruction may lead to carbon monoxide accumulation and reduced oxygen-carrying capacity.
Smoking also leads to cellular hyperplasia stimulating the production of more mucus reducing the airway diameter hence increasing difficulty in clearing secretions.
Smoker, compared to a non-smoker, is 10 times more likely to die of COPD
Prolonged exposures to harmful particles and gases from:
Infection. Infection is a major contributing factor to the aggravation and progression of COPD
Heredity. Alpha antitrypsin deficiency (produced in the liver and found in the lungs) accounts for about 1% of the cases. Emphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages.
Emphysema is an abnormal permanent enlargement of the air space distal to the terminal bronchioles accompanied by destruction of bronchioles:
It starts with Hyperinflation of alveoli which then causes the destruction of alveolar walls and destruction of alveolar-capillary walls. Once the alveolar walls are destroyed there is narrowing of the airways and loss of lung elasticity:
There are two types of emphysema:
The structural changes in emphysema are:
Small bronchioles become obstructed as a result of
Recurrent infections lead to production and stimulation of neutrophils and macrophages which then release proteolytic enzymes. These enzymes cause alveolar destruction, inflammation, exudation and edema of the bronchioles.
Elastin and collagen are destroyed. Air then goes to the lungs but it is unable to come out on its own and remains in the lings causing bronchioles to collapse.
Trapped air causes hyperinflation and over distention of the alveoli. As more alveoli coalesce, blebs and bullae may develop destroying the alveolar walls and capillaries causing reduced surface area for O2 diffusion.
Compensation is done by increasing respiratory rate to increase alveolar ventilation. Hypoxemia usually develops late in the disease
Pathologic lung changes in chronic Bronchitis are;
In chronic inflammation, the primary pathologic mechanism causing changes that lead to narrow airway lumen and reduced airflow due to hyperplasia of mucous glands, Inflammatory swelling, excess, thick mucus production.
Greater resistance to airflow increases the work of breathing
Bronchioles are clogged with mucus and pose a physical barrier to ventilation. Hypoxemia and hypercapnia due to lack of ventilation and O2 diffusion
The tendency to hypoventilate and retain CO2. Frequently patients require O2 both at rest and during exercise.
Cough is often ineffective to remove secretions because the person cannot breathe deeply enough to cause airflow distal to the secretions
Bronchospasm frequently develops more common with a history of smoking or asthma
Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema
Earliest symptoms are :
COPD Diagnostic Studies
st x-rays early in the disease may not show abnormalities
History and physical exam
Pulmonary function studies will indicate reduced FEV1/FVC and increased residual volume and total lung capacity
Chronic Obstructive Pulmonary Disease can be managed, but not cured
Treatment is different for each individual and is based on the severity of the symptoms
Early diagnosis and treatment can:
Bronchodilators as maintenance therapy:
Beta-adrenergic agonists such as Ventolin(MDI or nebulizer is preferred).Anticholinergics eg Atrovent. These drugs work by relaxing muscles around airways
Steroids to reduce inflammation
Oxygen therapy to help with shortness of breath by raising PO2 in inspired air and treat hypoxemia
Chest physiotherapy – to bring secretions into larger, more central airways
Encourage patient to remain as active as possible
Full stomachs press on diaphragm causing dyspnea and discomfort
Difficulty eating and breathing at the same time leads to inadequate amounts being eaten
The annual flu vaccine reduces the risk of flu and its complications
Pneumonia vaccine reduces the risk of the common cause of pneumonia
Pulmonary hypertension (pulmonary vessel constriction due to alveolar hypoxia and acidosis)
Cor pulmonale (Right heart hypertrophy + Right ventricular failure)
Acute Respiratory Failure