Emphysema
Jennifer Davis
Modesto Junior College
Abstract
Emphysema has long been lacking a clinical definition but instead is often defined in pathological terms. As a disease affecting the airspaces or parenchymal, and not the bronchi. The American Thoracic Society states that emphysema exists when “there is an anatomical alteration of the lung characterized by an abnormal enlargement of the airspaces distal to the non-respiratory bronchioles, accompanied by destructive changes of the alveolar walls”³. The characterization of emphysema pathologically includes all areas distal to the terminal bronchiole including; alveolar ducts, respiratory bronchioles, and terminal alveoli.
Emphysema
In a normal lung there is a healthy balance of chemicals that protect the lung fibers from destruction. These elastic fibers in the lungs allow it to expand and contract with each respiration. It is believed that in emphysema, this delicate balance is permanently altered. Once the elastic fibers are destroyed, the alveolar walls begin to breakdown resulting in a decrease of the alveolar-capillary diffusion surface area. Overtime, enough of the alveoli are destroyed that holes are left in the lung tissue and patients begin to become short of breath with mild exertion. This inconvenience often causes them to seek medical intervention. Unfortunately by this time, the irreparable damage has already been done. The term emphysema itself can also be used when describing several other conditions where the lungs hyper inflate without causing destruction to the alveoli. These conditions include; Congenital lobar emphysema, compensatory emphysema, and senile emphysema.
It’s not Bronchitis
Emphysema is just one of many conditions grouped under the COPD label, and is often classified on the same level as bronchitis. Though these two conditions may seem similar on the surface, they can be easily distinguished from one another by physiologic testing. Bronchitis manifests as an airway disease while emphysema is isolated to the pulmonary parenchyma. Emphysema and bronchitis may superficially have similar results on spirometry testing do to obstructed expiratory flows. If a patient has asthma, further distinction may be difficult between emphysema and bronchitis because of the hyper reactivity of the airways. Although there may be some crossover in many patients, such incidents should be seen as exceptions to the rule and this is often do to patients having both conditions. “Patients with emphysema are often underweight
and need to gain weight, whereas those with chronic bronchitis are likely to be overweight and need to lose weight.”
Risk Factors
While smoking cigarettes remains the major risk factor, with a ten times greater risk of developing emphysema than the general population, only ten to fifteen percent of smokers develop significant obstructive lung disease. Emphysematous patients tend to develop airflow obstruction over numerous years, often without the display of symptoms at all. They are found later in life to be clinically diagnosed with progressively detrimental symptoms which often lead to mortality. Other risk factors include age, exposure to environmental particles such as dust and gases, air pollution, fumes and chemicals. Age tends to be a significantly determining factor when it comes to the onset of emphysema symptoms. Although it takes years for the damage to occur, most people begin to manifest symptoms in their fifties. Occupational exposure to pollutants is a growing risk factor for emphysema. Fumes from certain chemicals such as chlorine and pesticides, as well as dust particles from wood, grains, and mining and cotton products also increase the odds that emphysema will develop.
Alpha 1 Deficiency
Heredity can play an important role in which smokers will develop emphysema. A rare, inherited protein called Alpha 1 Antitrypsin (1AT) can be deficient which may lead people younger than fifty to develop emphysema. It has been discovered that emphysema commonly occurs in patients who are lacking 1AT. This enzyme helps to protect the lung field from injury.
It is synthesized in the liver and inhibits elastase from breaking down lung tissue. Essentially it is the body’s self-defense mechanism against alveoli destruction. It has been shown that cigarette smoking decreases neutrophil elastase in the lower respiratory tract, making it more vulnerable to destruction. For each concentration of alpha 1 antitrypsin in the lower respiratory tract, it takes twice as long for an equivalent amount of neutrophil elastase to be inhibited in a smoker’s lung compared with the nonsmoker’s lung.² The majority of patients with emphysema have normal 1AT serum levels. Patients with this congenital form of emphysema have anatomical changes in the lung bases instead of the traditional upper lung fields. Evidence has shown that through intravenous administration of 1AT can help restore the imbalance caused by this deficit.