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Asthma-Emphysema

Asthma-Emphysema

Asthma-EmphysemaNow you have a general idea of the elements that make up your respiratory system after going through and how they normally work together. You’ve also seen where and how emphysema and chronic bronchitis create problems. Here we focus on the diseases themselves and tie all the pieces together. What does each disease look like? How and why are emphysema and chronic bronchitis so closely related? How does COPD progress over time?

NOTE: As you read through these descriptions, try to keep in mind that these two diseases—each in its own way obstructing the flow of air in and out of the lungs—usually occur together. We describe their mechanisms separately for ease of presentation and understanding. But in the real world, the two sets of processes usually work hand in hand.

Cigarette smoking is the overwhelmingly most important cause of COPD. It causes two major kinds of damage to the lungs—the air sac damage we call emphysema, and the airway/air sac damage we call chronic bronchitis. Realizing that smoking injures our lungs isn’t a modern notion.

Over 300 years ago, the seventeenth-century physician Tobias Venner published the first warning against smoking and lung damage in his book Via Recta and Vitam Longam {The Long and Healthy Life): “Tobacco . . . disturbeth the humors and spirits, corrupteth the breath . . . exisaccateth the windpipe, lungs, and liver.”

Compared to nonsmokers, cigarette smokers are ten times more likely to die from COPD, cigar smokers three times more likely, and pipe smokers one and one-half times more likely.

Avoid smoking

The next question: How does cigarette smoking cause lung damage that impairs their ability to work, and gets worse as time goes by?

Emphysema

Emphysema’s immediate cause depends on whether it is the first or second of the COPD diseases to appear. When it develops first, its cause is a presently incurable enzyme imbalance in the lungs that allows destruction of too many elastic fibers in the lungs’ framework and air sac walls. A tiny number of these patients inherit this enzyme imbalance. The vast majority develop it from smoking cigarettes for many years.

When chronic bronchitis—typically caused by smoking—is the first to develop, it eventually hyperinflates the lungs because mucus obstructing the smallest bronchioles prevents air sacs from fully emptying. Then elastin in these overstretched alveoli walls breaks down. The route is different, but the same point is reached.

What medical researchers have learned from studying people who have inherited this imbalance permits us to understand the mechanism behind this problem, regardless of its cause.

An important element in the body’s repair system are enzymes that destroy proteins—the basic building blocks of all tissue. They get rid of aging cells to make way for new ones, and help in other ways to fight disease. To prevent these enzymes from digesting too much protein, our body also produces regulatory enzymes that continuously circulate throughout our body in our plasma—the fluid in which our blood cells travel.

Alpha1-antitrypsin is the most abundant of these regulatory enzymes. It is manufactured in the liver, then released into the plasma for transport.

Its primary role is inhibiting the enzyme elastase, which is manufactured by a type of white blood cell and released into the plasma surrounding them. Elastase—as its name implies—digests elastin.

Elastin is the basic construction material in the lungs, providing the bulk of the framework and the alveoli walls. Elastase digests aging elastin cells so they can be replaced by new ones. Normally, alpha,-antitrypsin adequately controls the amount of elastase in the lungs so it doesn’t destroy healthy tissue too. But with too little alpha!-antitrypsin, elastase proliferates. It destroys healthy elastic cells. This is the beginning of emphysema—when it precedes chronic bronchitis.

Clinical scientists have gathered two kinds of proof linking this abnormal relationship to emphysema. In animal experiments, higher elastase levels clearly produce emphysema. In humans, inadequate alpha,-antitrypsin is the single factor always associated with COPD.

Inherited Alpha1-Antitrypsin Deficiency:

Our 31 chromosomes contain about 100,000 genes—the blueprints for all our inherited characteristics. We have two sets of chromosomes, one from each of our parents. A gene on chromosome 14 determines how much alpha1-antitrypsin our liver produces. Depending on what each parent passed on to them, some people have two normal alpha1-antitrypsin genes, some have two defective genes, and some have one of each.

When a gene pair has one defective member, the consequence generally depends on the trait. For traits needing only one active gene, the defective one is not called into service. But for traits that rely on both genes—and alpha1-antitrypsin is one of these—even one defective gene can cause trouble. And a pair of defective genes can wreak havoc.

With just one defective alpha1-antitrypsin gene, a person’s liver still produces roughly 75% of what it should. The subtle problems this can cause do not involve emphysema. But the person with two defective genes produces only 15% of this critical regulatory enzyme—too little to control the destruction of elastin. Most of these people eventually develop emphysema (and are also susceptible to chronic liver disease). The emphysema symptoms are usually obvious by age 35 if they smoke, and by age 45 if they don’t. (This deficiency is more common in some countries than others. It affects 1 of every 6,000 people in the United States, for example, but 1 of every 1,000 in Sweden.)

Self-Made Alpha1-Antitrypsin Deficiency:

Uncontrolled destruction of the lungs’ elastin by the elastase enzyme is also how smokers develop emphysema. In fact, cigarette smoke packs a triple whammy when it comes to injuring the lungs’ elastic network, by (1) inactivating alpha1-antitrypsin; (2) causing pulmonary inflammation, which brings still more elastase (via elastase-containing neutrophils) into the lungs; and (3) slowing production of new elastic cells.

Emphysema Develops:

By whichever route, destruction of too many elastic fibers in the lungs’ framework and air sac walls is the first step in emphysema. This loss of elasticity results in hyperinflated air sacs, and impairs the lungs’ ability to recoil effectively during expiration. The hyperinflated air sacs become permanently enlarged. Eventually the walls of these overstretched air sacs break down, merging neighboring alveoli into one large air sac. At the same time, the disease invades the walls of previously healthy alveoli.

Destruction of capillary-rich air sac walls means that much of the lungs’ capillary network—which is responsible for taking oxygen into the body and discarding carbon dioxide—is gradually lost. This continually reduces the amount of gas exchange that can occur. The inspiratory muscles start working harder to take air in.

Since the enlarged alveoli can no longer provide the force that normally keeps the smallest airways fully open during expiration, expiratory resistance increases considerably. In compensation, expiration becomes slower and longer, and often is eventually aided by the expiratory muscles even during nonstrenuous activities. But the increased force exerted by the expiratory muscles’ compensatory behavior compresses the small airways even further. Their collapse during expiration traps air in the attached alveoli. This process begins limiting the amount of stale air that can be breathed out, and therefore the amount of fresh air that is breathed in.

Expiratory resistance can eventually become so high that it actually prevents expiration from finishing before the next inspiration must begin. This increases air trapping, and limits even more the amount of air that can be moved in and out of the lungs.

Substantial air trapping—when more air than normal remains in the lungs at the end of each expiration—means the lungs can no longer return to their normal resting position. Because they must remain partially expanded, the inspiratory muscles cannot relax—stretch out to full length—in between breaths. A shorter muscle is less effective, and so must work harder. At some point, the accessory inspiratory muscles start to help out on a full-time basis.

An irony of this disease is that each new development increases the workload on the respiratory muscles, while at the same time diminishing further the amount of oxygen available to produce the energy this work requires.

So emphysema patients are characterized by hyperinflated lungs and by chronically diminished airflow—especially during expiration. Gas exchange is moderately disrupted. The consequences of these lung changes are most noticeable during activities requiring physical effort. Patients find themselves breathless doing things that once gave them no difficulty.

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  1. Patrick Perruzzi
    Patrick Perruzzi05-29-2012

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