Print Friendly

 

 

 

 

By Medifit Biologicals

 

EMPHYSEMA

Emphysema 4

EMPHYSEMA DEFINITION

Emphysema gradually damages the air sacs (alveoli) in your lungs, making you progressively more short of breath. Emphysema is one of several diseases known collectively as chronic obstructive pulmonary disease (COPD).

Smoking is the leading cause of emphysema.

Your lungs’ alveoli are clustered like bunches of grapes. In emphysema, the inner walls of the air sacs weaken and eventually rupture — creating one larger air space instead of many small ones. This reduces the surface area of the lungs and, in turn, the amount of oxygen that reaches your bloodstream.

When you exhale, the damaged alveoli don’t work properly and old air becomes trapped, leaving no room for fresh, oxygen-rich air to enter. Treatment may slow the progression of emphysema, but it can’t reverse the damage.

 

EMPHYSEMA CAUSES

In the vast majority of people, smoking is the cause of emphysema. Exactly how smoking destroys the air sac linings in the lungs isn’t known. However, population studies show that smokers are about six times more likely to develop emphysema than nonsmokers.

Estimates vary, but more than 24 million people in the U.S. likely have emphysema or another form of COPD, and probably many of them don’t know it. Emphysema and chronic bronchitis are the third-leading cause of death in the U.S.

Interestingly, most heavy smokers do not develop emphysema. Why some smokers get emphysema and others do not is unknown. All heavy smokers experience other negative health effects of smoking, though.

Emphysema 1

EMPHYSEMA PATHOPHYSIOLOGY

Once innate respiratory defenses of the lung’s epithelial cell barrier and mucociliary transport system are infiltrated by foreign/invading antigens (noxious cigarette ingredients, for instance), the responding inflammatory immune cells (including polymorphonuclear cells, eosinophils, macrophages, CD4 positive and CD8 positive lymphocytes) transport the antigens to the bronchial associated lymphatic tissue layer (BALT). It is here where the majority of the release of neutrophilic chemotactic factors is thought to occur. Proteolytic enzymes like matrix-metalloproteinases (MMPs) are mainly released by macrophages, which lead to destruction of the lung’s epithelial barrier.

Macrophages are found to be 5- to 10-fold higher in the bronchoalveolar lavage fluid of emphysematous pateints.Also, along with macrophages, the release of proteases and free radical hydrogen peroxide from neutrophils adds to the epithelial ruination, specifically with emphasis on the basement membrane. This is why neutrophils are thought to be highly important in the pathogenesis of emphysema at the tissue level, a differentiator to the mainly eosinophilic inflammatory response in airways affected by asthma.

After all, the T lymphocytes in the sputum of emphysematous smokers are mainly CD8 positive cells.[9] These cells release chemotactic factors to recruit more cells (pro-inflammatory cytokines that amplify the inflammation) and growth factors that promote structural change. The inflammation is further amplified by oxidative stress and protease production. Oxidants are produced from cigarette smoke and released from inflammatory cells. Proteases are produced by inflammatory, macrophage, and epithelial cells, which fuel bronchiolar edema from an elastin-destroying protease-antiprotease imbalance. This protease-menace is elastase, released by macrophages, and responsible for breakdown of the lung’s fragile elastic lamina (of which elastin is a structural protein component). This is believed to be central in the development of emphysema. Peptides from elastin can be detected in increased quantities in patients with emphysema and AAT.

The repair process of airway remodeling further exacerbates emphysema’s anatomical derangements with key characters such as vascular endothelial growth factor (VEGF), which is expressed in airway smooth muscle cells and is responsible for neovascularization and expression of increased and possibly abnormal patterns of fibroblastic development. It is these structural changes of mucus hyperplasia, bronchiolar edema, and smooth muscle hypertrophy and fibrosis in smokers’ airways that result in the small airways narrowing of less than two millimeters.

 

EMPHYSEMA SYMPTOMS

You can have emphysema for many years without noticing any signs or symptoms. The main symptom of emphysema is shortness of breath, which usually begins gradually. You may start avoiding activities that cause you to be short of breath, so the symptom doesn’t become a problem until it starts interfering with daily tasks. Emphysema eventually causes shortness of breath even while you’re at rest.

Illustration depicting emphysema, a condition characterized by damage to the alveoli. Alveoli are the small air sacs at the end of the respiratory tree (in the lungs). Long term exposure to compounds found in cigarette smoke (such as carbon monoxide and cyanide) are believed to be responsible for loss of elasticity in the alveoli, leading to emphysema and other lung diseases such as COPD (chronic obstructive pulmonary disease). The illustration also includes the appearance of healthy alveoli for comparison.

EMPHYSEMA DIAGNOSIS

A person with emphysema usually describes slowly worsening shortness of breath, over a period of months or years. He or she also likely smoked for many years. Symptoms may also include cough orwheezing.

Physical exam: In mild emphysema, a doctor’s examination may reveal no evidence of emphysema. In people with more advanced emphysema, a doctor may notice these findings:

  • Increased chest size or “barrel chest” (from abnormally expanded lungs in emphysema)
  • Decreased breath sounds through the stethoscope
  • Rounded fingertips (clubbing)
  • Pursed-lip breathing
  • Hypoxemia (hypoxia): Low oxygen levels in the blood, detected onpulseoximetry or arterial blood gas testing
  • Hypercarbia: High levels of carbon dioxide in the blood. This results from an inability to exhale properly in emphysema
  • Cyanosis: Blue-tinged lips, resulting from low oxygen in severe emphysema
  • Malnutrition: Muscles slowly waste away in advanced emphysema

Pulmonary function tests (PFTs): A person sits inside an enclosed booth and breathes into a tube. As someone performs various breathing maneuvers, PFTs measure:

  • How much air the lungs can hold
  • How rapidly a person can blow out air from their lungs
  • How much air remains trapped in the lungs after exhalation

Whether any airflow limitations improve with inhaledbronchodilator medicines, such as albuterol

People with normal lungs can blow out most of the air in their lungs in one second. With emphysema, it’s more likely to take longer to empty the lungs.

Chest X-ray film: A chest X-ray of someone with emphysema may show abnormally large lungs. In early emphysema, though, a chest X-ray film is usually normal. Diagnosing emphysema can’t be done with an X-ray alone.

Computed tomography (CT scan) of the chest: A CT scan in someone with emphysema may show small pockets of air throughout the lung. These areas of damaged lung are where air becomes trapped, making forceful exhalation difficult.

Complete blood count : This simple blood test usually shows normal amounts of white and red blood cells. In advanced emphysema, the red blood cell count may rise. Infections may cause an elevated white blood cell count.

Emphysema 3

EMPHYSEMA TREATMENT

Emphysema can’t be cured, but treatments can help relieve symptoms and slow the progression of the disease.

MEDICATIONS

Depending upon the severity of your symptoms, your doctor might suggest:

  • Bronchodilators. These drugs can help relieve coughing, shortness of breath and breathing problems by relaxing constricted airways, but they’re not as effective in treating emphysema as they are in treating asthma or chronic bronchitis.
  • Inhaled steroids. Corticosteroid drugs inhaled as aerosol sprays may help relieve shortness of breath. Prolonged use may weaken your bones and increase your risk of high blood pressure, cataracts and diabetes.
  • Antibiotics. If you develop a bacterial infection, like acute bronchitis or pneumonia, antibiotics are appropriate.

THERAPY

  • Pulmonary rehabilitation. A pulmonary rehabilitation program can teach you breathing exercises and techniques that may help reduce your breathlessness and improve your ability to exercise.
  • Nutrition therapy. You’ll also receive advice about proper nutrition. In the early stages of emphysema, many people need to lose weight, while people with late-stage emphysema often need to gain weight.
  • Supplemental oxygen. If you have severe emphysema with low blood oxygen levels, using oxygen regularly at home and when you exercise may provide some relief. Many people use oxygen 24 hours a day. It’s usually administered via narrow tubing that fits into your nostrils.

SURGERY

Depending on the severity of your emphysema, your doctor may suggest one or more different types of surgery, including:

  • Lung volume reduction surgery. In this procedure, surgeons remove small wedges of damaged lung tissue. Removing the diseased tissue helps the remaining lung tissue expand and work more efficiently and helps improve breathing.
  • Lung transplant. Lung transplantation is an option if you have severe emphysema and other options have failed.

By Medifit Biologicals

www.medifitbiologicals.com