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Emphysema |What is Emphysema | Emphysema Definition |What is Emphysema

Emphysema is a long-term, progressive disease of the lungs that primarily causes
shortness of breath due to over-inflation of the alveoli (air sacs in the lung). In people with emphysema the lung tissues involved in exchange of gases (oxygen and carbon dioxide) is impaired or destroyed. It is included in a group of diseases called chronic obstructive pulmonary disease or COPD. Emphysema is called an obstructive lung disease because the destruction of lung tissue around smaller airways (bronchioles), makes these airways unable to hold their shape properly when exhale. This makes them inefficient at transferring oxygen into the blood, and in taking carbon dioxide out of the blood.

 

 

Causes Of Emphysema 

The main cause of emphysema is long term exposure to airborne irritants,
including:

  • Tobacco smoke
  • Marijuana smoke
  •  Air pollution
  •  Chemical fumes and dust Cigarette smoking is by far the most
    dangerous behaviour that causes people to develop emphysema, and it is also the most preventable cause. Other risk factors include a deficiency of an enzyme called α-1- antitrypsin, air pollution, airway reactivity, heredity, male sex and age.
    The importance of cigarette smoking as a risk factor for developing emphysema cannot be overemphasized. Cigarette smoke contributes to this disease process in two ways. It destroys lung tissue, which results in the obstruction of air flow, and it causes inflammation and irritation of airways that can add to air flow obstruction.
  •  Destruction of lung tissue occurs in several ways. First, cigarette smoke directly affects the cells in the airway responsible for clearing mucus and other secretions. Occasional smoking temporarily disrupts the sweeping action of tiny hairs called cilia that line the airways. Continued smoking leads to longer dysfunction of the cilia. Long term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages. Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract. Furthermore, smoke causes mucous secretion to be increased, at the same time that the ability to clear the secretions is decreased. The resulting mucous deposition can provide bacteria and other organisms with a rich source of food and lead to infection.
  •  The immune cells in the lung, whose job is to prevent and fight infection, are also
    affected by cigarette smoke. They cannot fight bacteria as effectively, or clear the lungs of the many particles (such as tar) that cigarette smoke contains. In these ways, cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the inflammation
    caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells. of tiny hairs called cilia that line the airways. Continued smoking leads to longer dysfunction of the cilia. Long term exposure to cigarette smoke causes the cilia to disappear from the cells lining the air passages. Without the constant sweeping motion of the cilia, mucous secretions cannot be cleared from the lower respiratory tract. Furthermore, smoke causes mucous secretion to be increased, at the same time that the ability to clear the secretions is decreased. The resulting mucous deposition can provide bacteria and other organisms with a rich source of food and lead to infection.
  •  The immune cells in the lung, whose job is to prevent and fight infection, are also affected by cigarette smoke. They cannot fight bacteria as effectively, or clear the lungs of the many particles (such as tar) that cigarette smoke contains. In these ways, cigarette smoke sets the stage for frequent lung infections. Although these infections may not even be serious enough to require medical care, the inflammation
    caused by the immune system constantly attacking bacteria or tar leads to the release of destructive enzymes from the immune cells. α-1-antitrypsin deficiency α-1-antitrypsin (also known as α-1- antiprotease) AAT is a glycoprotein member of the serine protease inhibitor family that is synthesized in the liver and is secreted into the blood stream. It is a substance that fights a destructive enzyme in the lungs called trypsin (or protease). Trypsin is a digestive enzyme, most often found in the digestive tract, where it is used to help the body digest food. It is also released by immune cells in their attempt to destroy bacteria and other material. People with α-1-antitrypsin deficiency cannot fight the destructive effects of trypsin once it is released in the lung. The destruction of tissue by trypsin produces similar effects to those seen with cigarette smoking. The lung tissue is slowly destroyed, thus decreasing the ability of the lungs to perform appropriately. Foreign objects (e.g. bacteria) are trying to be destroyed but this enzyme destroys normal tissue since the second enzyme (antiprotease) responsible for controlling the first enzyme (protease) is not available or is poorly functioning. This is referred to as the “Dutch” hypothesis of emphysema formation.

The American Thoracic Society/ European Respiratory Society Guidelines recommend screening for AAT deficiency if emphysema is suspected in any patient younger than 45 years and with any of the following:

  • Absence of recognized emphysema, risk factors such as smoking or occupational inhalational exposure.
  •  Unexplained liver disease.
  •  Family history of AAT deficiency, COPD, bronchiectasis, or panniculitis.
  •  Positive c-ANCA (anti-neutrophilic cytoplasmic antibody) vasculitis.
  • Unclear/idiopathic bronchiectasis.
  • Asthma with persistent, fixed-airways obstruction despite therapy.

 

Risk Factors Of Emphysema

Factors that increase risk of developing emphysema include:

  • Smoking: Emphysema is most likely to develop in cigarette smokers, but cigar and pipe smokers also are susceptible. The risk for all types of smokers increases with the number of years and amount of tobacco smoked.
  •  Age: The lung damage that occurs in emphysema develops gradually; most people with tobacco-related emphy sema begin to experience symptoms of the disease between the ages of 40 and 60.
  •  Exposure to second-hand smoke: Second-hand smoke, also known as
    passive or environmental tobacco smoke, is smoke that you inadvertently inhale from someone else’s cigarette, pipe or cigar. Being around second hand smoke increases your risk of emphysema.
  •  Occupational exposure to fumes or dust: Breathe fumes from certain chemicals or dust from grain, cotton, wood or mining products, are more likely to develop emphysema. This risk is even greater in cigarette smokers.
  •  Exposure to indoor and outdoor pollution: Breathing indoor pollutants, such as fumes from heating fuel, as well as outdoor pollutants, car exhaust, for instance increases risk of emphysema.