Treatment of Cystic Fibrosis - Essay Example

Mucus provides a lining cavity to the organs, and the individual suffering from the disease has mucus that is sticky and thick. It also affects the lungs by building up and blocking the airways that carry the air in and out of the lungs. Thus, the blockage does not allow bacteria to grow and resulting in infections. In most cases, the disease affects the intestines by mucus blocking tubes in the pancreas hence the digestive enzymes are inhibited from reaching the small intestine for digestion.

Sweat becomes salty as a result of the disease where upon sweating an individual loses a lot of salts. This affects the balance of minerals that are present in the blood and is likely to result in health problems. It causes fatigue, dehydration, increased heart rate, decreased heart pressure, and heat stroke. In men, the disease can result in infertility while in women, it reduces the chances of getting pregnant.

The disease results when there is a mutation in the gene cystic fibrosis transmembrane conductance regulator. This gene is important in that it creates digestive juices, mucus, and sweat. A sole copy of the gene is needed so that it can prevent cystic fibrosis (Langwith, 2009). In most people, these copies are usually two. Cystic fibrosis occurs when an individual is unable to have at least one of the gene versions that are unaltered so that the cystic fibrosis transmembrane conductance regulator can be formed. The cystic fibrosis transmembrane conductance regulator is a channel of ions that transports the thiocyanate and chloride ions across the cell membranes of the epithelial thus resulting in cystic fibrosis.

In patients with Cystic Fibrosis, mutation of cystic fibrosis transmembrane conductance regulator is unable to control the epithelial sodium channel (ENaC). The epithelial sodium channel becomes hyperactive and as a result, too much of the sodium from the body causes mucus to become thick. The current drug to counteract cystic fibrosis is the one that mutates the 2000cystic fibrosis transmembrane conductance regulator (Giddings, 2009). A more efficient way to counter cystic fibrosis would be a therapy that would help act on the epithelial sodium channel rather than correcting the cystic fibrosis transmembrane conductance regulator.

Another way would be to inhibit the epithelial sodium channel to treat hypertension. This can be done using a grouping of microscopy and genetic automation to assess how they would affect the epithelial sodium channel. This study has helped bring down the activity of the epithelial sodium channel and the genes that are involved in the process. When it was tested it inhibited cystic fibrosis in the lungs of patients and thus it was discovered to be very promising in the treatment of cystic fibrosis. These results have been applauded in the pharmaceutical industry as a drug.