Idiopathic pulmonary fibrosis. The lungs take in air through the wind pipe called trachea to its branching airway called bronchi. These branch down into very smaller bronchioles and then into millions of air sacs called as alveoli…
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Idiopathic pulmonary fibrosis. The lungs take in air through the wind pipe called trachea to its branching airway called bronchi. These branch down into very smaller bronchioles and then into millions of air sacs called as alveoli. Oxygen passes through these tiny walls of alveoli into the tiny blood vessels that are present near to them. Similarly the carbon-di-oxide is transferred from the blood vessels to the alveoli which are then removed out of the lungs through the process of exhalation. Thus the oxygen required by the blood vessels is taken in by the cells. The most important part of respiration is the alveoli. These alveoli are sometimes damaged by unknown causes and results in the thickening of the walls. As the wall thickens the transfer of oxygen to the blood vessels decrease, this result in the increase of the blood pressure inside the blood vessels and finally leads to the heart failure. Such a condition is called as Idiopathic pulmonary fibrosis. The process by which these alveoli cells are damaged is unknown. This damage is passed to the epithelial cells and the changes in these muscles causes serious abnormalities. Idiopathic pulmonary fibrosis is a serious chronic disease of the respiratory system. Here the alveoli present in the lung tissues becomes damaged and scarred. It is also called as cryptogenic fibrosing alveolitis. The main reason for the cause of this disease was thought to be inflammation that occurs in the alveoli of the lungs and that inflammation was thought to increase and cause scarring and fibrosis. Recently it is called as one type of idiopathic interstitial pneumonia and a distinct clinical disorder. The words idiopathic and cryptogenic means “of unknown cause”, that is the occurrence of this disease is unknown. , pulmonary means “affecting the lungs”, as the alveoli of the lungs re affected it is called so. Fibrosis means “thickening”, here the thickening of the walls of the alveoli occurs and Alveolitis means “inflammation of the alveoli”. The main causative agent for this disease is unknown. It is suggested that either drug toxicities, environmental factors such as pollutants in the environment, cigarette smoking, viral infections and the presence of reflux diseases or vascular diseases can be the causative agent for this disease. Some genetic factors are also found to be involved in the occurrence of this disease. The mutations at the surfactant protein C and the polymorphisms at the tumor necrosis factor alpha are also found to cause IPF. The over expression of this disease is found to occur at mutations at the transforming growth factor Beta 1. The pulmonary function studies performed to analysis IPF has concluded that the oxygen and air supply is very much reduced in this case because of the thickening of the alveoli due to inflammation. (Noth, 2007). This disease is a very rare disease. 3 among 10,000 people are prone for this disease. This can occur at any age but the persons between 50 – 70 years are developing this disease more commonly. This disease is more common among men than women. The environmental factors are found to play a major role in the incorporation of this disease. The dusts from the diamond polishing, the pollen grains, the heavy industrial smoke. Industrial car cleaning, the people working in the mines, and those who are exposed to very finite particles are having more risk for the IPF to occur. Pathophysiology: The pathophysiology of this disease is less understood. The alveolar epithelial cell injury and the apoptosis of the cells are the earlier pathogenesis for this disease. (Horowitz, 2006). The interactions between the epithelial and mesenchymal cells are interrupted at the basement. The key control point for the pathogenesis was found to be basement membrane and the extra cellular matrix. The changes in the alveoli cells include alterations in type II alveolar epithelial cells, proliferation of the infected cells and the damage, bronchiolarization, regenerative hyperplasia and bronchiolarization. These regions are
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Due to reduced elasticity and a larger fibrous barrier, diffusion of oxygen and carbon dioxide between the alveoli and blood stream is hindered. This hindrance causes low lung compliance and lowers the effective rate of gaseous diffusion between alveoli and blood stream.
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