Pulmonary Fibrosis Research Paper
Pulmonary fibrosis (PF) is the condition in which the alveolar wall is thickened by scarring, causes the patients to have shortness of breath, fatigue and lower the oxygen saturation. PF may have definable causes but in many cases, the causes remain unknown. Those cases with unknown causes called idiopathic pulmonary fibrosis (IPF).
Air is drawn in by the nose and mouth, passes through the bronchi to the bronchioles and finally reaches millions of alveoli. Around the alveolar is a group of many capillaries and between the alveolar wall and capillary membrane is a small space called interstitial space. Oxygen (O2) in the alveolar after inhalation goes through the alveolar wall, the interstitial space and capillary membrane to go inside the capillary
in order for the hemoglobin to carry them to the heart. Carbon dioxide (CO2) goes through the opposite pathway from the oxygen and exit the body by exhalation. In IPF, the interstitial space is thickened by scarring causes oxygen is hard to reach the capillary. The scar also makes the lung stiffed and hard to recoil. Because of stiffness, it lowers the lung capacity and restricts the ability of oxygen cross through the alveolar wall lead to shortness of breath. The number of scars is increased over time; make the lung more stiff, lower the capacity and more restrict of the ability to cross through the alveolar wall.
In clinical of IPF cases, we usually see a patient in their middle age (50 - 70 years old) presents with new onset of progressive exertional dyspnea and non-productive cough, most have symptoms for 12-18 months prior to definitive evaluation and constitutional symptoms are uncommon. Beside dyspnea, the patient may also lost weight, have fever, fatigue, myalgia or arthralgia. When we do the physical examination, we may find bibasilar late inspiratory fine crackles, tachypnea. The heart sound is usually normal until it reaches the middle-late stages in which we'll find augmented P2, right-sided heave and S3 gallop. We may also see cyanosis, rash, arthritis, myositis or clubbing.
IPF usually affects middle aged and older adults. It varies from person to person. Thus some patients will happen quickly and some will process much slower. Even though in some cases, the procession is very slow, it still intervenes with patient's daily activities. In many years, there was no cure for IPF, only supportive treatments were available. However, there is a new hope for patients with IPF - It's Nintedanib.
Nintedanib was approved by the U.S. Food and Drug Administration (FDA) in October 2014 and by the European Commission In January 2015 as a drug to treat IPF. The experiment for this drug is developed by Boehringer Ingelheim
Air is drawn in by the nose and mouth, passes through the bronchi to the bronchioles and finally reaches millions of alveoli. Around the alveolar is a group of many capillaries and between the alveolar wall and capillary membrane is a small space called interstitial space. Oxygen (O2) in the alveolar after inhalation goes through the alveolar wall, the interstitial space and capillary membrane to go inside the capillary
in order for the hemoglobin to carry them to the heart. Carbon dioxide (CO2) goes through the opposite pathway from the oxygen and exit the body by exhalation. In IPF, the interstitial space is thickened by scarring causes oxygen is hard to reach the capillary. The scar also makes the lung stiffed and hard to recoil. Because of stiffness, it lowers the lung capacity and restricts the ability of oxygen cross through the alveolar wall lead to shortness of breath. The number of scars is increased over time; make the lung more stiff, lower the capacity and more restrict of the ability to cross through the alveolar wall.
In clinical of IPF cases, we usually see a patient in their middle age (50 - 70 years old) presents with new onset of progressive exertional dyspnea and non-productive cough, most have symptoms for 12-18 months prior to definitive evaluation and constitutional symptoms are uncommon. Beside dyspnea, the patient may also lost weight, have fever, fatigue, myalgia or arthralgia. When we do the physical examination, we may find bibasilar late inspiratory fine crackles, tachypnea. The heart sound is usually normal until it reaches the middle-late stages in which we'll find augmented P2, right-sided heave and S3 gallop. We may also see cyanosis, rash, arthritis, myositis or clubbing.
IPF usually affects middle aged and older adults. It varies from person to person. Thus some patients will happen quickly and some will process much slower. Even though in some cases, the procession is very slow, it still intervenes with patient's daily activities. In many years, there was no cure for IPF, only supportive treatments were available. However, there is a new hope for patients with IPF - It's Nintedanib.
Nintedanib was approved by the U.S. Food and Drug Administration (FDA) in October 2014 and by the European Commission In January 2015 as a drug to treat IPF. The experiment for this drug is developed by Boehringer Ingelheim