What is the pathophysiology of rheumatoid arthritis?
scientists did not acquire fully accurate pathophysiology of rheumatoid arthritis (RA), but many discoveries now extend the extent of the beneficial treatment of this immune system disorder that affects almost 2 million people in the United States. Rheumatoid arthritis is one of a group of diseases called autoimmune diseases in which the immune cells of the body accidentally attack their own tissues or organs of the body. In the case of RA, the attack occurs in the joints of the body and creates inflammation, pain and impaired movement. The antibody, called the rheumatoid factor, causes the immune system incorrectly identifying the healthy joint tissue of the body as a foreign tissue and targeting them to destruction. Although the exact cause of rheumatoid arthritis is unknown, there are obviously several factors, including sex, infection, genetics, smoking and poorly regulated immune system.
women develop rheumatoid arthritis three times more often than men, especially a durpvní postpartum year. Women usually develop the first symptoms during the third to the fifth decadeof life. Scientists assume that female sex hormones that tend to promote inflammation play a role in the pathophysiology of rheumatoid arthritis. The increased incidence of RA in women reflects a formula observed in other autoimmune diseases.
Scientists also believe that infection can serve as a triggering event in the pathophysiology of rheumatoid arthritis. In response to infection, the body produces proteins, called antibodies that attack foreign particles. If antibodies are not sufficiently specific to bacteria, they can connect to normal body cells that somehow resemble bacteria, deactivate cells and indicate them to eliminate immune cells. Many doctors suspect Parvovirus, rubella, herpes and mycoplasm, causing "walking pneumonia," to be agents who potentially stimulate RA.
While it is a pitchMNO only in 20 percent of the general population, genetically coded cell marker, HLA-DR4, occurs in more than two-thirds of Caucasian patients with RA. The genetic code for this antigen marker is placed on a short arm of the sixth chromosome in humans. Patients with marker have an increased chance of developing rheumatoid arthritis due to those who do not do so. However, the presence of marker does not guarantee the onset of rheumatoid arthritis. Scientists believe that the brand indicates only genetic predisposition.
Cigarette smoking will double the risk of developing the pathophysiology of rheumatoid arthritis. Patients who have been smoking for more than 25 years have a triple increase in the likelihood of rheumatoid arthritis with the development of bone erosion. The use of tobacco increases the number of white blood cells and the level of circulating blood antibodies, a rheumatoid factor. The connection between smoking and RA is stronger in men than women.
undoubtedly immune cells and cell -lined cells convey chronic inflammatory inflammation of revMatoid arthritis. White blood cells flow into the joints and cause pain, swelling, heat and redness. Cells also release chemical mediators, including cytokines, antibodies, interleukins and tumor necrosis (TNF), which promote scarring and destruction of joint lining and cartilage. In the late stages of the bone, it erodes and disrupts the joint. Cytokines also produce pathophysiology of rheumatoid arthritis of the whole body such as muscle pain, weight loss and fever.