Arthritis Research Paper Arthritis is a Essay

Arthritis Essay, Research Paper

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Arthritis is a general term for about 100 diseases that produce either INFLAMMATION of connective tissues, peculiarly in articulations, or noninflammatory devolution of these tissues - Arthritis Research Paper Arthritis is a Essay introduction. The word means “ joint redness, ” but because other constructions are besides affected, the diseases are frequently called connective tissue diseases. The footings rheumatism and arthritic diseases are besides used. Besides conditions so named, the diseases include urarthritis, lupus erythematosus, ancylosing spondylitis, degenerative articulation disease, and many others, among them the more late identified LYME DISEASE. Causes of these upsets include immune-system reactions and the wear and tear of aging, while research indicates that the nervous system may frequently be every bit involved. About one out of seven Americans exhibit some signifier of arthritis. INFLAMMATORY CONNECTIVE TISSUE DISEASES This varied group of diseases green goodss redness in the connective tissues, peculiarly in the articulations. The marks of redness & # 8211 ; heat, inflammation, swelling, and hurting & # 8211 ; may be evident. Microscopic scrutiny of the lesions reveals outstanding blood vass, unnatural accretions of white blood cells, and changing grades of lesion mending with marking. In some diseases, the redness is clearly an immune reaction, the organic structure & # 8217 ; s defence against occupying micro-organism. In others, the cause is different or unknown. Infectious Arthritis This disease is most common in immature grownups. Infection in a joint is normally caused by bacteriums or other micro-organisms that invade the articulation from its blood vass. Within hours or a few yearss the joint, normally the articulatio genus or cubitus, becomes inflamed. There is an unnatural accretion of synovial, or joint, fluid, which may be cloudy and incorporate big Numberss of white blood cells. Gonococcal arthritis, a complication of gonorrhoea, is the most common signifier of infective arthritis. Treatment with antibiotics and aspiration of synovial fluid is normally quickly effectual, and merely minor residuary harm is done to the joint. Occasionally the infection is prolonged and produces joint devastation and requires surgery. Arthritic Fever This is a signifier of infective arthritis caused by haemolytic streptococci, a bacteria. Unlike typical infective arthritis, nevertheless, the disease is most common in kids aged 5 to 15 old ages, begins hebdomads after the oncoming of the streptococcic infection, and streptococcuss can non be isolated from the joint fluid. The inflammatory procedure may affect the bosom and bring forth arthritic bosom disease. The symptoms of RHEUMATIC FEVER normally occur 2 to 3 hebdomads after the oncoming of a terrible streptococcic sore pharynx. Acute hurting and swelling “ migrate ” from joint to joint over a period of several yearss. The redness, which persists for less than three months, can normally be controlled by acetylsalicylic acid and remainder, and it produces no residuary malformation. Less than 1 per centum of kids with streptococcic sore pharynxs develop arthritic febrility, and a little figure of these will develop arthritic bosom disease. Arthritic febrility merely seldom occurs if the streptococcic sore pharynx is treated early with an antibiotic such as penicillin. The redness of the articulations and the bosom in arthritic febrility seemingly occurs because the organic structure & # 8217 ; s immune response to the streptococci amendss tissues. For this ground, arthritic febrility has been termed an autoimmune disease. Gout and Pseudogout The inflammatory procedure in these diseases is unrelated to infection. Rather, redness is incited by the deposition in the articulation of uric acerb nowadays in the blood stream. An onslaught of acute gouty arthritis is caused by the formation of acuate crystals of the deposited uric acid. When these crystals are ingested by white blood cells, the cells release enzymes that evoke rednesss. Uric acid is a normal breakdown merchandise of urine metamorphosis. Abnormally elevated blood degrees of uric acid, which are associated with gouty arthritis, arise through either inordinate production of uric acid or decreased elimination of uric acid by the kidneys. Some instances of hyperuricemia and urarthritis are caused by known specific enzymatic defects. Many are associated with metabolic changes that occur in fleshiness. When extreme, the gouty procedure consequences in big sedimentations of uric acid, or chalkstone, around articulations. Acute onslaughts subside when the patient receives anti-inflammatory drugs. Further onslaughts may be prevented by colchicine, a drug that inhibits the consumption of crystals by white blood cells. Serum uric acid degrees decline and tophi decide when the extra uric acid production is controlled by weight decrease and by drugs such as Zyloprim, a purine parallel that inhibits both formation of purines and their dislocation to uric acid. The disease normally affects work forces over age 40. The symptoms of pseudogout may mime GOUT, but the redness is initiated by crystals of Ca pyrophosphate. They can be distinguished from uric acid crystals by polarisation microscopy. The disease is treated with anti-inflammatory drugs. Rheumatoid Arthritis The symptoms of arthritic arthritis are attributable to redness of the connective tissues, but the cause is unknown. The major disablement produced by rheumatoid arthritis has prompted a world-wide plan of research devoted to happening its cause and remedy. In arthritic arthritis, the synovial membranes, or interior liners of the joint capsules, are inveterate inflamed. The synovial mass proliferates and thereby destroys gristle, bone, and next constructions. The widespread inflammatory procedure besides involves other tissue such as blood vass, tegument, nervousnesss, musculuss, bosom, and lungs. The consequence is painful articulations, loss of mobility, and generalized tenderness and depression. Rheumatoid arthritis is preponderantly a disease of adult females between the ages of 20 and 60. Probably many persons have such a mild signifier of the disease that they ne’er seek medical attention. The typical patient with freshly diagnosed rheumatoid arthritis is a 35-year-old adult female who has been kicking for months of generalised achings and stiffness, peculiarly in her custodies and fingers, for an hr after originating ; swelling and hurting in fingers, custodies, carpuss, and elbows ; straitening weariness in the early afternoon ; and trouble in kiping. The affected articulations a

re tender. The fingers have a sausage-like appearance because of swelling at the proximal interphalangeal joints. The wrists, too, are swollen by overgrowth of synovium, and there are rheumatoid nodules at the elbows. Laboratory studies of the blood may reveal the presence of rheumatoid factors, proteins produced by the immune system in response to the rheumatic process. Although rheumatoid arthritis may prove to be infectious, it is not a conventional contagious disease. The minor tendency for familial occurrence is probably attributable to genetic factors. Immunology, including autoimmunity, is clearly important. Rheumatoid factors (anti-antibodies) form immune complexes that incite inflammation, and lymphocyte accumulations in the body cause swelling of tissues, including synovia. Systemic LUPUS ERYTHEMATOSUS is about one-tenth as common as rheumatoid arthritis. It has an even stronger predilection for women, especially those in the child-bearing ages. It is characterized by inflammation of blood vessels and potential involvement of several tissues and organs, particularly the skin, joints, kidneys, lungs, heart, nervous system, and blood cells. Some patients are acutely affected with a febrile disease that is life threatening because of renal disease, nervous system disease, or accompanying infections. Most have a more indolent disease that produces moderate disability from nondeforming arthritis, skin eruptions, and fatigue. As in rheumatoid arthritis, the body seems to react against itself rather than against an invading microorganism. Anti-self antibodies react with intact blood cells, nuclear components, and blood-vessel walls. The complexes that form in the patient’s blood precipitate in basement membranes of skin, kidneys, and nervous system and thus cause inflammation. Juvenile rheumatoid arthritis usually begins by age 5 or in the early teens. In most cases, tests for rheumatoid factors are negative and the disease becomes inactive by age 15. Ankylosing SPONDYLITIS occurs more commonly in men than women; it affects the spine and sacroiliac joints in particular, with resultant fusion of vertebrae and immobility. Tests for rheumatoid factors are negative, and tests for the tissue antigen HLA B27 are usually positive. NONINFLAMMATORY CONNECTIVE TISSUE DISEASES The joints and other connective tissues can be involved by trauma, endocrine disorders, metabolic abnormalities, congenital deformities, and other disease processes. The most important one is degenerative joint disease (OSTEOARTHRITIS). Degenerative Joint Disease. This is the most common form of arthritis and affects virtually all older adults to one degree or another. Most have few, if any associated symptoms, and the disease is diagnosed only because X rays of the vertebrae show characteristic spurs or because the fingers are knobbed by bony proliferations (Heberden’s nodes) at the distal interphalangeal joints. In some the spurs encroach on nerves as they emerge from the spinal canal and produce nerve-root syndromes. In others, the malpositioned joints are a source of ligamentous strain and abnormal muscular tension. The result is pain that becomes worse as the day goes on. Occasionally a severe form of the disease affects the hips. The destructive process results in restricted mobility of the hip joints and disabling pain, and major surgery may be required. The destroyed tissue is removed and replaced by a new joint made of plastic, an operation that is usually dramatically effective. Degenerative processes affect the ligaments and intervertebral disks of the spine. If a disk slips out, the syndrome of herniated disk may ensue. This is common in middle-aged men and usually affects the lumbar vertebrae, producing nerve-root irritation and ligamentous strain with resultant low-back pain and neurological deficits. Unless the symptoms remit with rest and analgesics, the disk may need to be surgically removed. These degenerative processes are in part caused by wear and tear. They affect primarily weight-bearing joints and joints subject to trauma or to malpositioned anatomy. Joints damaged by other forms of arthritis are prone to later degenerative joint disease. Heberden’s nodes are more prominent in the right hand of right-handed individuals and in the fingers of typists. Traumas produce microfractures in the cartilage that lines the articulating surfaces exposing raw underlying bone. The bone cells then release enzymes that destroy the protein and polysaccharide components of bone. Frayed pieces of cartilage may be taken up by white blood cells and thus add an element of inflammation. TREATMENT OF ARTHRITIS Accurate diagnosis and proper treatment usually follow naturally from the history, physical exam, and laboratory tests and from consideration of the pathophysiologic mechanisms. Infectious arthritis usually responds dramatically to appropriate antibiotics. The noninfectious inflammatory diseases are treated with drugs that suppress inflammation. Many of these drugs, for example, aspirin, indomethacin, and ibuprofen, appear to work by inhibiting synthesis of prostaglandins that mediate inflammation. Although certain adrenal cortical steroids are powerful inhibitors of inflammation, toxic side effects limit their usefulness. Similarly, drugs that inhibit proliferation of cells in the inflammatory masses have potentially severe side effects. Drugs that inhibit undesirable inflammation may also inhibit desired inflammatory responses. A result is a high frequency of secondary infections. More specific therapy, for example, allopurinol and colchicine in gout, is dependent on knowledge of the precise biochemical mechanisms of disease pathogenesis. Researchers are also studying the use of drugs that act on the nervous system. Despite the wear-and-tear origin of degenerative joint disease, it, too, may respond well to so-called anti-inflammatory drugs. Perhaps they are primarily acting as analgesics (pain-killers), or they may act by decreasing the secondary inflammation that follows joint trauma. Franklin Mullinax Bibliography: Arthritis Foundation, Understanding Arthritis (1986); Kelley, William N., et al., eds., Textbook of Rheumatology, 2d ed., (1985); McCarty, Daniel F., ed., Arthritis and Allied Conditions, 11th ed. (1988); Moll, J. M. H., Rheumatology in Clinical Practice (1987).

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