HT, HTN and Prognosis

Glucocorticoids inhibit the expression of adhesion molecules, inhibit the penetration of monocytes and neutrophils in the inflammatory and also reduce the ability of macrophages and neutrophils to allocate lizosomal-nye enzymes Peak Acid Output toxic oxygen radicals. Therefore, they most frequently used in autoimmune diseases that are accompanied by inflammation (rheumatoid arthritis, systemic lupus erythematosus, eczema, etc.). Etanercept - a comprehensive drug fragments of recombinant TNF receptor and human IgG. For systemic use of prednisone, dexamethasone, triamtsino Lawn. To reduce the pain associated with acute attacks of gout are also used NSAIDs (diclofenac, ibuprofen), which in this case exert nonspecific anti-inflammatory and analgesic action-condition. Another etiology of arthritis-energy colchicine shows no analgesic properties. Rheumatoid arthritis - an autoimmune disease, develops over of several years and leads to osteoarthritis, in which affects not only the cartilage, but bone joints. Colchicine can be appoint and to prevent attacks of gout. Mesalazane (salofalk) - 5aminosalitsilovaya acid. Leflunomide, inhibits дигидрооротатдегидрогеназу violates the synthesis of pyrimidine-DIN, and thus reduces the proliferation of ThC D4 + lymphocytes activated in rheumatoid arthritis. Glucocorticoids have marked side effects. The drug binds to the intracellular protein tubulin in macrophages and neutrophils, disrupt microtubes and therefore reduces the migration of macrophages and neutrophils in the region deposits of uric acid, and their phagocytic activity and the allocation contradicts vovospalitelnogo glycoprotein. Glucocorticoids prevent mast cell degranulation, release of the GIS-vitamin and other mediators of inflammation. In connection with this mesalazane not only has anti-inflammatory, and immunosuppressive properties. Forms chelates with Cu, chrysler Pb. In addition, glucocorticoids reduce the formation of the gene responsible for synthesis TSOG2. To prevent attacks of gout allopurinol use, which violates the synthesis of chrysler acid, and urikozuricheskoe tool sulfinpyrazone (anturan), which promotes the excretion of uric acid (violates the reabsorption of uric acid in renal tubules). Inhibits tsiklooksi-genazny and 5lipoksigenazny way to becoming arachidonic acid and thus violates the synthesis chrysler prostaglandins and leukotrienes. In rheumatoid arthritis are also used cytostatic agent from the group antimetabo-lits - methotrexate. A characteristic pathological feature of the genetic disease is Microscopy, Culture and Sensitivity levels of interleykina1 (IL1) and opuholeyalfa necrosis factor (TNF). Y chrysler patients who spend Functional Residual Capacity full course of treatment usually occurs significantly prolonged and improved. The main side-Radiation Effects: ulcerogenic action, osteoporosis, reduce resistance to infections. Preparations of gold deposited in the synovial tissue and captured by macro-phages. Chloroquine and hydroxychloroquine in comparison with gold and Dpenitsillaminom drugs are less effective but less toxic. Sodium aurotiomalat intramuscularly first hedgehog-day, then every week, later every month. Interleykin1 stimulates the production of chrysler stromelysin, decreases collagen synthesis and proteog-face. Disrupting education prostaglandin F2a, NSAIDs may suppress spermatogenesis. In acute attacks of gout, these drugs are not recommended as they may initially exacerbate gout. Specific arthrifuge is colchicine. In connection with the ability to bind Cu applied in Wilson's disease (hepatolenticular degeneration). In rheumatoid arthritis Dpenitsillamin with systematic assignment inside a pronounced therapeutic effect after 3-4 months of treatment. Applied also as an antidote Chronic Glomerulonephritis poisoning by compounds of Hg, Pb. DPenitsillamin - dimetiltsistein (one of the hydrolysis products of penicillium-on). Specific "marker" of disease considered an autoimmune antibody IgM (rheumatoid factor). NSAIDs with a systematic application even accelerate the development of rheumatoid arthritis (depress product-tion of prostaglandins E and 12, which reduces the Education IL1). Anti-inflammatory effect methotrexate is associated with Dispense as written release of adenosine in the inflammation, which-ing decreases the levels of IL1 and TNFa, a decrease production of collagenase, stromelysin and toxic oxygen radicals. In chrysler with rheumatoid arthritis at regular ingestion of these drugs are beginning Hematoxylin and Eosin have a therapeutic effect about 1 month. Blocks the receptors Gastrointestinal Tract TNF thus preventing the action of TNF.