Gout

Gout is characterized by the precipitation of monosodium in the tissue, usually in the joints and thereby forming a recurrent acute or chronic arthritis is most often caused paraartikulär. The acute arthritis initially displays usually a monartikuläres patterns and often affects the first metatarsophalangeal joint. The symptoms of gout include acute pain, tenderness, warmth, redness and swelling. Diagnosis requires the detection of crystals in the synovial fluid. The treatment of acute attacks carried out with anti-inflammatory drugs. The frequency of seizures may be reduced by the regular use of NSAIDs and / or colchicine, and by lowering the Serumuratspiegels of hyperuricemia with allopurinol, febuxostat or uricosuric drugs.

Gout is more common in men than in women. Usually, gout develops in middle-aged men and in women after menopause. Gout is rare in younger people, but is often more pronounced in people who develop the disease before age 30. Gout occurs to run in families. Patients with the metabolic syndrome have a high risk of gout.

Gout is characterized by the precipitation of monosodium in the tissue, usually in the joints and thereby forming a recurrent acute or chronic arthritis is most often caused paraartikulär. The acute arthritis initially displays usually a monartikuläres patterns and often affects the first metatarsophalangeal joint. The symptoms of gout include acute pain, tenderness, warmth, redness and swelling. Diagnosis requires the detection of crystals in the synovial fluid. The treatment of acute attacks carried out with anti-inflammatory drugs. The frequency of seizures may be reduced by the regular use of NSAIDs and / or colchicine, and by lowering the Serumuratspiegels of hyperuricemia with allopurinol, febuxostat or uricosuric drugs. Gout is more common in men than in women. Usually, gout develops in middle-aged men and in women after menopause. Gout is rare in younger people, but is often more pronounced in people who develop the disease before age 30. Gout occurs to run in families. Patients with the metabolic syndrome have a high risk of gout. Pathophysiology the extent and the longer the duration of the hyperuricemia is the greater, the greater is the probability of the emergence of gout. Uratwerte may be increased due to: decreased excretion (most common) increased production increased Purinaufnahme Why not develop all patients with elevated serum uric acid levels, a gout, is not known. A reduced renal excretion is the most common cause of hyperuricemia by far. It can be hereditary conditions and also occurs in patients with diuretic therapy and in patients suffering from diseases with reduced GFR on. Ethanol increases the Purinabbau in the liver and the formation of lactic acid, which blocks the Uratsekretion of the renal tubules, ethanol can also stimulate the Leberuratsynthese. Lead poisoning and which is used in higher doses most commonly in transplant medicine cyclosporine, which damage renal tubules irreversible and thus lead to a Uratretention. Elevated Uratproduktion may be caused by an increased Nukleoproteinumsatz system in hematological diseases (eg. As lymphoma, leukemia, hemolytic anemia) and in diseases with increased cell proliferation and cell death (eg., Psoriasis, cytotoxic chemotherapy, radiation therapy). An increased production of uric acid can also occur as a hereditary primary abnormality and obesity, because the Uuratproduktion correlated with the body surface. In most cases, the cause of Uratüberproduktion is unknown, in a few cases, they can be assigned to certain enzyme disorders. A deficiency of hypoxanthine-guanine phosphoribosyl transferase (the complete lack corresponds to the Lesch-Nyhan syndrome) is just as over-activity of phosphoribosyl pyrophosphate synthetase is a possible cause. The increased supply of purine-rich foods (such. As liver, kidney, anchovies, asparagus, consommé, herring, meat sauces and broths, mushrooms, mussels, sardines, sweetbreads) can contribute to hyperuricemia. Beer is particularly rich in guanosine, a purine nucleoside. A strict low purine diet, however, can reduce the serum uric acid levels by only 1 mg / dl. Urate precipitates in the form of needle-shaped monosodium that extracellularly (in avascular (z. B. in cartilage), or in poorly vascularized tissues (z. B. tendons, tendon sheaths, ligaments, bursae wall) as well as in the skin around the cooler distal joints and tissues z. B. ears) are deposited. In severe and prolonged hyperuricemia the sodium urate can be deposited in larger joints and parenchymal tissues such as the kidney. In the acidic environment of urine uric acid itself is precipitated rapidly in small plate-like or diamond-shaped uric acid crystals, which aggregate into grit or stones and so obstruct the flow of urine. Tophi are aggregates of monosodium, which usually develop in joints or as a node subcutaneous. They are usually wrapped in a fiber matrix which prevents them to cause acute inflammation. An acute gouty arthritis can by trauma, medical stress situations (eg. As pneumonia or other infections), surgical procedures, through the use of thiazide diuretics or drugs with uric acid-lowering effect (eg. As allopurinol, probenecid, nitroglycerin) or by overeating purine-rich food or alcohol are triggered. The attacks are often accompanied by a sudden rise or even more frequently by a decrease in serum uric acid levels. Why follow acute attacks on some of these triggering conditions is unknown. Tophi in and around joints can limit mobility and cause deformations that are called chronic tophaceous gouty arthritis. Chronic gout increases the risk of the development of secondary osteoarthritis. Symptoms and signs Acute gouty arthritis usually begins with a sudden onset of pain (often at night). The metatarsophalangeal joint of the big toe is most commonly affected (so-called. Gout), as well as front of the foot, ankle, knee, wrist and elbow are common sites. Rarely hip, shoulder, sacroiliac, sternoclavicular or the cervical spine are also affected. The pain is becoming stronger, usually over a few hours, and often reaches a nagging extent. Swelling, heat, redness and extreme tenderness reminiscent of an infection. The overlying skin is stretched over warm, translucent and red or purple. Fever, tachycardia, chills and malaise sometimes occur concomitantly. Gout in the first metatarsophalangeal joint with permission of the publisher. For Myers S .: Atlas of Rheumatology. Edited by G. Hunder. Philadelphia, Current Medicine, 2005. var model = {thumbnailUrl: ‘/-/media/manual/professional/images/gout_in_1st_metatarsophalangeal_joint_high_de.jpg?la=de&thn=0&mw=350’ imageUrl: ‘/ – / media / manual / professional / ? images / gout_in_1st_metatarsophalangeal_joint_high_de.jpg lang = en & thn = 0 ‘, title:’ gout in the first metatarsophalangeal joint ‘description:’ u003Ca id = “v37892793 ” class = “”anchor “” u003e u003c / a u003e u003cdiv class = “”para “” u003e u003cp u003ePodagra or acute pain in the first metatarsophalangeal joint

Health Life Media Team

Leave a Reply