gout(redirected from Chrystal synovitis)
Also found in: Dictionary, Thesaurus, Legal, Encyclopedia.
Causes and symptoms
Without treatment, acute attacks of gout usually last a few days or weeks. The symptoms then disappear completely until the next attack. As the disease progresses, the attacks tend to last longer and the intervals between attacks become shorter.
A definite diagnosis of gout is made by identifying needle-shaped sodium urate crystals in the synovial fluid aspirated from an affected joint. The crystals may be seen inside polymorphonuclear leukocytes. Acute gouty arthritis is an example of an acute inflammatory process. Serial serum uric acid levels are also monitored; levels consistently above 8 mg/100 ml are an abnormal finding.
goutA metabolic disorder characterised by increased uric acid in the blood and joints, resulting in recurring painful arthritis and renal dysfunction with deposits of uric acid in the urinary tract, which in some cases is caused by either of two X-linked enzymes.
One-half of cases present with the classic “podagra” which affects the metatarsophalangeal joint; up to 90% suffer podagra at some time during their disease. With time, the attacks become polyarticular. Gouty tophi accumulate on the ears and over joints. Patients with gout are at high risk of forming kidney stones, which, in extreme cases, can cause renal failure.
Alcoholism, hereditary defect of hypoxanthine-guanine phosphoribosyl transferase (HG-PRT), phosphoribosylpyrophosphate synthetase superactivity, obesity, hypertension, renal dysfunction, drugs; family history of gout is present in about half of cases.
Increased uric acid, often ≥ 410 µmol/L–US: 7.0 mg/ml, a level found in a significant minority of men (90% of gout occurs in men).
Crystals in joints, body fluids, tissues.
Colchicine, NSAIDs, corticosteroids.
Diet, allopurinol, sulfinpyrazone, salicylates.
goutOrthopedics A condition characterized by ↑ uric acid in the blood and joints, resulting in recurring painful arthritis, renal function and deposits of uric acid in the urinary tract, linked to 2 X-linked enzymes Risk factors Hereditary defects of HG-PRT–hypoxanthine-guanine phosphoribosyl transferase, obesity, weight gain, alcohol intake, HTN, renal dysfunction, drugs Lab ↑ uric acid, often ≥ 410 µmol/L–US: 7.0 mg/ml, a level found in a significant minority of ♂–90% of gout occurs in ♂ Diagnosis Crystals in joints, body fluids, tissues; family Hx of gout is present in ±1⁄2 of cases;1⁄2 present with the classic 'podagra'–1st metatarsophalangeal joint; up to 90% suffer podagra at some time during their disease Acute treatment Colchicine, NSAIDs, corticosteroids Interval Diet Chronic Allopurinol, sulfinpyrazone, salicylates. See Congenital gout, PseudoGout, Saturnine gout.
gout(gowt) [Fr. goute, fr L. gutta, a drop]
Most hyperuricemic people are asymptomatic between acute attacks. When an attack of acute gouty arthritis develops, it usually begins at night with moderate pain that increases in intensity to the point where no body position provides relief. Low-grade fever and joint inflammation (hot, exquisitely tender, dusky-red or cyanotic joints) may be present. See: illustration
Colchicine, nonsteroidal anti-inflammatory agents, or corticosteroids are used to treat acute gouty attacks. Long-term therapy aims at preventing hyperuricemia by giving uricosuric drugs such as probenecid, or xanthine oxidase inhibitors such as allopurinol. Patients with gout have a tendency to form uric acid kidney stones. The diet should be well balanced and devoid of purine-rich foods, e.g., anchovies, sardines, liver, kidneys, sweetbreads, lentils, beer, wine, and other alcoholic beverages, because these raise urate levels. Fluid intake should be encouraged.
During the acute phase, bedrest is prescribed for at least the first 24 hr, and affected joints are elevated, immobilized, and protected by a bed cradle. Analgesics are administered, and hot or cold packs applied, depending on which the patient finds most helpful. The patient is taught about these measures. Colchicine, nonsteroidal anti-inflammatory agents, prednisone, or other prescribed drugs are administered. Allopurinol may be prescribed as maintenance therapy after acute attacks to suppress uric acid formation and control uric acid levels, thus preventing future attacks. Patients should be warned to report adverse effects of allopurinol, e.g., drowsiness, dizziness, nausea, vomiting, urinary frequency, dermatitis. A low-purine diet is recommended. The importance of gradual weight reduction is explained if obesity, which places additional stress on painful joints, is a factor. If soft-tissue tophi are present, e.g., near joints in fingers, knees, or feet, the patient should wear soft clothing to cover these areas and should use meticulous skin care and sterile dressings to prevent infection of open lesions.
Surgery may be required to excise or drain infected or ulcerated tophi, to correct joint deformities, or to improve joint function. Even minor surgery may precipitate gouty attacks (usually within 24 to 96 hr after surgery); therefore, the patient should be instructed about this risk and medications administered as prescribed to prevent acute attacks. The goal of chronic management of gout is to maintain serum uric acid levels below 6 mg/dl. At these levels chronic complications of gout are limited.
abarticular goutPeriarticular gout.
saturnine goutLead gout.
goutAn acute inflammatory joint disorder (ARTHRITIS) caused by deposition of monosodium urate monohydrate crystals around joints, tendons and other tissues, especially the near joint of the big toe. This occurs when there is excess uric acid in the body, probably as a result of a genetic abnormality. There is excruciating pain and inflammation. Treatment is by non-steroidal anti-inflammatory drugs (NSAIDS), such as indomethacin (indometacin) or naproxen, used early and throughout the attack. Colchicine is also effective. Gout can be prevented by the use of allopurinol which lowers the levels of uric acid in the blood. See also GOUTY TOPHI.
Patient discussion about gout
Q. Is gout hereditary? My Mother has gout for a few years now. Is it hereditary? Does this mean I too will get it in the future?
If other members of your family have had gout, you’re more likely to develop it also, yet, just because someone in the family suffers from gout does not mean everyone in that family will have the disease. This risk varies from person to person.
for further reading , you can visit my blog :
Q. How is gout treated? After a lot of tests, my Doctor concluded that I have gout. What treatment should I expect? Is gout curable?
Colchicine is used to treat acute gout attack and usually begins working within few hours of taking it. Low doses of colchicine are also used to prevent attacks. These drugs are recommended for people who have had multiple attacks of gout, kidney stones due to uric acid, or tophi.
The goal of lowering the blood uric acid is to slowly dissolve deposits of uric acid in the joint.
Q. what is the connection between gout and drinking cokes? There was an article in your magazine earlier this year about how drinking cokes could affect gout....can I get a copy of that artical?
This is because soft drinks contain large quantities of high-fructose corn syrup (HFCS), a common sweetener in soft drinks, which results in Hyperuricemia in blood.
Hyperuricemia, in turn predispose the body for gout.
(taken from : http://en.wikipedia.org/wiki/Gout )