caused by the build up of uric acid in the joints‚ tissue deposition of uric acid crystals‚ and joint destruction if left untreated. Uric acid is a byproduct of purine metabolism. Lacking uricase‚ humans remove uric acid primarily by renal excretion. "Normally‚ uric acid dissolves in your blood and passes through your kidneys into your urine. But sometimes your body either produces too much uric acid or your kidneys excrete too little uric acid. When this happens‚ uric acid can build up‚ forming sharp
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anti-inflammatory drugs (ibuprofen and others)‚ and corticosteroids. Other medications decrease the level of uric acid in the blood and prevent the deposit of uric acid in joints (gouty arthritis)‚ the kidneys (stones)‚ and in tissue (tophi)‚ helping to prevent further attacks and complications. Gout is a type of arthritis caused by a buildup of uric acid crystals in the joints. Uric acid is a breakdown product of purines that are part of many foods we eat. Some people may develop chronic
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Fatima Khan Q: WHAT IS THE CLINICAL IMPORTANCE OF URIC ACID AND CREATININE? ANSWER: URIC ACID Uric acid is a weak organic acid‚ the end product of purine nucleotides degradation. The findings of human pathological levels of uric acid in serum and urine have in most patients serious clinical implications. Uric acid is a useful diagnostic tool as screening for most of purine metabolic disorders. The importance of uric acid measurement in plasma and urine with respect of metabolic disorders is
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Grand Canyon University Biology 100 Lecture Abstract Homeostatic imbalance is the disturbance of normal homeostasis in the body. This paper is on the disease of gout caused by a homeostatic imbalance. Due to the kidney’s inability to filter uric acid it starts to build up in the joints and cause pain‚ tenderness‚ redness‚ warmth and swelling in the joints. Gout usually attacks the joint of the big toe‚ but it can also attack the joints in the knees‚ ankles‚ feet‚ hands‚ wrists and elbows. Unfortunately
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analyzed for biochemical parameters such as serum urea‚ uric acid and electrolytes. Serum urea was measured using the commercially available kit (Liquicheck AGAPPE Diagnostics LTD)‚ following the GLDH-Urease method (Tietz‚ 1976). The amount of creatinine in serum was estimated using Liquicheck AGAPPE Diagnostics commercial kit according to Picrate method (Cook‚ 1975). Serum uric acid level was determined using commercially available Biosystems Uric acid kit by Uricase method (Fossati et al.‚ 1980). Estimation
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analyzed for biochemical parameters such as serum urea‚ uric acid and electrolytes.Serum urea was measured using the commercially available kit (Liquicheck AGAPPE Diagnostics LTD)‚ following the GLDH-Urease method (Tietz‚ 1976). The amount of creatinine in serum was estimated using Liquicheck AGAPPE Diagnostics commercial kit according to Picrate method (Cook‚ 1975). Serum uric acid level was determined using commercially available Biosystems Uric acid kit by Uricase method (Fossati et al.‚ 1980). Estimation
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Student Name: Dealon Rouse | Patient Initials: JB | Admission Diagnosis: Left Total Knee Arthroplasty &Excision of Left Knee Mass Related to Gouty Arthritis | Date(s) of Care: 11/10/11- 11/12/11 | Age: 46 | | Date of Admission: 11/10/11 | Gender: Male | | Marital Status: Married | Room #: 507 | Code Status: Full Code | Occupation: Electrician | Race: Hispanic | Isolation Type: | Religion: Roman Catholic | | Allergies: No Known Allergies | History of Present Illness:
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of hypoxanthine to xanthine to uric acid. At therapeutic concentrations it does not inhibit other enzymes involved in purine and pyrimidine synthesis. Its key pharmological action is that is reduces serum uric acid levels in the body. Uloric’s pharmacodynamic properties include a dose dependent decrease in 24-hour mean serum uric acid concentrations and an increase in 24-hour mean serum xanthine concentrations. In addition‚ it decreases daily urinary uric acid excretion and an increase in total
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electrolyte depletion such as hypokalemia. Less common side effects include jaundice‚ ringing in the ears (tinnitus)‚ sensitivity to light (photophobia)‚ rash‚ pancreatitis‚ nausea‚ diarrhea‚ abdominal pain‚ and dizziness. Increased blood sugar and uric acid levels also may occur. When hypertonic fluids are infused‚ osmosis pulls water out of the cells and causes the cells to shrink resulting cells to get rid of excessive free water. The side effect includes‚ when they shrink at the site of IV
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purine salvage pathway. Mutation in the HPRT gene are manifested at varying degrees of expressivity. For example‚ in men with 20% HPRT deficiency‚ hyperuricemia is a common result. This leads to high levels of uric acid in the blood‚ which causes gouty arthritis and/or the formation of uric acid stone in the urinary tract. Collectively‚ these symptoms categorize Kelly-Seegmiller syndrome. Female carriers of the disease are at increased risk for gouty arthritis. LNS can also cause deleyed growth and
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