Uric Acid Test PDF

 Uric acid is the end product of 1. purine metabolism in the liver, (adenine and guanine) is present in RNA and DNA. 2. a high turnover of nucleoproteins(purine, pyrimidine) in the bone marrow and GIT.  In plasma, uric acid is present as monosodium salt.  The pool of uric acid in the bod...

 Uric acid is the end product of 1. purine metabolism in the liver, (adenine and guanine) is present in RNA and DNA. 2. a high turnover of nucleoproteins(purine, pyrimidine) in the bone marrow and GIT.  In plasma, uric acid is present as monosodium salt.  The pool of uric acid in the body is about 1200 mg, out of which about half amount undergoes turnover daily, that is, about 600 mg/dl is formed daily, and about the same amount is lost. 90% about 25% are destroyed by bacteria in the colon. about 75% are exerted through urine Uric acid excretion from the body  Type of sample and precaution A random sample can be used. Serum/plasma is stable for 3 to 5 days at 4 °C. Precautions EDTA and fluoride cause positive interference with the uricase method. For a urine sample, collected 24 h sample. Do not refrigerate and add NaOH to keep urine alkaline. Severe exercise increases the level of uric acid. Indications This is done to diagnose gout. This test is also helpful in assessing recurrent urinary stone formation. This test is done in leukemic patients and renal failure To monitor some cancer treatments because rapid cell turnover from such treatment can increase uric acid levels. increased level of uric acid, that is due to: 1) Excessive cell breakdown. 2) catabolism of nucleic acid. 3) Failure to excrete as in renal failure.  The normal concentration of uric acid in serum is 3.5–7.2 mg/dL Average values are slightly higher in males. (lower in women by about 1 mg/dL).  The blood level of the uric acid depends upon: 1) The rate of synthesis in the liver. 2) The rate of excretion by the kidneys.  Hyperuricemia: 1. Acute and chronic nephritis Hypouricemia: 2. Urinary obstruction 1. Proximal renal damage. 3. High purine diet 2. Drugs such as (salicylates, 4. Diabetic ketoacidosis allopurinol) 5. Malignant tumors 3. Wilson disease 6. Several genetic inborn errors affect the 4. Fanconi syndrome breakdown of purines. 5. Acromegaly Lesch Nyhan syndrome (due to deficiency of 6. Celiac disease enzyme hypoxanthine-guanine phosphoribosyl transferase) The enzyme is responsible for 7. Xanthine oxidase recycling purines by converting guanine and deficiency. hypoxanthine into guanosine monophosphate and inosine monophosphate, respectively. Lack of the enzyme causes an increase in guanine and hypoxanthine, which eventually gets converted into uric acid. 7. Von Gierke disease leads to acidosis because lactate competes with urate excretion Kings’ Disease Gout is Kings’ disease a metabolic disease caused by the overproduction or under-excretion of uric acid. Due to  its poor solubility,  excess urate in the blood crystallizes and forms deposits in soft tissues such as  kidneys (causing nephropathy)  toes and joints (causing gouty arthritis). Allopurinol is used to treat gout due to its suicide inhibition effect on xanthine oxidase. Temperature-dependent precipitation of uric acid crystals in tissues at below normal temperature is believed to be the cause of gout Uric acid soluble in water, precipitated out as crystals when its concentration exceeds 80 mg/dl and the aqueous solution becomes supersaturated as follows: 1. in soft tissues causing gout 2. in the urethra causing stones 3. in the kidney causing nephron damage Diagnosis of gout 1. Increase of the uric acid level (In most cases, there is an increase in the uric acid level in the blood. This increase could be only present during attacks.) 2. Leukocytosis & increase of ESR (There is an increase in the number of WBCs in the blood and an increase of ESR as gout is an inflammatory process ) 3. Synovial fluid analysis (Needle shaped crystals) Crystals of urate in polarized light