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CC finals readings > URIC ACID > Flashcards

URIC ACID Flashcards

1
Q

product of catabolism of the purine nucleic acids. Although it is filtered by the glomerulus and secreted by the distal tubules into the urine, most uric acid is reabsorbed in the proximal tubules and reused

A

Uric acid

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2
Q

Uric acid is relatively insoluble in plasma and, at high concentrations, can be deposited in the

A

joints and tissue, causing painful inflammation

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3
Q

Purines, such as

A

adenine and guanine

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4
Q

such as adenine and guanine from the breakdown of ingested nucleic acids or from tissue destruction, are converted into uric acid, primarily in the liver.

A

Purines

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5
Q

Uric acid is transported in the plasma from the liver to the kidney, where it is filtered by the

A

glomerulus

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6
Q

98% to 100% of the uric acid from the glomerular filtrate occurs in the proximal tubules

A

Reabsorption

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7
Q

Renal excretion accounts for about 70% of uric acid elimination; the remainder passes into the

A

GI tract and is degraded by bacterial enzymes

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8
Q

Nearly all of the uric acid in plasma is present as

A

monosodium urate

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9
Q

At the pH of plasma (pH ~ __), urate is relatively insoluble; at concentrations greater than 6.8 mg/dL, the plasma is saturated

A

7

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10
Q

may form and precipitate in the tissues

A

urate crystals

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11
Q

In acidic urine (pH < ____), uric acid is the predominant species and uric acid crystals may form.

A

5.75

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12
Q

Uric acid is measured to confirm diagnosis and monitor treatment of _____, to prevent uric acid nephropathy during chemotherapeutic treatment, to assess inherited disorders of purine metabolism, to detect kidney dysfunction, and to assist in the diagnosis of renal calculi.

A

gout

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13
Q

based on the oxidation of uric acid in a protein-free filtrate, with subsequent reduction of phosphotungstic acid in alkaline solution to tungsten blue

A

Caraway method

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14
Q

Caraway method method lacks

A

specificity

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15
Q

the enzyme that catalyzes the oxidation of uric acid to allantoin, are more specific and are used almost
exclusively in clinical laboratories. The simplest of these methods measures the differential absorption of uric acid and allantoin at 293 nm.21 The difference in absorbance before and after incubation with uricase is proportional to the uric acid concentration

A

Methods using uricase (urate oxidase, EC 1.7.3.3)

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16
Q

can cause high background absorbance, reducing sensitivity

A

Proteins

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17
Q

can cause negative interference

A

hemoglobin and xanthine

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18
Q

measure the hydrogen peroxide produced as uric acid is converted to allantoin

A

Coupled enzyme methods

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19
Q

used to catalyze a chemical indicator reaction. The color produced is proportional to the quantity of uric acid in the specimen

A

Peroxidase or catalase (EC 1.11.1.6)

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20
Q

this kind have been adapted for use on traditional wet chemistry analyzers and for dry chemistry slide analyzers

A

Enzymatic methods

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21
Q

which destroy peroxide, if present in sufficient quantity, can interfere

A

Bilirubin and ascorbic acid

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22
Q

Commercial reagent preparations often include
___________________________________ to minimize these interferences

A

potassium ferricyanide and ascorbate oxidase

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23
Q

typically using UV detection, have been developed

A

HPLC (high-performance liquid chromatography)

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24
Q

Uric acid may be measured in

A

heparinized plasma, serum, or urine

25
Q

should be removed from cells as quickly as possible to prevent dilution by intracellular contents

A

Serum

26
Q

may affect uric acid concentration overall, but a recent meal has no significant effect and a fasting specimen is unnecessary

A

Diet

27
Q

should be avoided

A

Gross lipemia

28
Q

may falsely decrease results obtained by peroxidase methods

A

High bilirubin concentration

29
Q

with concomitant glutathione release, may result in low values

A

Significant hemolysis

30
Q

shown to increase values for uric acid

A

Drugs such as salicylates and thiazides

31
Q

after red blood cells have been removed

A

Uric acid is stable in plasma or serum

32
Q

Serum samples may be stored refrigerated for _____days

A

3 to 5

33
Q

should not be used for specimens that will be tested by a uricase method

A

Ethylenediaminetetraacetic acid (EDTA) or fluoride additives

34
Q

Urine collections must be

A

alkaline (pH 8)

35
Q

expressed in conventional units of milligrams per deciliter can be converted to SI units using the molecular mass of uric acid (168 g/mol)

A

Results

36
Q

Abnormally increased plasma uric acid concentration is found in

A

gout,
increased catabolism of nucleic acids, and
renal disease

37
Q

disease found primarily in men and is usually first diagnosed between 30 and 50 years of age. Affected individuals have pain and inflammation of the joints caused by precipitation of sodium urates.

A

Gout

38
Q

result of overproduction of uric acid, although may be exacerbated by a purine-rich diet, drugs, and alcohol.

A

hyperuricemia

39
Q

In women, urate concentration rises after

A

menopause

40
Q

may develop hyperuricemia and gout. In severe cases, deposits of crystalline uric acid and urates called tophi form in tissue, causing deformities

A

Postmenopausal women

41
Q

Another common cause of elevated plasma uric acid concentration is increased metabolism of cell nuclei, as occurs in patients on chemotherapy for such proliferative diseases as

A

leukemia, lymphoma, multiple myeloma, and polycythemia

42
Q

which inhibits xanthine oxidase (EC 1.1.3.22), an enzyme in the uric acid synthesis pathway, is used for treatment

A

Allopurinol

43
Q

may exhibit elevated uric acid concentration

A

Patients with hemolytic or megaloblastic anemia

44
Q

Increased urate concentrations may be found following ingestion of a _____________________________________ or as a result of increased tissue catabolism due to inadequate dietary intake (starvation)

A

diet rich in purines (e.g., liver, kidney, sweetbreads, and shellfish)

45
Q

associated with significant increases in physiological uric acid concentrations

A

Inherited disorders of purine metabolism

46
Q

X-linked genetic disorder (seen only in males) caused by the complete deficiency of hypoxanthine–guanine phosphoribosyltransferase (EC 2.4.2.8), an
important enzyme in the biosynthesis of purines

A

Lesch-Nyhan syndrome

47
Q

Mutations in the first enzyme in the purine synthesis pathway, phosphoribosylpyrophosphate synthetase (EC 2.7.6.1), also cause

A

elevated uric acid concentration

48
Q

produced in excess and compete with urate for renal excretion in these diseases

A

Metabolites such as lactate and triglycerides

49
Q

Hyperuricemia as a result of decreased uric acid excretion is a common feature of

A

toxemia of pregnancy (preeclampsia) and lactic acidosis

50
Q

causes elevated uric acid concentration because filtration and secretion are impaired

A

Chronic renal disease

51
Q

formation of kidney stones (renal calculi), may occur due to a variety of predisposing factors and conditions

A

Uric acid nephrolithiasis

52
Q

In acidic urine, the relatively insoluble uric acid precipitates to form calculi, which can cause

A

intense flank pain

53
Q

may be dissolved by alkalinization of the urine or treated by increased fluid intake and administration of xanthine oxidase inhibitors to reduce uric acid production

A

stones

54
Q

less common than hyperuricemia and is usually secondary to severe liver disease or defective tubular reabsorption, as in Fanconi syndrome (a disorder of reabsorption in the proximal convoluted tubules of the kidney)

A

Hypouricemia

55
Q

Decreased plasma uric acid can be caused by chemotherapy with 6- mercaptopurine or azathioprine, inhibitors of de novo purine synthesis, and as a result of overtreatment with allopurinol. Some studies have shown an association between low uric acid concentrations and neurodegenerative conditions such as

A

Alzheimer’s and Parkinson’s diseases

56
Q

Decreased uric acid Concentration

A

Liver disease
Defective tubular reabsorption (Fanconi syndrome)
Chemotherapy with azathioprine or 6-mercaptopurine
Overtreatment with allopurinol

57
Q

increased uric acid Concentration

A

Gout
Treatment of myeloproliferative disease with cytotoxic
drugs
Hemolytic and proliferative processes
Purine-rich diet
Increased tissue catabolism or starvation
Enzyme deficiencies
Lesch-Nyhan syndrome (hypoxanthine guanine phosphoribosyltransferase deficiency)
Phosphoribosylpyrophosphate synthetase deficiency
Glycogen storage disease type I (glucose-6-phos-
phatase deficiency)
Fructose intolerance (fructose-1-phosphate aldolase deficiency)
Toxemia of pregnancy
Lactic acidosis
Chronic renal disease
Drugs and poisons

58
Q
A

Lesch-Nyhan syndrome (hypoxanthine guanine phosphoribosyltransferase deficiency)
Phosphoribosylpyrophosphate synthetase deficiency
Glycogen storage disease type I (glucose-6-phosphatase deficiency)

CC finals readings (16 decks)

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