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[MT 6317] Clinical Chemistry Laboratory > [2S] UNIT 9.2 Uric Acid Determination > Flashcards

[2S] UNIT 9.2 Uric Acid Determination Flashcards

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1
Q

One of the NPNs present in the bloodstream

A

Uric Acid

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2
Q

Organ in trouble when there is elevation of NPNs in the bloodstream

A

Kidneys

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3
Q

Only NPN that tells that the liver is in trouble if it is elevated in the bloodstream

A

Ammonia

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4
Q

Toxic byproduct that needs to be converted to urea for detoxification

A

Ammonia

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5
Q

Other NPNs circulating in the plasma

Not considered as waste product

A

Amino acids

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6
Q

Other NPNs circulating in the plasma

● Waste products
● Body needs to get rid of

A

Urea, Uric acid, Creatinine, Ammonia

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6
Q

End product of purine catabolism

A

Uric Acid

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7
Q

End product of protein catabolism

A

Urea

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8
Q

T/F: Urea is higher compared to creatinine

A

T

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9
Q

Precursor of uric acid

A

Xanthine

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10
Q

Where is uric acid produced?

A

Liver

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11
Q

Xanthine is acted upon by what enzyme and to be converted to?

A

○ Acted upon by Xanthine oxidase
○ To be converted to uric acid

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12
Q

It is a waste product

A

Uric Acid

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13
Q

Main product of the catabolism of exogenous (dietary) and endogenous purine nucleosides (Adenine and Guanine)

A

Uric Acid

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14
Q

T/F: Most uric acids are reabsorbed and 1% is excreted

A

T

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15
Q

T/F: Decrease in serum uric acid is common

A

F; uncommon

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16
Q

T/F: Although uric acid measurement may assess kidney function, uric acid is not as reliable as that of urea and creatinine.

A

T

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17
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

1st organ

A

Liver

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17
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

■ Cells that make up the lobules
■ It is where uric acid is produced

A

Hepatocytes

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18
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Functional unit of the liver

A

Lobules

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19
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Very vascular organ riched with blood vessels

A

Liver

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20
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

In the liver, ______ synthesize the uric acid

A

Hepatocytes

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21
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

travels in the bloodstream in order for them to be disposed properly

A

Hepatocytes

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22
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Urinary bladder → urethra (vary in size)

A

Inner Medulla

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22
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

This network of blood vessels are connected to the kidneys

A

Hepatocytes

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23
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

3rd site

A

Kidney (Outer Cortex)

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24
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Produce uric acid (waste product) → throw it in the _____

A

blood

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25
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Calyxes and Pelvis → Drains in the ureter and urinary bladder

A

Inner Medulla

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26
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Functional unit of kidney

A

Nephron

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27
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

T/F: We can live with only 1 nephron and 1 kidney

A

F; we cannot live with only 1 nephron

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28
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

Each kidney contains approximately 1 million to ____ nephrons

A

1.5 million

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29
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

● Found in medulla
● Contains blood vessel

A

Nephron

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30
Q

HOW IT TRAVELS FROM HEPATOCYTE TO KIDNEYS

● Part of nephron that acts as a filter
● Tuft of capillaries

A

Glomerulus

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31
Q

Why is it reabsorbed if it is a waste product?

A

It uses raw material for the synthesis of purines

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32
Q

If the physician is requesting for uric acid, it means he/she is suspecting that the patient has inflammatory condition in the joints

A

Gout

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33
Q

Effective Chemotherapy = ↑ uric acid _ plasma

A

↑

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33
Q

CHEMOTHERAPY

More cells destroyed _ uric acid

A

↑ (megalo & cancer)

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34
Q

● Men age 30-50 years old are more commonly affected
● Females: menopausal

A

Gout

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35
Q

● Decrease concentration of uric acid
● The cells that produces uric acid are destroyed

A

Liver Disease

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36
Q

● Decrease concentration of uric acid
● 90% of uric acid is reabsorbed in the proximal convoluted tubule
● There will be no reabsorption of uric acid

A

Renal / Tubular Failure

37
Q

Mixture of enzymatic and chemical method

A

Method of Determination

38
Q

Measure the reaction at an absorbance of _____

A

293 nm

38
Q

Historical method for the determination of uric acid

A

Conversion of uric acid to allantoin

39
Q

METHOD OF DETERMINATION

Decrease in absorbance is _____ proportional to the concentration of uric acid

A

directly

40
Q

Principle of the reagent used in the experiment:

Uric acid + O2 + 2 H2O2 → allantoin + CO2 + H2O2

A

Uricase

41
Q

In the presence of uricase, uric acid is converted to?

A

allantoin and hydrogen peroxide

41
Q

Principle of the reagent used in the experiment:

2 H2O2 + 4-AAP + EHSPT → quinoneimine + HCl + 4 H2

A

Peroxidase

42
Q

Under catalysis of peroxidase with amino-4-antipyrine (4-AAP) and EHSPT, hydrogen peroxide reacts to give a?

A

red-violet quinoneimine dye

43
Q

hasten the oxidation of uric acid to allantoin

A

Uricase

44
Q

Quinoneimine uses a light with a wavelength of ___
nm

A

540

44
Q

T/F: Concentration of quinoneimine (indicator) is directly proportional to uric acid

A

T

45
Q

T/F: ENZYMATIC ASSAYS ARE MORE SPECIFIC
THAN CHEMICAL ASSAYS

A

T

46
Q

BUA Main form in Plasma

A

Monosodium Urate

47
Q

Principle of Caraway Method

A

Reduction-Oxidation Reaction

48
Q

CLINICAL APPLICATIONS

T/F: Confirm diagnosis and monitor treatment of gout

A

T

49
Q

CLINICAL APPLICATIONS

T/F: Prevent uric acid nephropathy during chemotherapeutic treatment

A

T

50
Q

CLINICAL APPLICATIONS

T/F: Assist in the diagnosis of renal calculi

A

T

50
Q

CLINICAL APPLICATIONS

T/F: Assess inherited disorders of pyrimidine metabolism

A

F; purine

51
Q

CLINICAL APPLICATIONS

T/F: Detect liver dysfunction

A

F; kidney

52
Q

Based on reduction of phosphotungstic acid in alkaline solution to tungsten blue

A

CHEMICAL: Caraway

53
Q

In carbonate solution (Na2CO3/OH-):
uric acid + H3PW12O40 + O2 → allantoin + tungsten blue + CO2

A

CHEMICAL: Caraway

53
Q

Non-specific and requires protein removal

A

CHEMICAL: Caraway

54
Q

● Uses uricase enzyme to catalyze oxidation of uric acid to allantoin
● More specific and more commonly used

A

Enzymatic Methods

55
Q

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

A

ENZYMATIC: Coupled Enzymatic Reaction

56
Q

Color produced is directly proportional to uric acid
concentration

A

ENZYMATIC: Coupled Enzymatic Reaction

57
Q

2 Sources of error in coupled enzymatic reaction

A

Reducing Agents
- High bilirubin
- Ascorbic acid / Vit C

58
Q

Measures differentiation absorbance before and after incubation with uricase at 293 nm

A

ENZYMATIC: Spectrophotometric Assay

59
Q

Difference is directly proportional to uric acid
concentration

A

ENZYMATIC: Spectrophotometric Assay

60
Q

2 Sources of error in spectrophotometric assay

A

Presence of protein
Hemoglobin & Xanthine

61
Q

OTHER METHODS

Typically uses UV detection

A

High Performance Liquid Chromatography (HPLC)

61
Q

OTHER METHODS

● Proposed candidate reference method
● Detects characteristic fragments following ionization
● Quantifies uric acid using isotopically labeled compound

A

Isotope Dilution Mass Spectrometry (IDMS)

62
Q

Specimen used

A

Heparinized plasma, urine or serum

63
Q

T/F: Heparin inhibits uricase enzymes

A

F; EDTA & Fluoride

64
Q

Uric Acid Reagent Kit

A

Phosphate buffer (pH 7.0), EHSPT, Amino-4-antipyrine, Uricase, peroxidase, ferrocyanide, sodium azide

65
Q

ASSAY REQUIREMENTS

● Wavelength:
● Optical path:
● Temperature:
● Read against ________

A

546 nm
1 cm
37° C
reagent blank

66
Q

HYPER OR HYPOURICEMIA

Gout

A

Hyperuricemia

67
Q

HYPER OR HYPOURICEMIA

Treatment of myeloproliferative disease with cytotoxic drugs

A

Hyperuricemia

68
Q

HYPER OR HYPOURICEMIA

Hemolytic and proliferative
processes

A

Hyperuricemia

69
Q

HYPER OR HYPOURICEMIA

Purine-rich diet

A

Hyperuricemia

70
Q

HYPER OR HYPOURICEMIA

Toxemia of pregnancy

A

Hyperuricemia

71
Q

HYPER OR HYPOURICEMIA

Increased tissue catabolism or starvation

A

Hyperuricemia

72
Q

HYPER OR HYPOURICEMIA

Lactic acidosis

A

Hyperuricemia

73
Q

HYPER OR HYPOURICEMIA

Chronic renal disease

A

Hyperuricemia

74
Q

HYPER OR HYPOURICEMIA

Lesch-nyhan syndrome (hypoxanthine guanine phosphoribosyltransferase deficiency)

A

Hyperuricemia

74
Q

HYPER OR HYPOURICEMIA

Fructose intolerance (fructose-1-phosphate aldolase deficiency)

A

Hyperuricemia

74
Q

HYPER OR HYPOURICEMIA

Drugs and poisons

A

Hyperuricemia

75
Q

HYPER OR HYPOURICEMIA

Phosphoribosylpyrophosphate synthetase deficiency

A

Hyperuricemia

75
Q

HYPER OR HYPOURICEMIA

Liver disease

A

Hypouricemia

76
Q

HYPER OR HYPOURICEMIA

Glycogen storage disease type 1 (glucose-6-phosphate deficiency)

A

Hyperuricemia

77
Q

HYPER OR HYPOURICEMIA

Defective tubular reabsorption (Fanconi syndrome)

A

Hypouricemia

78
Q

HYPER OR HYPOURICEMIA

Chemotherapy with azathioprine or 6-mercaptopurine

A

Hypouricemia

79
Q

HYPER OR HYPOURICEMIA

Overtreatment with allopurinol

A

Hypouricemia

80
Q

CONCENTRATION OF STANDARD

Plasma / Serum

A

6 mg/dL

81
Q

CONCENTRATION OF STANDARD

Urine

A

88 mg/dL

82
Q

Conversion factor of mg to mmol/L

A

0.0595

83
Q

REFERENCE RANGE PLASMA / SERUM

Male

a. 3.5-7.2 mg/dL
b. 2.0-5.5 mg/dL
c. 2.6-6.0 mg/dL
d. 250-750 mg/day

A

a. 3.5-7.2 mg/dL

84
Q

REFERENCE RANGE PLASMA / SERUM

Female

a. 3.5-7.2 mg/dL
b. 2.0-5.5 mg/dL
c. 2.6-6.0 mg/dL
d. 250-750 mg/day

A

c. 2.6-6.0 mg/dL

85
Q

REFERENCE RANGE PLASMA / SERUM

Child

a. 3.5-7.2 mg/dL
b. 2.0-5.5 mg/dL
c. 2.6-6.0 mg/dL
d. 250-750 mg/day

A

b. 2.0-5.5 mg/dL

86
Q

REFERENCE RANGE

Urine 24h

A

250-750 mg/day

[MT 6317] Clinical Chemistry Laboratory (10 decks)

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