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MT6317 CLIN CHEM 1 > U4 LEC: NPNs: URIC ACID (PT. 1) > Flashcards

U4 LEC: NPNs: URIC ACID (PT. 1) Flashcards

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1
Q

Product of catabolism of purine bases

A

Uric Acid

catabolism also happens in the liver

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2
Q

Purine bases

A

Adenine, Guanine

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3
Q

Readily filtered by?

A

glomerulus

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4
Q

Uric acid undergoes?

A

reabsorption and secretion

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5
Q

____% reabsorbed in the _________

A

98-100, proximal convoluted tubules

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6
Q

_____% excreted in the _________

A

<1%, distal tubules

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7
Q

Renal excretion

A

70%

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8
Q

GI excretion

A

30%

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9
Q

Relatively insoluble in plasma as _______ at _______

A

monosodium urate, pH 7.0

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10
Q

At what concentrations does plasma become saturated and may form urate crystals in the tissues?

A

> 6.8 mg/dL

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11
Q

At what pH does uric acid crystals form?

A

< 5.75 (acidic urine)

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12
Q

Where does monosodium urate crystals deposit into?

A

tissues and joints

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13
Q

Where do you see uric acid crystals in pH <5.75?

A

acidic urine

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14
Q

The accumulation of high concentrations of crystals is called?

A

Tophi

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15
Q

The inflammation after accumulation in joints and tissues is called?

A

gouty arthritis

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16
Q

Gout has _____ uric acid, saturated plasma

A

increased

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17
Q

Inflammation can also lead to?

A

edema (swelling / pamamanas due to liquid)

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18
Q

Method of reliving Gouty Arthritis

A

use 50-100mL syringe to aspirate synovial fluid from the knee

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19
Q

Clinical applications of Uric Acid

A
  • confirm diagnosis and monitor treatment of gout
  • assess and prevent uric acid nephropathy during chemotherapeutic management
  • assess inherited disorders of purine metabolism
  • detect kidney dysfunction
  • assist in the diagnosis of renal calculi
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20
Q

Clinical Application

Confirm diagnosis and monitor treatment of?

A

gout

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21
Q

This refers to uric acid in blood.

A

Monosodium urate

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22
Q

Clinical Application

Assess and prevent uric acid nephropathy during?

A

chemotherapeutic management

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23
Q

T/F: In chemotherapy, there is increase in the uric acid, and decreased WBC.

A

True

Cell lysis > kakalat nucleic acids > high purines

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24
Q

Clinical Application

Assess inherited disorders of?

A

purine metabolism

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25
Q

Clinical Application

Detect?

A

kidney dysfunction

98% is reabsorbed dapat by the kidneys so UA can be a marker

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26
Q

Clinical Application

Assist in the diagnosis of?

A

renal calculi

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27
Q

T/F: Uric acid can form renal calculis.

A

True

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28
Q

Most common kidney stone

A

Calcium Oxalate (CaOx)

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29
Q

Calcium Oxalate can be seen in conditions of?

A
  • Chronic UTI
  • Parahyperthyroidism (production of excessive calcium)
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30
Q

Hyperuricemia

A

> 6.0 mg/dL

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31
Q

Gout is present in males between?

A

30 to 50 yrs of age

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32
Q

Gout is present in females after?

A

menopausal

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33
Q

Normal value of UA

A

until 7.2

pero dapat daw di ka na umabot dito !

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34
Q

Food rich in purines

A
  • street foods (laman loob; liver, isaw)
  • beer
  • red meat
  • dark meat of fish
  • monggo
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35
Q

Pain and inflammation of joints are caused by?

A

precipitation of sodium urates

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36
Q

Hyperuricemia is seen in what percentage of patients?

A

25% to 30%

result of overproduction of uric acid

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37
Q

T/F: You can be hyperuricemic and not have gout.

A

True

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38
Q

Hyperuricemia can cause?

A

formation of renal calculi

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39
Q

Hyperuricemia can also cause?

A

increased nuclear breakdown

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40
Q

Increased nuclear breakdown

seen in patients undergoing chemotherapy for?

A
  • leukemia
  • lymphoma
  • multiple myeloma
  • polycythemia
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41
Q

Increased nuclear breakdown

UA monitoring is done to avoid?

A

nephrotoxicity and renal calculi

42
Q

Increased nuclear breakdown

Treatment

A

Allopurinol

43
Q

Increased nuclear breakdown

Allopurinol inhibits or attacks what enzyme?

A

Xanthine oxidase

44
Q

Increased nuclear breakdown

Xanthine Oxidase converts _______ to UA

A

Hypoxanthine and Xanthine

45
Q

Increased nuclear breakdown

can also cause?

A
  • Hemolytic/megaloblastic anemia
  • Purine-rich diet
46
Q

UA can also be used to detect?

A

kidney diseases (impaired filtration and secretion)

47
Q

T/F: With impaired filtration and secretion, Uric Acid may increase in the blood.

A

True

48
Q

T/F: Uric Acid is not a good indicator for renal function.

A

True

if problema is nasa distal = small amt lang ang nasa urine

49
Q

This syndrome is an X-linked genetic disorder.

A

Lesch-Nyhan Syndrome

50
Q

Lesch-Nyhan Syndrome

only seen in?

A

males (commonly in male children)

51
Q

Lesch-Nyhan Syndrome

Absolute/complete deficiency of?

A

Hypoxanthine-Guanine Phosphoribosyltransferase (HGPT)

52
Q

Lesch-Nyhan Syndrome

This enzyme is responsible for utilization of purine bases in the nucleotide salvage pathway.

A

Hypoxanthine-Guanine Phosphoribosyltransferase (HGPT)

53
Q

Lesch-Nyhan Syndrome

Lack of HGPT prevents reutilization of purine bases in the?

A

nucleotide salvage pathway

54
Q

Lesch-Nyhan Syndrome

Consequentially results in?

A

increased UA in plasma and urine

55
Q

Lesch-Nyhan Syndrome

Characteristics

A
  • deformities
  • neurologic symptoms
  • mental retardation
  • self mutilation
56
Q

Lesch-Nyhan Syndrome

____ purine synthesis, _______ degradation product

A

increasing

57
Q

Disease Correlation

A
  • mutations on Phosphoribosyl synthetase
  • Toxemia of pregnancy (preeclampsia)
  • Lactic acidosis
58
Q

Disease Correlation

Glycogen storage disorder

A

Type I (Von Gierke)

gluconeogenesis (nucleic acids to energy)

59
Q

Disease Correlation

Atrophy (tissues will eat theirselves)

A

Increased tissue catabolism or starvation

60
Q

Causes of Hyperuricemia

Decreased UA excretion

A
  • Preeclampsia
  • Lactic acidosis
61
Q

Causes of Hypouricemia

Secondary to?

A

severe liver disease

62
Q

Causes of Hypouricemia

Defective tubular reabsorption (tuloy tuloy ineexcrete, nasa ihi and di nabalik sa blood)

A

Fanconi Syndrome

63
Q

Causes of Hypouricemia

Chemotherapy with?

A
  • 6-mercatopurine
  • azathiopurine
64
Q

Causes of Hypouricemia

6-mercatopurine and azathiopurine inhibits?

A

de novo purine synthesis

65
Q

Causes of Hypouricemia

______ of Allopurinol

A

Overproduction

66
Q

Reference method for Uric Acid

A

Isotope dilution mass spectrometry (IDMS)

67
Q

Direct REDOX Method is called?

A

Caraway / Henry’s Method

68
Q

Caraway / Henry’s Method

Utilizes?

A

Phosphotungstic acid

69
Q

Caraway / Henry’s Method

Will produce?

A

Tungsten blue and allantoin

70
Q

Caraway / Henry’s Method

End product of purine metabolism in lower forms

A

Allantoin
(UA to Allantoin)

71
Q

Caraway / Henry’s Method

________ of Uric Acid in PFF

A

Oxidation

72
Q

Caraway / Henry’s Method

__________ of Phosphotungstic Acid

A

Reduction

73
Q

Caraway / Henry’s Method

False increaase

A
  • turbidity
  • aspirin and metabolite
  • acetaminophen
  • caffeine
  • theophylline
74
Q

Iron Reduction Method

Ferric iron will become?

A

ferrous iron

75
Q

Most common method for Uric Acid

A

Enzymatic Method

76
Q

Enzymatic Method

Utilizes what enzyme?

A

Uricase

77
Q

Uricase Method is also known as?

A

Blauch and Koch

78
Q

Uricase Method

Conversion of?

A

UA to Allantoin

79
Q

T/F: With the help of Uricase, the amount of UA is proprtional to converted amount of Allantoin

A

True

80
Q

Uricase Method

Measurement at?

A

290-293nm

81
Q

Uricase Method

more specific but proteins may cause?

A

high background absorbance

82
Q

Uricase Method

Negative interference due to?

A
  • Hemoglobin
  • Xanthine
83
Q

This refers to a colorimetric method.

A

Coupled Enzymatic Method

84
Q

Coupled Enzymatic Method

After conversion to Allantoin, utilizes?

A

H2O2 (Peroxide) and indicator dye to produce colored compound

85
Q

Coupled Enzymatic Method

These may destroy peroxide (wala masyado sasama sa colored compound), may lead to false decrease

A
  • Bilirubin
  • Ascorbic acid
86
Q

Coupled Enzymatic Method

Remedy for Peroxide

A

Addition of:
- Potassium ferricyanide
- Ascorbate oxidase

87
Q

IDMS

Detection of?

A

characteristic fragments after ionization

88
Q

IDMS

Quantification using?

A

isotopically labeled compound

89
Q

Specimen Requirements

A
  • heparinized plasma
  • serum
  • urine
90
Q

Specimen Requirements

may affect UA concentration

A

Diet

91
Q

T/F: Recent intake of food will not have a significant effect, hence, it is a non fasting test.

A

True

92
Q

Specimen Requirements

This should be avoided

A

Gross lipemia (turbidity causes interference)

93
Q

Specimen Requirements

May result to low values

A

Hemolysis with concomitant glutathione release

94
Q

Specimen Requirements

May increase UA values

A
  • Salicylates
  • Thiazides
95
Q

Specimen Requirements

Serum samples may be refrigerated for?

A

3 to 5 days

96
Q

Specimen Requirements

Anticoagulants that should not be used

A
  • EDTA
  • Sodium Fluoride

inhibits Uricase

97
Q

Specimen Requirements

Urine specimen

A

must be alkalinzed to pH 8(add chemicals)

98
Q

Conversion Factor

A

0.06

99
Q

Reference Values

Male

A

3.5-7.2 mg/dL (0.21-0.43 mmol/L)

100
Q

Reference Values

Female

A

2.6-6.0 mg/dL (0.16-0.36 mmol/L)

101
Q

Reference Values

Child

A

2.0-5.5 mg/dL (0.12-0.33 mmol/L)

102
Q

Reference Values

Adult, Urine 24 h

A

250-750 mg/d (1.5-4.4 mmol/d)

MT6317 CLIN CHEM 1 (11 decks)

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