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CC1 LECTURE DEAN > URIC ACID AND AMMONIA > Flashcards

URIC ACID AND AMMONIA Flashcards

1
Q

waste product normally formed in the body

A
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2
Q

major product of the catabolism of purine nucleosides:

A

adenosine & guanosine

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3
Q

Intermediate:

A

Xanthine

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4
Q

The bulk of purines ultimately excreted as uric acid in the urine arises from degradation of [?]

A

endogenous nucleic acids

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5
Q

released inside the body

A

endogenous

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6
Q

can be reused or recycled to form new nuceotides

A

purines

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7
Q

Reutilization of the major purine bases (?) is achieved through “salvage” pathways

A

adenine, hypoxanthine and guanine

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8
Q

[?] of the free bases causes re-synthesis of the respective nucleotide monophosphates

A

Phosphoribosylation

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9
Q

[?] - present as insoluble mosodium urate crystals

A

96.8% of uric acid in plasma

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10
Q

% is excreted through the urine

A

75%

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11
Q

Bacterial degradation in GIT:

A

allantoin and other compounds

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12
Q

RENAL HANDLING of URIC ACID

A
  1. Glomerular filtration
  2. Reabsorption at the pct
  3. Active secretion
  4. Reabsorption at the dct
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13
Q

Net excretion:

A

10%

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14
Q

FACTORS AFFECTING BUA LEVEL

  1. Diet: [?]
  2. Age & gender: increase w/ [?]; higher in [?] (gouty arthritis)
  3. 2x greater concentration in [?] than in plasma
  4. Avoid the use of [?] because it forms salts that cause turbidity
  5. UA is stable in [?] for several days at RT and longer at ref. temp.
  6. [/] increases its stability
A

legumes, seeds, internal organs
age; males
RBC
K oxalate
serum
Thymol

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15
Q

measures uric acid as an intact molecule

A

DIRECT METHOD: Phosphotungstic Acid (PTA)

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16
Q
  • oxidizing agent
  • reducing agent
A

Phosphotungstic Acid - oxidizing agent
Uric acid - reducing agent

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17
Q

degraded to form allantoin and CO2

A

DIRECT METHOD: Phosphotungstic Acid (PTA)

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18
Q

PTA is converted to tungsten blue (colorimetric)

A

DIRECT METHOD: Phosphotungstic Acid (PTA)

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19
Q

DIRECT METHOD: Phosphotungstic Acid (PTA) INTERFERENCES
1. Endogenous:
2. Exogenous:

A

glucose, ascorbic acid, glutathione, ergothionine cysteine (from hemolysis)
acetaminophen (paracetamol), aspirin (anti-cancer), gentisic acid, caffeine, theobromine, theophylline

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20
Q

The decrease in the UA concentration is determined by measuring the absorbance in the range of 290 – 300 nm (UV light)

A

A. Blaunch and Koch (UV test with uricase)

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21
Q

Trinder – Uricase method
Reduced chromogens:

A

DHBS: 3,5 – dichloro – 2- dihydroxy benzene sulfonic acid
PAP: 4 – aminophenazone

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22
Q

Trinder – Uricase method
Enzymes:

A

Oxidase or Uricase
Peroxidase

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23
Q

Trinder – Uricase method
End-product:

A

Quinoneimine (pink)

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24
Q

Uricase – catalase system

Formaldehyde + Acetyleacetone -
Formaldehyde + PAP -

A

yellow lutidine
trinder pink compound

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25
Q

Bittner method

Two sample measurements:
First:
Second:

A

treated with uricase to destroy uric acid
uricase is absent - Difference represents true UA

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26
Q

TPTZ Method by Morin
TPTZ :

A

2,4,6- tripyridyl – 5 – triazine

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27
Q

Amperometric Principle:

A

Polarographic method

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28
Q

HYPERURICEMIA Increased Formation Primary

A
  • Idiopathic: unknown cause
  • Inherited metabolic disorders: Lesch-Nyhan Syndrome
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29
Q

HYPERURICEMIA Increased Formation Secondary

A
  • Excess dietary purine intake
  • Increased nuclear breakdown (e.g. Leukemia high in lymphoblasts)
  • Psoriasis
  • Altered ATP metabolism
  • Tissue hypoxia
  • Pre-eclampsia
  • Alcohol
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30
Q

HYPERURICEMIA Decreased Excretion Primary

A
  • Idiopathic
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31
Q

HYPERURICEMIA Decreased Excretion Secondary

A
  • Renal failure
  • Drug therapy: salicylate/aspirin (promote circulation/prevent clotting)
  • Poisons: heavy metal
  • Pre-eclampsia
  • Organicacids
  • Trisomy21 (Down syndrome )
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32
Q

: x-linked genetic disorder (female carrier but does not express the trait – the male offspring will)

A

Lesch-Nyhan syndrome

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33
Q

deficiency of the enzyme, Hypoxanthineguaninephosphoribosyl transferase (muricase)

A

Lesch-Nyhan syndrome

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34
Q

Lesch-Nyhan syndrome symptoms

A

Delayed motor development
Self-destructive behavior (chewing off fingertips and lips)
Gout - like swelling
Kidney and bladder stones

35
Q

: prevents reutilization of purine bases in the nucleotide salvage pathway

A

Abnormal phosphoribosyl pyroPO4 synthetase

36
Q

: monosodium urate precipitates from supersaturated body fluids

A

GOUT

37
Q

CLASSIFICATION OF GOUT

A

Gouty arthritis
Gout nephropathy
Acute intradeposition of urate cyrstals
Urate nephrolithiasis

38
Q
  • urate crystals in joint fluids (precipitate fluids: tophi)
A

Gouty arthritis

39
Q
  • swelling and painful joints; affecting the joints (big toe) and fingers
A

Gouty arthritis

40
Q

HYPOURICEMIA
[?] - reduction in signs of organ

A

Atrophy of the liver

41
Q

Reference Interval (uricase method)
Female

Male

Conversion factor:

A

2.6-6.0 mg/dL

3.5-7.2 mg/dL

0.059

42
Q

chemical cpd of ammonia

A

NH2CHCOOH

43
Q

from [?] thru the action of digestive and bacterial enzymes on proteins in the GIT

A

deamination of amino acids

44
Q

used in the liver for

A

urea production

45
Q

plasma level in circulation is extremely low (?)

A

15 – 45 µg/dL

46
Q

increased in concentration in the blood in cases of

A

severe liver damage

47
Q

most ammonia in the blood exists as

A

ammonium ion

48
Q

concentration is not dependent on

A

renal function

49
Q

high ammonia :

A

neurotoxic

50
Q

Increased ammonium ions

A

encephalopathy

51
Q

METHODS for AMMONIA DETERMINATION:

A
  1. Conway and Cook Diffusion Method
  2. Forman’s Resin Absorption Method
  3. Kunahashi, Ishihora and Euhera Method
  4. Van Anken Enzymatic Method
  5. Ion Selective Electrode
52
Q

• specimen is alkalinized to convert NH4 ions to NH3

A

Conway and Cook Diffusion Method

53
Q

• NH3 is trapped in acid medium of diffusion cell

A

Conway and Cook Diffusion Method

54
Q

• Quantitated by titration or colorimetry

A

Conway and Cook Diffusion Method

55
Q

• Time consuming with poor accuracy and precision

A

Conway and Cook Diffusion Method

56
Q

• Uses cation-exchange resin

A

Forman’s Resin Absorption Method

57
Q

• NH3 absorbed by the resin and eluted

A

Forman’s Resin Absorption Method

58
Q

• Quantitated by Berthelot reaction or by Nesslerization

A

Forman’s Resin Absorption Method

59
Q

Forman’s Resin Absorption Method
N.V.:

A

16 – 33 µmol/L

60
Q

• NH3 is obtained through the use of a Dowax column

A

Kunahashi, Ishihora and Euhera Method

61
Q

• Assayed using the Berthelot method

A

Kunahashi, Ishihora and Euhera Method

62
Q

• Based on the diffusion of NH3 through a selective membrane into NH4 chloride causing pH change which is determined potentiometrically

A

Ion Selective Electrode

63
Q

• Good precision and accuracy

A

Ion Selective Electrode

64
Q

SOURCES OF AMMONIA CONTAMINATION:

A
  1. Smoking
  2. Laboratory atmosphere
  3. Poor venipuncture technique
  4. Metabolism of nitrogenous constituents
65
Q

should be avoided by patient and phlebotomist

A

Smoking

66
Q

must be done in a lab w/ restricted traffic

A

Blood collection & NH3 analysis

67
Q

Glassware: soaked in

A

hypochlorite solution (52.5g/L)

68
Q

Use of heparin lock

A

Poor venipuncture technique

69
Q

Probing for a vein

A

Poor venipuncture technique

70
Q

Partial fill of the evacuated tube

A

Poor venipuncture technique

71
Q

blood into a syringe & transferring it into an anti-coagulated tube

A

Poor venipuncture technique

72
Q

Acceptable anticoagulants:

A

EDTA and non-NH4 heparin salts

73
Q

NH3 values in [?] are significantly but variably higher than in plasma

A

serum

74
Q

Metabolism of nitrogenous constituents
Minimized by:
placing the specimen in [?]
centrifuging [?]
performing the assay [?]

A

ice water
w/o delay
immediately

75
Q

I. PRIMARY OR INHERITED HYPERAMMONEMIA:

A

A. Enzyme defects in the Kreb’s Henseleit Cycle
B. Defects in the metabolism of amino acids
C. Defects in the metabolism of organic compounds

76
Q

Defects in the metabolism of amino acids:

A

Lysine & Ornithine

77
Q

Defects in the metabolism of:

A

Propionic acid
Methylmalonic acid
Isovaleric acid

78
Q

II. ACQUIRED HYPERAMMONEMIA

A

A. Severe liver disease:
Acute
Chronic
B. Impaired venous drainage (from intestine to liver by portal vein)
C. Impaired renal excretion

79
Q

– toxic or fulminant viral hepatitis & Reye’s syndrome

A

Acute

80
Q

– cirrhosis

A

Chronic

81
Q

Hepatic encephalopathy among cirrhotic patients is caused by:

A

• GIT bleeding
• Excess dietary proteins
• Constipation
• Infections
• Drug effects

82
Q

Impaired renal excretion

A

Decreased urine output → Increased BUN reabsorbed → increased excretion of urea into intestines converted to ammonia

83
Q

Reference Interval
adult
child (10days to 2y)

A

19-60 ug/dL
68-136 ug/dL

CC1 LECTURE DEAN (14 decks)

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