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CC1 LECTURE DEAN > URIC ACID AND AMMONIA > Flashcards

URIC ACID AND AMMONIA Flashcards

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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
Bittner method Two sample measurements: First: Second:
treated with uricase to destroy uric acid uricase is absent - Difference represents true UA
26
TPTZ Method by Morin TPTZ :
2,4,6- tripyridyl – 5 – triazine
27
Amperometric Principle:
Polarographic method
28
HYPERURICEMIA Increased Formation Primary
- Idiopathic: unknown cause - Inherited metabolic disorders: Lesch-Nyhan Syndrome
29
HYPERURICEMIA Increased Formation Secondary
- Excess dietary purine intake - Increased nuclear breakdown (e.g. Leukemia high in lymphoblasts) - Psoriasis - Altered ATP metabolism - Tissue hypoxia - Pre-eclampsia - Alcohol
30
HYPERURICEMIA Decreased Excretion Primary
- Idiopathic
31
HYPERURICEMIA Decreased Excretion Secondary
- Renal failure - Drug therapy: salicylate/aspirin (promote circulation/prevent clotting) - Poisons: heavy metal - Pre-eclampsia - Organicacids - Trisomy21 (Down syndrome )
32
: x-linked genetic disorder (female carrier but does not express the trait – the male offspring will)
Lesch-Nyhan syndrome
33
deficiency of the enzyme, Hypoxanthineguaninephosphoribosyl transferase (muricase)
Lesch-Nyhan syndrome
34
Lesch-Nyhan syndrome symptoms
Delayed motor development Self-destructive behavior (chewing off fingertips and lips) Gout - like swelling Kidney and bladder stones
35
: prevents reutilization of purine bases in the nucleotide salvage pathway
Abnormal phosphoribosyl pyroPO4 synthetase
36
: monosodium urate precipitates from supersaturated body fluids
GOUT
37
CLASSIFICATION OF GOUT
Gouty arthritis Gout nephropathy Acute intradeposition of urate cyrstals Urate nephrolithiasis
38
- urate crystals in joint fluids (precipitate fluids: tophi)
Gouty arthritis
39
- swelling and painful joints; affecting the joints (big toe) and fingers
Gouty arthritis
40
HYPOURICEMIA [?] - reduction in signs of organ
Atrophy of the liver
41
Reference Interval (uricase method) Female Male Conversion factor:
2.6-6.0 mg/dL 3.5-7.2 mg/dL 0.059
42
chemical cpd of ammonia
NH2CHCOOH
43
from [?] thru the action of digestive and bacterial enzymes on proteins in the GIT
deamination of amino acids
44
used in the liver for
urea production
45
plasma level in circulation is extremely low (?)
15 – 45 µg/dL
46
increased in concentration in the blood in cases of
severe liver damage
47
most ammonia in the blood exists as
ammonium ion
48
concentration is not dependent on
renal function
49
high ammonia :
neurotoxic
50
Increased ammonium ions
encephalopathy
51
METHODS for AMMONIA DETERMINATION:
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
• specimen is alkalinized to convert NH4 ions to NH3
Conway and Cook Diffusion Method
53
• NH3 is trapped in acid medium of diffusion cell
Conway and Cook Diffusion Method
54
• Quantitated by titration or colorimetry
Conway and Cook Diffusion Method
55
• Time consuming with poor accuracy and precision
Conway and Cook Diffusion Method
56
• Uses cation-exchange resin
Forman’s Resin Absorption Method
57
• NH3 absorbed by the resin and eluted
Forman’s Resin Absorption Method
58
• Quantitated by Berthelot reaction or by Nesslerization
Forman’s Resin Absorption Method
59
Forman’s Resin Absorption Method N.V.:
16 – 33 µmol/L
60
• NH3 is obtained through the use of a Dowax column
Kunahashi, Ishihora and Euhera Method
61
• Assayed using the Berthelot method
Kunahashi, Ishihora and Euhera Method
62
• Based on the diffusion of NH3 through a selective membrane into NH4 chloride causing pH change which is determined potentiometrically
Ion Selective Electrode
63
• Good precision and accuracy
Ion Selective Electrode
64
SOURCES OF AMMONIA CONTAMINATION:
1. Smoking 2. Laboratory atmosphere 3. Poor venipuncture technique 4. Metabolism of nitrogenous constituents
65
should be avoided by patient and phlebotomist
Smoking
66
must be done in a lab w/ restricted traffic
Blood collection & NH3 analysis
67
Glassware: soaked in
hypochlorite solution (52.5g/L)
68
Use of heparin lock
Poor venipuncture technique
69
Probing for a vein
Poor venipuncture technique
70
Partial fill of the evacuated tube
Poor venipuncture technique
71
blood into a syringe & transferring it into an anti-coagulated tube
Poor venipuncture technique
72
Acceptable anticoagulants:
EDTA and non-NH4 heparin salts
73
NH3 values in [?] are significantly but variably higher than in plasma
serum
74
Metabolism of nitrogenous constituents Minimized by: placing the specimen in [?] centrifuging [?] performing the assay [?]
ice water w/o delay immediately
75
I. PRIMARY OR INHERITED HYPERAMMONEMIA:
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
Defects in the metabolism of amino acids:
Lysine & Ornithine
77
Defects in the metabolism of:
Propionic acid Methylmalonic acid Isovaleric acid
78
II. ACQUIRED HYPERAMMONEMIA
A. Severe liver disease: Acute Chronic B. Impaired venous drainage (from intestine to liver by portal vein) C. Impaired renal excretion
79
– toxic or fulminant viral hepatitis & Reye’s syndrome
Acute
80
– cirrhosis
Chronic
81
Hepatic encephalopathy among cirrhotic patients is caused by:
• GIT bleeding • Excess dietary proteins • Constipation • Infections • Drug effects
82
Impaired renal excretion
Decreased urine output → Increased BUN reabsorbed → increased excretion of urea into intestines converted to ammonia
83
Reference Interval adult child (10days to 2y)
19-60 ug/dL 68-136 ug/dL

CC1 LECTURE DEAN (14 decks)

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