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CLIN CHEM LAB > NON-PROTEIN NITROGENOUS COMPOUNDS 2 > Flashcards

NON-PROTEIN NITROGENOUS COMPOUNDS 2 Flashcards

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1
Q

metabolic waste product of purine metabolism

A

URIC ACID

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2
Q

_______reabsorbed by PCT

A

98-100%

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3
Q

URIC ACID

small amount are secreted by _______

A

DCT (Distal convoluted tubule)

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4
Q

___________is formed from the breakdown of nucleic acids and in is an end product of purine metabolism

A

Uric acid

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5
Q

__________ is transported by the plasma from the liver to the kidney, where it is filtered and where about ______ is excreted

A

Uric acid - 70%

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6
Q

The remainder of uric acid is excreted into the _________

A

GI tract

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7
Q

At concentrations greater than _______ the plasma is saturated

A

relatively insoluble (blood pH)
6.8 mg/dl

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8
Q

Resulting to _____________

A

urate crystal formations

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9
Q

Why measure uric acid?
(5)

A

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

(5)

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10
Q

In disease correlation there are three elevated Uric acid disease (3)

A
  1. Gout
  2. Increased catabolism of nucleic acids
  3. Renal diseases

GIR

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11
Q

-precipitation of sodium urates in the joints
cause hyperuricemia
prone to renal calculi
tophi formations (tissues)

A
  1. Gout
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12
Q

DISEASE CORRELATION

In patients with proliferative disorders on “chemotheraphy”

  • monitoring Uric acid level to avoid nephrotoxicity
A

leukemia
lymphoma
multiple myeloma
polycythemia

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13
Q

treatment of proliferative disorders

A

TX: Allopurinol

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14
Q

DISEASE CORRELATION
other renal disease:

A
  • hemolytic or megaloblastic anemia
  • lesch nyhan syndrome
  • glycogen storage disease
  • G-6-PD deficiency

HLGG

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15
Q

Filtration and secretion are impaired

A

Chronic renal disease

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16
Q
  • X linked genetic disorder
  • Complete deficiency of hypoxanthine guanine phosphoribosyltransferase
A

Lesch-Nyhan Syndrome

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17
Q

Prevents reutilization of purine bases resulting to increased Uric acid

A

Lesch-Nyhan syndrome

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18
Q
  • Toxemia of pregnancy and lactic acidosis
  • Ingestion of purine-rich diet
  • starvation

TIS

A

Hyperuricemia

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19
Q

hyperuricemia
ingestion of purine rich diet

A

liver, kidney, shellfish, legumes

LKSL

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20
Q

Secondary to liver disease
defective tubular reabsorption

A

hypouricemia

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21
Q

disorder of reabsorption in the PCT

A

Fanconi’s Syndrome

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22
Q
  • 6-mercaptopurine or azathioprine
  • overtreatment with allopurinol
A

Chemotheraphy

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23
Q

Based on the oxidation of UA in PFF with subsequent reduction of phospotungstic acid to tungsten blue

A
  1. Caraway Method
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24
Q

provides alkaline pH for color development

A

Sodium carbonate

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25
Q

small collection of sodium urate crystals
in the joint

A

Tophi

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26
Q

→ Has a MW of 168 Da

A

Filtered by the glomerulus

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27
Q

Exogenous

A

diet

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28
Q

Endogenous

A

liver, intestine and other
tissues

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29
Q

Guanine will be acted upon by _________________

A

guanine deaminase

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30
Q

→ Guanosine will be converted to Guanine via ______________

A

nucleosidase

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31
Q

Guanine will be acted upon by _________________

A

guanine deaminase

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32
Q

Earlier uric acid crystal formation due to the
abnormal levels of UA in the urine is demonstrated
by the orange colored deposits in the diapers

A

Lesch Nyhan syndrome

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33
Q

Urate stones can also develop and is demonstrated
by the blood in urine

A

Lesch Nyhan syndrome

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34
Q

Toxemia of pregnancy and lactic acidosis
▪ Ingestion of Purine-rich diet
− Liver, kidney, shellfish, legumes
▪ Starvation; tissue catabolism induced by inadequate
dietary intake

A

Hyperuricemia

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35
Q

− Competition with the rate of renal excretion because
of the excess metabolites such as TAGs and lactate

A

▪ G6PD deficiency

36
Q

− A disorder of reabsorption in the PCT

A

▪ Fanconi’s Syndrome:

37
Q

▪ Secondary to liver disease
▪ Defective tubular reabsorption

A

→ Hypouricemia

38
Q

− 6-mercaptopurine or azathioprine
− Overtreatment with allopurinol

A

Chemotherapy

39
Q

✓ Taken by RBCs and can decrease the formation
of certain genetic material
✓ Inhibit purine synthesis
✓ Inhibits xanthine oxidase

A
40
Q

Based on the oxidation of UA in PFF, with subsequent
reduction of phosphotungstic acid to tungsten blue
Lacks specificity

A
  1. Caraway Method
41
Q

Uricase catalyzes the oxidation of UA to allantoin
→ Measures the differential absorption of uric acid and
allantoin at 293 nm
→ Uricase is also known as urate oxidase
● More specific
● Hemoglobin and xanthine can cause negative interference

A
  1. Uricase Method
42
Q

Uricase is also known as __________

A

urate oxidase

43
Q

Uricase method

→ Measures the differential absorption of uric acid and
allantoin at _______

A

293 nm

44
Q

Lesch nyhan syndrome

Earlier uric acid crystal formation due to the
abnormal levels of UA in the urine is demonstrated
by the __________ colored deposits in the diapers

A

color orange

45
Q

Caraway method

Due to the reaction above there will be formation of
________, _________ and__________

A

tungsten blue, allantoin, and carbon dioxide

46
Q

Uricase method

_______ and ________ can cause negative interference

A

Hemoglobin and xanthine

47
Q

Measures the hydrogen peroxide produced as UA is
converted to allantoin

A

Coupled Enzymatic Methods

48
Q

catalyze a chemical indicator
reaction

A

Peroxidase or catalase

49
Q

medical term for kidney
stones; composed of minerals and salts

A

Renal calculi

50
Q

e is the appropriate term for the uric
acid IN THE BLOOD

A

Monosodium urate

51
Q

l if it is IN THE URINE

A

Uric acid crystal

52
Q

uric acid crystals have a shape of ____________

A

rhombus shape

53
Q

The remainder of uric acid is excreted into the
GI tract __________

A

will be defecated

54
Q

Transported by the plasma from the liver to the
kidney, where it is filtered and where about
70% is excreted _________

A

Via urination

55
Q

● Interference: bilirubin and ascorbic acid can destroy peroxide

A
56
Q

Coupled enzymatic method

Interference: __________ can destroy peroxide

A

bilirubin and ascorbic acid

57
Q

increased blood cells

A

Polycythemia

58
Q

Uric acid is oxidized to allantoin by ________

A

Enzymatic colorimetric

59
Q

The generated hydrogen peroxide reacts with
4-aminophenazone/ESPT to quinoneimine

A

enzymatic colorimetric

60
Q

→ DHBS stands for _____________

A

3,5 - dichloro-2-hydroxybenzenesulfonic
acid

61
Q

Within ___________ of liver failure, there is high probability
that a person may die

A

30 minutes

62
Q

ENZYMATIC COLORIMETRIC

The generated hydrogen peroxide reacts with
__________

A

4-aminophenazone / Ethyl-sulphopropyl
toluidine (ESPT) to quinoneimine

63
Q

Inhibits the action of the enzyme XANTHINE
OXIDASE
➢ With this, xanthine will not be converted into
uric acid, thus lowering uric acid concentration
in the blood

A

Allopurinol

64
Q

catalyzes the oxidation of hypoxanthine to
xanthine, and of xanthine to uric acid
➢ responsible for the synthesis of uric acid

A

xanthine oxidase

65
Q

Produced in the catabolism or deamination of amino acids
and by bacterial metabolism in the lumen of the intestine

A

AMMONIA

66
Q

Removed from the circulation and converted to urea in the
liver

A

AMMONIA

67
Q

is consumed by the parenchymal cells in the liver
for the conversion of ammonia to ure

A

Ammonia

68
Q

→ Ammonia can be secreted by the kidneys as _________and acts to buffer the urine

A

ammonium ions

69
Q

▪ Fasting is not required
− Diet can affect uric acid levels but recent meals have
no effect
▪ Avoid lipemic and hemolyzed specimens
▪ May be refrigerated for 3-5 days

A

Serum

70
Q

Falsely decreased results to peroxidase methods
✓ Addition of potassium ferricyanide and ascorbate oxidase

A

Ascorbic acid

71
Q

—Salicylates
→ Thiazide

A

Drugs

72
Q

In ascorbic acid there are addition of _____________

A

Addition of potassium ferricyanide and ascorbate oxidase

PF and AO

73
Q

In ascorbic acid there are addition of _____________

A

Addition of potassium ferricyanide and ascorbate oxidase

PF and AO

74
Q

→ Both can cause false increase

A

salicylates and thiazides

75
Q

Disease Correlation

A

Hepatic failure
● Severe liver disease (most common cause of distrubed
ammonia catabolism); increased ammonia level
● Inherited deficiency of urea cycle enzymes

76
Q

● Complicated by its low concentration, instability, and
pervasive contamination
● Glutamate dehydrogenase assay

A

Analytical methods

77
Q

→ Causes swelling in the liver and brain
→ Often affects children and teenagers recovering from a
viral infection, most commonly the flu or chickenpox

A

Reye’s Syndrome

78
Q

ammonia concentration
increases rapidly following specimen collection
because of in vitro amino acid deamination

A

WHOLE BLOOD

79
Q

Venous blood should be obtained ___________ and placed on ice immediately

A

WITHOUT TRAUMA

80
Q

most preferred tube use in ammonia

A

Heparin (green tube)

81
Q

Samples should be centrifuged at __________
within ______ minutes of collection and the plasma
or serum removed
* Hemolysis should be avoided

A

0 degrees to 4 degrees celcius at 20 minutes

82
Q

In specimen requirement _______ should be avoided

A

hemolysis

83
Q

Most common on automated
instruments
o Accurate and precise

A

Glutamate dehydrogenase assay

84
Q

Give me the 2 chemical methods of analytic methods ammonia

A
  1. ion-selective electrode
  2. spectrophotometric
85
Q

Give me 1 enzymatic methods of analytic method in ammonia

A
  1. glutamate dehydrogenase

CLIN CHEM LAB (14 decks)

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