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Clinical Chemistry > Non-protein Nitrogen Compounds > Flashcards

Non-protein Nitrogen Compounds Flashcards

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1
Q

What are the end products of nucleic acid and protein metabolism?

A

Urea, Amino acids, Uris acid, creatinine, creatine, ammonia.

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2
Q

Th concentration of nitrogen-contains compounded was quantified….

A

Spectrophotometrically by converting nitrogen to ammonia, with the subsequent reaction being Nessler’s reagent (producing a yellow color)

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3
Q

Majority of Non-protein Nitrogen compounds arise from

A

Catabolism of proteins and nucleic acids

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4
Q

UREA-BUN is the main major end product of

A

Protein metabolism

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5
Q

UREA-BUN is formed

A

In the liver and most is excreted in the urine as a waste product. While some of it is reabsorbed depending on the state of hydration and the urine flow rate.

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6
Q

Reference range for Nitrogen in Adults

A

In plasma or serum: 6-20 mg/dl
In urine, 24 hours: 12-20 g/d

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7
Q

UREA-BUN is used to evaluate

A

Renal function, Nitrogen balance, hydration status, Adequacy of dialysis, and aid in diagnosis of renal disease.

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8
Q

The UREA-BUN enzymatic is

A

The most frequently used method

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9
Q

The Talke-Schubert method

A

Is the most common quantitation, it couples the urease reaction with glutamate dehydrogenase

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10
Q

The rate of NADH disappearance in the Talke-Schubert method is measured at

A

340 nm

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11
Q

The amount of NAD measured in the Talke Schubert method is

A

Proportional to the amount of BUN in the sample

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12
Q

The colorimetric berthelot reaction involves

A

An ammonium ion from urease reaction is measured by color change associated with a pH indicator (Blue indophenol)

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13
Q

The Direct Method- Colorimetric for UREA-BUN involves

A

Urea reacting with diacetylmorphine monoxime under strong acidic conditions and heat.

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14
Q

The Direct Method-Colorimetric in analyzing UREA-BUN produces what color and measures what?

A

It condenses to produce a red color and directly measures urea content.

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15
Q

The Conductometric/Electrode method in UREA-BUN

A

Is specific and rapid, and measures there rate of increase in conductivity when ammonium ions are being produced from urea.

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16
Q

The reference method in UREA-BUN analytical methods

A

Includes an isotope dilution mass spectrometry

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17
Q

The Specimen required in the analyzing of UREA include

A

The use of plasma, serum, or urine. Sodium citrate and. Sodium fluoride tubes would not be recommended due to their inhibitory effects on urease. A non-hemolyzed sample.

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18
Q

Azotemia

A

Is when there is an elevated concentration of nitrogen compounds (urea) being retained in the blood

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19
Q

Uremia

A

Is when there is a very high plasma urea concentration accompanied by renal failure. Could include electrolyte and water imbalance and could be fatal if not treated with dialysis.

20
Q

Prenal Azotemia

A

Is when there is a reduced renal blood flow, resulting in less urea filtered. Could result in Congestive heart failure, hemorrhage and dehydration.

21
Q

Renal Azotemia

A

Is when there is decreased renal function, which will then in turn increase plasma urea concentration. Which could result in kidney disease, glomerular nephritis, renal failure.

22
Q

Postrenal Azotemia

A

is when there is an obstruction of urine flow within the urinary tract below the kidneys causing waste build-up in the kidneys.

Ie: kidney stones

23
Q

Uric Acid is the end-product of

A

The breakdown of purine nucleic acids, which most is reabsorbed in the proximal tubules and reused.

24
Q

Uric acid is relatively

A

Insoluble in the plasma, and can be deposited into tissue and joints at high concentrations causing inflammation. Which could precipitate as urate crystals if levels are elevated above 6.8 mg/dl.

25
Q

In acidic urine (pH < 5.75)

A

Uric acid is predominant thus forming Uric acid crystals.

26
Q

Purines such as guanine and adenine from the breakdown of nucleic acids or tissue destruction are

A

Converted into Uric acid mainly within the liver- purine metabolism.

27
Q

70% of Uric acid is

A

Eliminated and the remainder passes into the GI tracts where it is degraded by bacterial enzymes.

28
Q

Nearly all the Uric acid within the plasma is

A

Present as mono-sodium urate

29
Q

Uric Acid can help the assessment of

A

Gout, Inherited disorders of purine metabolism, renal calculi, Toxemia of pregnancy, Leukemia, Lymphoma, Uric acid neuropathy during chemotherapy, and kidney disfunction.

30
Q

The Uric Acid Caraway method

A

Is the most common analytical method that requires protein free filtrate. Which has Uric Acid oxidized and phosphptungistic reduced to tungsten blue and allantoin at an alkaline pH.

Lacks specificity
Interference from glucose, glutathione, and ascorbic acid.

31
Q

The Uricase method in Uric Acid analytical methodology

A

Is a more specific method, that has uricase catalyzing the oxidation of Uric acid to allantoin. Exclusively used in clinical labs.

32
Q

The simple method in Uric acid analytical methodology

A

Utilizes differential spectrophotometry, absorbing Uric acid at 293nm.

Absorbance difference between before and after is proportional to the Uric acid concentration present.

33
Q

The Coupled Method in Uric Acid Analytical Methodology

A

Measures the hydrogen peroxide produced as Uric acid and converted to allantoin

34
Q

Catalase or peroxidase issued to

A

Catalyze a chemical indicator reaction, with the color being produced proportional to the quantity of Uric acid present in the coupled method (Uric acid)

35
Q

Uric acid specimen requires

A

The use of serum, plasma, and urine. The removal of serum from cells to prevent dilution. Refrigeration for 3-5 days to stabilize. Fasting not needed. Avoid grossly lipemic samples.

36
Q

Increase of bilirubin concentrations

A

Falsely decreases Uric acid levels when using the peroxidase method

37
Q

Significant hemolysis, with concomitant glutathione release will

A

Decrease the Uric acid result values

38
Q

Drugs such as salicylates and thiazides

A

Will increase the Uric acid result values

39
Q

Hyperuricemia (GOUT) is

A

Most common in men (30-50 years), resulting in pain and inflammation f joints due to precipitation of sodium urates. Plasma Uric acid concentration >60 mg/dl. It is caused by overproduction of Uric acid, purine rich diet, drugs, and alcohol.

Susceptible to renal calculi

In women it is commonly seen after menopause, and In severe cases could cause Deformities from crystalline Uric acid in tissue.

40
Q

Hyperuricemia (Leukemia, Lymphoma, Multiple Myeloma, and polycythemia)

A

These could be a result from increased metabolism of cell nuclei. The monitor of Uric acid concentration is need to avoid nephrotoxicity. Utilization of Allopurinol is used for treatment.

41
Q

Hemolytic or Megaloblastic Anemia, Diet, and starvation

A

Can result in the elevation of Uric acid (Hypruricemia)

42
Q

Inherited Disorders of Purine metabolism

A

Could be known as the Lesch-Nyah’s syndrome, with mutations in the 1st enzyme in purine synthesis pathway. And The secondary to glycogen storage disease, and fructose intolerance.

43
Q

Decreased Uric Acid Excretion could result in

A

Toxemia of pregnancy (preeclampsia), lactic acidosis, and chronic renal disease (excretion and secretion impairment)

44
Q

Uric Acid Nephrolithiasis

A

Is the formation of kidney stones (renal calculi), acidic urine also present with insoluble Uric acid precipices forming calculi (flank pain). Is treated by increase fluid intake and administering xanthine oxidase inhibitors.

45
Q

Hypouriecemia

A

Is a less common condition which includes low Uric acid. And is secondary to severe liver disease, and defective tubular reabsorption (Fanconi syndrome). May be caused by chemotherapy and over treatment of allopurinol. Also associated with Parkinson’s and Alzheimer’s .

46
Q

Fanconi syndrome

A

Is the disorder of reabsorption in proximal convoluted tubules of kidneys

Clinical Chemistry (10 decks)

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