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Clinical Chemistry LEC > Non-Protein Nitrogens (Urea, Uric Acid, Creatinine & Ammonia) > Flashcards

Non-Protein Nitrogens (Urea, Uric Acid, Creatinine & Ammonia) Flashcards

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1
Q

4 types of Non-Protein Nitrogens

A
  • Urea
  • Creatinine
  • Uric Acid
  • Ammonia
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2
Q

NPN with the HIGHEST concentration in the blood

A

Urea

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3
Q

Major excretory product of protein metabolism.

A

Urea

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4
Q

Ammonia is bound with Carbon Dioxide to form

A

Carbamoyl Phosphate

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5
Q

This enzymatically catalyzed process is also an important pathway to reduce the levels of ammonia in the blood.

A

Urea Cycle

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6
Q

Urea is commonly termed as?

Since?

A

Blood Urea Nitrogen (BUN) since urea was based on the measurement of your Nitrogen

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7
Q
  • Most of the urea in the glomerular filtrate is excreted in the ____________
  • Some urea is reabsorbed by ________________ during passage of the filtrate through the renal tubules.
A
  • Urine
  • Passive Diffusion
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8
Q

Formula for Urea

A

BUN x 2.14

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9
Q

Protein will undergo ___________ to get amino acids.

A

Proteolysis

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10
Q

Amino acids will undergo _____________ or oxidative deamination to get ammonia

A

Transamination

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11
Q
  • Transfer of your amino group
  • Removal of your amino group
A
  • Transamination
  • Oxidative deamination
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12
Q

Urea is formed in the liver, especially in the __________

A

Hepatocytes

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13
Q
  • A portion of your hepatocytes where the forming of Urea BEGINS
  • A portion of your hepatocytes where the forming of Urea ENDS
A
  • Mitochondria
  • Cytoplasm
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14
Q

CO2 and NH3 is converted into

A

Carbamoyl Phosphate

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15
Q

The enzyme to catalyze carbamoyl phosphate is?

A

Carbamoyl Phosphate synthetase 1

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16
Q

Carbamoyl Phosphate will combine with ___________ to form ______________

A
  • ornithine
  • citrulline
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17
Q

the enzyme to catalyze Citrulline is

A

Ornithine transcarbamylase

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18
Q

another importance of the Urea Cycle is to prevent the accumulation of _________

A

Ammonia

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19
Q

2 Areas where your Urea can be excreted

A
  • Kidneys
  • GI tract (Gastro Intestinal)
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20
Q

90%, is present and can be detected in urine

A

Kidneys

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21
Q

10%, through the action of the bacteria, urea will be converted back to ammonia which then be reabsorbed and recycled in the liver

A

GI tract

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22
Q

Concentration of urea in the blood is affected by the:

A
  • Protein content of the diet
  • Rate of protein metabolism
  • Renal function and Perfusion
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23
Q

Passage of your fluid through your blood vessels to an organ or tissue.

A

Perfusion

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24
Q

2 types of Urea Disorders

A
  • Azotemia
  • Uremia
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25
Q

Elevation of urea in the blood

A

Azotemia

26
Q

Azotemia + renal failure

A

Uremia

27
Q

3 causes of Azotemia in the blood:

A
  • Prerenal
  • Renal
  • Postrenal
28
Q

Occurs as a result of reduced renal blood flow

A

Prerenal

29
Q

Occurs as a result of decreased renal function

A

Renal

30
Q

Occurs due to obstruction of urine flow anywhere in the urinary tract by renal calculi, tumors of the bladder or prostate, or severe infection.

A

Postrenal

31
Q

5 examples of Prerenal Azotemia

A
  • Congestive Heart failure
  • Shock, hemorrhage
  • Dehydration
  • Increased protein catabolism
  • high-protein diet
32
Q

2 examples of Renal Azotemia

A
  • Acute and chronic renal failure
  • Renal disease, glomerular nephritis and tubular necrosis
33
Q

Inflammation in your glomerulus;
no proper filtration of urea

A

Nephritis

34
Q

Death in body tissue;
tubules cannot reabsorb properly

A

Necrosis

35
Q

1 Example of a Postrenal Azotemia

A

Urinary tract obstruction

36
Q

4 causes of decreased concentration of Urea

A
  • Low protein intake
  • Severe vomiting and diarrhea
  • Liver disease
  • Pregnancy (due to hormonal changes)
37
Q

Normal BUN/Creatinine ratio

A

10:1 to 20:1

38
Q

Formed from creatine and creatine phosphate in the muscle;
Released to the plasma in proportion to muscle mass

A

Creatinine

39
Q

Creatinine is synthesized by 3 amino acids which are:

A
  • Arginine
  • Glycine
  • Methionine
40
Q

The 3 Amino acids will undergo transamination forming:

A

Guanidinoacetic acid

41
Q

The transamination between the 3 amino acids and guanidinoacetic acid is catalyzed by the enzyme:

A

L-Arginine:glycine amidinotransferase (AGAT)

42
Q

Creatine with the help of creatine kinase will form phosphocreatine aka ____________

A

Creatine Phosphate

43
Q

Creatinine is a byproduct of ________ and ___________

A

Creatine & Phosphocreatine

44
Q

3 Clinical applications of Creatinine measurement

A
  • Determine the sufficiency of kidney function
  • Determine the severity of kidney damage
  • Monitor the progression of kidney disease
45
Q

4 reasons why Creatinine is a nice measurement.

A
  • it is filtered by the glomerulus
  • it is neither reabsorbed nor secreted
  • relatively constant in the plasma/blood
  • not affected by anything unlike urea that is affected by diet
46
Q

3 Muscle diseases on Creatinine:

A
  • Muscular dystrophy
  • Poliomyelitis
  • Trauma
47
Q

It is the progressive weakness and loss of muscle mass

A

Muscular dystrophy

48
Q

It affects our spinal cord that can cause paralysis

A

Poliomyelitis

49
Q

Product of the catabolism of PURINE NUCLEIC ACIDS (Guanine & Adenosine)

A

Uric Acid

50
Q

Relatively insoluble in plasma and in high concentrations, can be deposited in the joints and tissue causing pain and inflammation

A

Uric Acid

51
Q

Example of an inflammation caused by Uric Acid

A

Gouty Arthritis

52
Q

5 causes in increased concentration of Uric Acid

A
  • Gout
  • Treatment of myeloproliferative disease with cytotoxic drugs
  • Hemolytic and proliferative processes
  • Purine-rich diet
  • Increased tissue catabolism and starvation
53
Q

8 diseases caused by Enzyme deficiencies on uric acid:

A
  • Lesch-Nyhan syndrome
  • Phosphoribosyltransferase synthetase deficiency
  • Glycogen storage disease type-1
  • Fructose intolerance
  • Toxemia in pregnancy
  • Lactic acidosis
  • Chronic renal disease
  • Drugs and poisons
54
Q

4 causes in decreased concentration of Uric Acid

A
  • Liver disease
  • Defective tubular reabsorption
  • Chemotherapy with Azathioprine
  • Overtreatment with allopurinol
55
Q

Pain and inflammation of the joints due to precipitation of monosodium urates

A

Gout

56
Q

Produced in the deamination of amino acids during protein metabolism

A

Ammonia

57
Q

Consumed by the parenchymal cells of the liver in the production of urea.

A

Ammonia

58
Q

3 clinical application of ammonia measurement

A
  • Hepatic failure
  • Reye’s syndrome
  • Inherited defects in the urea cycle
59
Q

Disease that is common in children;
Acute metabolic disorder of the liver;
A child’s blood sugar would typically drop, while the level of ammonia and acidity in The body would increase;
Liver may swell and may develop fatty deposits

A

Reye’s syndrome

60
Q

Cerebral Edema;
Intracranial HTN;
Neuronal Dysfunction

A

Hepatic Encephalopathy

61
Q

The result of overproduction of uric acid and may be exacerbated by a purine-rich diet, drugs, and alcohol

A

Hyperuricemia

62
Q

Less common than hyperuricemia and is usually secondary to severe liver disease or defective tubular reabsorption.

A

Hypouricemia

Clinical Chemistry LEC (4 decks)

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