Non-Protein Nitrogen Flashcards

1
Q

What are Proteins (CHON)?

A

Made up of carbon, hydrogen, oxygen, and nitrogen (CHON, CHO=carbohydrates). The Building Blocks

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2
Q

WHAT ARE BLOOD NITROGEN COMPOUNDS (CHON + NPN)?

A

Made up of proteins (building blocks) and non-protein nitrogenous compounds

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3
Q

What is Total Nitrogen?

A

Measures all chemically bound nitrogen in the sample (can be applied to biological samples like plasma and urine)

UREA and NITROGEN are measures

Useful in assessing nitrogen balance

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4
Q

HOW TO QUANTITATE NPN?

A

Whole Blood + Protein Precipitants = Protein-Free Filtrate (PFF)

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5
Q

When did NPN originate?

A

originated in the early days of Clinical Chemistry when analytical methods require removal of CHONs before analysis (not done anymore though)

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6
Q

Clinically Significant NPN Compounds

A

Urea
Amino Acids
Uric acid
Creatinine
Creatine
Ammonia

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7
Q

% of total Protein (Urea)

A

45-50

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8
Q

% of total Protein (Amino Acids)

A

25

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9
Q

% of total Protein (Uric Acid)

A

10

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10
Q

% of total Protein (Creatinine)

A

5

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11
Q

% of total Protein (Creatine)

A

1-2

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12
Q

% of total Protein (Ammonia)

A

0-2

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13
Q

What is BLOOD UREA NITROGEN (BUN)?

A

Major excretory product of CHON metabolism

BUN because historic assays for measuring urea were based on the N content in urea. Urea N has been used to refer to urea determination (indirect measurement)

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14
Q

REASONS WHY PLASMA UREA IS MEASURED

A
  1. Evaluate renal function
  2. Assess hydration status
  3. Determine N balance
  4. Aid in the Dx. of renal dss
  5. Verify adequacy of dialysis
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15
Q

REFERENCE RANGE FOR UREA

A

6-20 mg/dL

↑w/ age. Children have lower values

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16
Q

What is UREMIA?

A

Failure of excretory, regulatory & endocrine
function of the kidney

(If left untreated, it can progress to stupor, coma &
death. Treatment = dialysis and kidney transplant)

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17
Q

What is AZOTEMIA?

A

The INCREASE in BUN, CREA & other products of CHON metabolism

(A symptom of UREMIA)

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18
Q

THREE MAIN CATEGORIES OF ↑ UREA

A

PRERENAL

RENAL

POSTRENAL

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19
Q

PRERENAL

A

A. ↓ in blood flow = less blood is delivered to the kidney = less urea is filtered
● Congestive heart failure
● Surgical shock
● Hemorrhage
● Dehydration

B. ↑ amount of CHON metabolism
● Stress
● Fever
● Major illness
● Corticosteroid therapy
● G.I hemorrhage

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20
Q

RENAL

A

About KIDNEYS
● Acute & chronic renal failure
● Glomerular nephritis
● Tubular necrosis

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21
Q

POSTRENAL

A

AFTER KIDNEYS
● Renal calculi (or kidney stones)
● Prostate or bladder tumor
● Severe infection

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22
Q

THREE MAIN CATEGORIES OF ↓ UREA

A

↑ CHON (protein) synthesis

↓ CHON intake

↓ UREA formation

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23
Q

↑ CHON (protein) synthesis

A

As indicates of late pregnancy and infancy

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24
Q

↓ CHON intake

A

STARVATION and malnutrition

25
Q

↓ UREA formation

A

Liver Disease

26
Q

UREA NITROGEN / CREATININE RATIO

A

This ratio normally at 10:1 to 20:1 aids differentiation of the cause of abnormal urea concentration.

27
Q

Cause: Prerenal Azotemia

A

Urea: ↑

Creatinine: N°

Ratio: ↑

28
Q

Cause: Renal Azotemia

A

Urea: ↑

Creatinine: ↑

Ratio: N°

29
Q

Cause: Postrenal Azotemia

A

Urea: ↑

Creatinine: ↑

Ratio: ↑

30
Q

Cause: ↓ Urea Production (ie. acute tubular
necrosis)

A

Urea: ↓

Creatinine: N°

Ratio: ↓

31
Q

Ammonia (Site)

A

Primary site of ammonia (NH3) is in the small intestine

32
Q

3 routes of formation of ENDOGENOUS NH3 (ammonia produced by the body):

A
  1. By-product of CHON metabolism
  2. Urea reenters small intestine for microbial
    breakdown
  3. Some results from anaerobic metabolism in
    skeletal muscle during exercise
33
Q

Primary Causes of ↑NH3 in Adults

A

Hepatic encephalopathy

Renal Failure

Pulmonary Problems

Reye’s Syndrome

Any abnormality in Krebs-Henseleit Cycle

34
Q

Hepatic encephalopathy

A

Venous blood doesn’t pass through the liver in large enough quantities for detoxification

Personality changes develop, neurological
alterations appear & coma as end result of liver
damage

May involve liver necrosis or cirrhosis

35
Q

Renal failure

A

Inability to excrete sufficient urea & NH3

36
Q

Pulmonary problems

A

Secondary to altered blood pH, w/c
distorts equilibrium between NH3
(ammonia) & NH4+ (ammonium)

37
Q

Reye’s Syndrome

A

● Acute metabolic liver disorder
● Occurs most commonly in children
● Serious disease that can be fatal
● Preceded by viral infection & AD of aspirin

38
Q

Any abnormality in Krebs-Henseleit Cycle

A

impaired metabolism (hereditary disorders in urea cycle enzymes)

39
Q

Uric Acid (BUA = BLOOD URIC ACID)

A

End product of purine nucleoside catabolism

Main Sources: endogenous purines and
dietary purines

40
Q

Endogenous Purines?

A

Adenosine & Guanosine nucleotides from tissue destruction

41
Q

Dietary Purines?

A

from the breakdown of ingested nucleic
acids; what we eat

42
Q

How Uric acid is made?

A

ENDOGENOUS PURINES + DIETARY PURINES → [goes to] LIVER → [and converted to] URIC ACID → (400mg from endogenous purines + 300mg from dietary purines) [will go to] → BLOODSTREAM → (although reabsorbed in the proximal convoluted tubule) 50% of total BUA is secreted in the urine.

43
Q

URIC ACID PATHWAYS AFTER going to the BLOODSTREAM: (FOR 70% BUA ELIMINATION IN RENAL EXCRETION)

A

KIDNEY → most of the uric acid are filtered → 98-100% are reabsorbed in the Proximal Convoluted Tubules → about 40% is reabsorbed in the Distal Convoluted Tubules through active transport processes → only 6-12% Uric Acid is excreted in the urine (400-500 mg/dL)

44
Q

URIC ACID PATHWAYS AFTER going to the BLOODSTREAM: (FOR REMAINING 30% IN RENAL EXCRETION)

A

INTESTINES → degradation by bacterial enzymes (in
stool exam) → 200-500mg eliminated in the stool

45
Q

What is URIC ACID in PLASMA present as?

A

Monosodium urate

46
Q

Importance of MEASUREMENT OF BUA

A

Provides useful info for:

  1. Gout - to confirm diagnosis and monitoring
  2. Chemotherapy Patients - for monitoring to prevent uric acid nephropathy or nephrotoxicity
  3. Inherited disorders of Purine Metabolism – assessment
  4. Kidney disfunction – detect
  5. Renal calculi – assist diagnosis (specifically uric acid stone)
47
Q

Reference Range for URIC ACID
↑ synthesis of purine precursors = ↑ uric acid
(↑ input = ↑ output)

A

MALE up to 7.0 mg/dL

FEMALE up to 6.0 mg/dL

48
Q

What is URICEMIA?

A

INCREASED URIC ACID in the blood

49
Q

CAUSES OF HYPERURICEMIA

A
  1. Alcohol and excess dietary purine intake
  2. Gout
  3. Tissue Hypoxia
  4. Increased NA turnover when there is increased
    metabolism of cell nuclei
  5. Inherited disorders of purine metabolism
  6. Increased renal absorption
  7. Decreased excretion
  8. Thiazide diuretics
  9. Lead poisoning
  10. Starvation
  11. Hemolytic or megaloblastic anemia
  12. Bone disease
50
Q

CAUSES OF HYPOURICEMIA

A
  1. Secondary to liver disease
  2. Fanconi syndrome – defective reabsorption in PCT
  3. Chemotreatment w/ 6-mercaptopurine or azathioprine
  4. Overtreatment w/ allopurinol (treatment for increase in uric acid)
  5. Exposure to toxic agents
51
Q

Creatinine is a function of:

A

a. Relative muscle mass – higher muscle mass, the
higher creatinine production. An obese individual
can be expected to have lower creatinine than
non obese individual with the same body mass.

b. Rate of creatine turnover

c. Renal function (> 6-8% eliminated by PCT secretion)

52
Q

Creatinine is a function of:

A

a. Relative muscle mass – higher muscle mass, the
higher creatinine production. An obese individual
can be expected to have lower creatinine than
non obese individual with the same body mass.

b. Rate of creatine turnover

c. Renal function (> 6-8% eliminated by PCT secretion)

53
Q

CREATINE AND CREATININE (CREA)

A

Crea means CREATININE in requisition slips, not CREATINE (We measure the former)

54
Q

CREA and GFR (Glomerular Filtration Rate)

A

CREA is inversely proportional to GFR and although an imperfect measurement, it is commonly used to assess renal filtration function (Always better to use GFR)

55
Q

Importance of MEASUREMENT OF CREA

A

Provides info for:

● Determining sufficiency of kidney function

● Monitor organ function after transplantation

● Determining severity of kidney disease

● Monitor progression of kidney disease

● ↑ CREA = obstruction or interferences w/ glomerular filtration

● CREA is inversely proportional to GFR

● ↑ CREA = ↓ GFR (even if not measured) = renal damage

● CREA is an insensitive marker, may not be measurably ↑ until >50% renal function has deteriorated

56
Q

What is Creatine?

A

Precursor of Creatinine (CREA)

57
Q

Importance of MEASUREMENT OF CREATINE

A

Used in:

● To evaluate Muscle Disease = ↑ creatine,
↑ urinary CREA, N° (Normal) CREA in blood

● Used for assessment of:
- Muscular dystrophy
- Poliomyelitis
- Hyperthyroidism
- Trauma

● Measurement of CK is better for Diagnosis bec. creatine measurement is usually not available in clinical laboratories

58
Q

Importance of MEASUREMENT OF URINE CREA

A

Used in:

● A measure of completeness of 24-hr urine

● Urinary constituents may be expressed as a ratio to creatinine quantity rather as mass excreted per day

59
Q

What does Blood Urea Nitrogen (BUN) measure?

A

Measures Ammonia instead of Urea