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Michelle: Clinical Chem > Week 3: NPN Compounds > Flashcards

Week 3: NPN Compounds Flashcards

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1
Q

List clinically significant non-protein nitrogen (NPN) compounds

A
  1. Urea
  2. Amino acids
  3. Uric acid
  4. Creatinine
  5. Creatine
  6. Ammonia
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2
Q

Explain the chemical structure, synthesis and mode of excretion of urea

A

Chemical structure + Synthesis: Formed in liver from CO2 + ammonia that comes from aa deamination

Excretion: Major excretory product of protein catabolism. Synthesis in liver -> blood -> kidney -> glomerular filtration -> urine

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3
Q

What are clinical applications of BUN measurement?

A
  • Assess renal function
  • Assess hydration status
  • Determine nitrogen balance
  • Aid diagnosis
  • Verify dialysis adequacy
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4
Q

Where is urea at its highest concentration in the nephron?

A

Ascending limb and collecting tube

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5
Q

Define azotemia

A

Elevated urea concentration

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6
Q

What can cause azotemia?

A
  • Carnivorous diet
  • Prerenal
  • Renal
  • Postrenal
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7
Q

Define uremia/uremic syndrome

A

Severe azotemia + renal failure

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8
Q

Explain how prerenal azotemia occurs

A

Result of reduced blood flow to kidney such that less urea is filtered through the glomerulus into the urine. Rather, it builds up instead

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9
Q

List causes of prerenal azotemia (hint: conditions that reduce functional blood volume OR increases protein catabolism)

A
  • congestive heart failure
  • shock (shuts off GI + liver)
  • hemorrhage
  • dehydration
  • burns
  • high protein diet
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10
Q

Explain how renal azotemia occurs

A

The kidney itself is abnormally functioning, which compromises urea excretion

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11
Q

List causes of renal azotemia

A
  • acute + chronic renal failure
  • glomerular nephritis
  • tubular necrosis (lack of oxygen to kidney tissues)
  • other intrinsic renal diseases
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12
Q

Explain how postrenal azotemia occurs

A

Obstruction of urine flow due to renal calculi, prostate or bladder tumors, or severe infection

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13
Q

List causes of reduced urea nitrogen

A
  • Low protein intake
  • Severe vomiting and/or diarrhea (loss)
  • Liver disease (lack of synthesis)
  • Increase in protein synthesis
  • Pregnancy
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14
Q

Urea is often reported in terms of ____ concentration rather than urea concentration

A

Nitrogen

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15
Q

What is the principle of BUN measurement?

A

Urease hydrolyzes urea to the ammonium ion, which oxidizes NADH. NADH absorbance is proportional to [BUN]. Absorbance decreases as reaction progresses

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16
Q

What are the specimen requirements for urea?

A

Plasma, serum, or urine

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17
Q

Common interfering substances in BUN measurement?

A
  • Ammonium ions
  • High citrate and fluoride bc inhibit urease
  • Susceptible to bacterial decomp so refrigerate specimen
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18
Q

What’s the adult urine urea nitrogen?

A

12-20 g/dL

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19
Q

What’s the adult BUN?

A

6-20 mg/dL

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20
Q

Explain the chemical structure, synthesis and mode of excretion of creatinine

A

Chem structure: Arg, Gly, + Met
Synthesis: Liver
Creatine - water = Creatinine
Creatine phosphate - phosphoric acid = Creatinine

Excretion: Waste product of creatine + creatine-P. Excreted into plasma at constant rate to muscle mass (stable), and urine

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21
Q

There are several kinds of creatine kinases (CK). Identify where the following are found:
CKbb
CKmb
CKmm

A

CKbb = brain tissue
CK mb = cardiac tissue
CK mm = skeletal tissue

22
Q

Plasma creatinine concentration is a function of ____ and ____

A

Creatine turnover + renal function (so Creatinine is a way to indirectly measure GFR)

23
Q

What is elevated creatinine associated with?

A

Abnormal renal function (abnormal GFR)

24
Q

How does plasma concentration of creatinine relate to GFR?

A

Inversely proportional

25
Q

What is the creatinine clearance equation?

A

(Urine creatinine/Plasma Creatinine) * (Urine volume ml/ Time min) *(1.73/BSA)

26
Q

State the principle of the chemical reaction used in creatinine measurement

A

Jaffe reaction, where creatinine reacts with picric acid in alkaline solution to produce a red-orange chromogen

27
Q

State most common interfering substances in Jaffe reaction for creatinine measurment

A
  • Glucose
  • Ketoacids
  • Uric acid

All falsely increase measured creatinine

28
Q

List specimen requirements for creatinine measurement by Jaffe reaction

A

Plasma, serum, or urine

29
Q

Which two molecules are key players in the creatinine reaction?

A

CK and NADH (latter gets used up)

30
Q

What is the prerenal azotemia BUN: Creatinine ratio?

A

> 20:1

31
Q

What is the normal or postrenal azotemia BUN: Creatinine ratio?

A

10:1 to 20:1

32
Q

What is the intrarenal azotemia BUN: Creatinine ratio?

A

<10:1

33
Q

What does elevated plasma creatinine and reduced GFR indicate?

A

Renal damage

34
Q

List factors that can influence estimated GFR (eGFR)

A
  • Age
  • Sex
  • Muscle mass
  • Race
35
Q

Discuss creatinine measurement in muscle wasting disease

A
  • Elevated urinary creatinine
  • Normal plasma creatinine
36
Q

Explain the chemical structure, synthesis, and mode of excretion of uric acid

A

Chem structure + synthesis: Breakdown product of purine metabolism (adenosine/guanine) in liver

Excretion: Uric acid -> kidney -> glomerular filtration -> urine, GI tract, or reabsorbed in proximal collection tubule

37
Q

Discuss methodologies for uric acid measurement

A
  • Primary method: uricase converts uric acid to allantoin and measure UV absorbance at 293 nm (uric acid has UV absorbance but allantoin does not)
  • Other methods combine uricase with catalase or peroxidase to act on H2O2 product from allantoin production
38
Q

Discuss renal disease in terms of uric acid measurement

A

Abnormally increased uric acid concentration because filtration and secretion are impaired.

39
Q

Discuss gout in terms of uric acid measurement

A

Abnormally increased uric acid concentration due to presence of MSU crystals

40
Q

Discuss increased cell turnover in terms of uric acid measurment

A

Abnormally increased uric acid concentration due to patients on chemotherapy for overproliferative diseases as leukemia, lymphoma, multiple myeloma, and polycythemia.

41
Q

Gout occurs in what demographic mainly?

A
  • Men
  • Onset 30-50 years old
42
Q

What is Lesch-Nyhan Syndrome?

A
  • Self-mutilating behavior apparent in 85% of males affected with LNS
  • Purine catabolism disorder
  • X-linked genetic disorder
43
Q

What is Fanconi’s Syndrome?

A

Proximal tubular function of kidney is impaired -> hypouricemia

44
Q

Describe hypouricemia

A
  • Secondary to liver disease
  • Defective renal tubular absorption (Fanconi’s)
  • Chemotherapy that inhibits purine synthesis may cause it
  • Allopurinol over treatment may cause it
45
Q

Explain the chemical structure, synthesis, and mode of excretion of ammonia

A

Chem structure + synthesis: Product of aa deamination by intestinal bacteria, exercise, consumed by liver parenchymal cells to convert to urea

Excretion: Excreted as ammonium ion by kidney and acts as urine buffer

46
Q

Explain ammonia toxicity

A

Free ammonia is toxic, but it’s present in plasma at low concentrations

47
Q

What is the most common cause of abnormal ammonia levels and why?

A

Severe liver disease because ammonia is not removed from circulation. Elevated ammonia levels are neurotoxic and often associated with encephalopathy and coma

48
Q

Specimen collection requirements of ammonia?

A
  • Cold chain (on ice)
  • Stable for 30 min after collection
  • False elevation if tube cap off
49
Q

What is Reye’s Syndrome?

A
  • Most common in children
  • High ammonia levels and fatty liver
  • Often preceded by viral infection treated with aspirin
  • Encephalopathy
50
Q

What is ammonia used to diagnose?

A

Inherited deficiencies of urea cycle enzymes

51
Q

Analytic methods of ammonia measurement?

A
  1. Glutamate dehydrogenase shows decrease in absorbance as NADH is oxidized at 340 nm
  2. Direct ISE: features pH change as ammonia diffuses through semi-permeable membrane (potentiometric)

Michelle: Clinical Chem (4 decks)

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