Week 3: NPN Compounds Flashcards

(51 cards)

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are clinical applications of BUN measurement?

A
  • Assess renal function
  • Assess hydration status
  • Determine nitrogen balance
  • Aid diagnosis
  • Verify dialysis adequacy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where is urea at its highest concentration in the nephron?

A

Ascending limb and collecting tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define azotemia

A

Elevated urea concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What can cause azotemia?

A
  • Carnivorous diet
  • Prerenal
  • Renal
  • Postrenal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define uremia/uremic syndrome

A

Severe azotemia + renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain how renal azotemia occurs

A

The kidney itself is abnormally functioning, which compromises urea excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain how postrenal azotemia occurs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Nitrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the specimen requirements for urea?

A

Plasma, serum, or urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What’s the adult urine urea nitrogen?

A

12-20 g/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What’s the adult BUN?

A

6-20 mg/dL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What is the creatinine clearance equation?
(Urine creatinine/Plasma Creatinine) * (Urine volume ml/ Time min) *(1.73/BSA)
26
State the principle of the chemical reaction used in creatinine measurement
Jaffe reaction, where creatinine reacts with picric acid in alkaline solution to produce a red-orange chromogen
27
State most common interfering substances in Jaffe reaction for creatinine measurment
- Glucose - Ketoacids - Uric acid All falsely increase measured creatinine
28
List specimen requirements for creatinine measurement by Jaffe reaction
Plasma, serum, or urine
29
Which two molecules are key players in the creatinine reaction?
CK and NADH (latter gets used up)
30
What is the prerenal azotemia BUN: Creatinine ratio?
>20:1
31
What is the normal or postrenal azotemia BUN: Creatinine ratio?
10:1 to 20:1
32
What is the intrarenal azotemia BUN: Creatinine ratio?
<10:1
33
What does elevated plasma creatinine and reduced GFR indicate?
Renal damage
34
List factors that can influence estimated GFR (eGFR)
- Age - Sex - Muscle mass - Race
35
Discuss creatinine measurement in muscle wasting disease
- Elevated urinary creatinine - Normal plasma creatinine
36
Explain the chemical structure, synthesis, and mode of excretion of uric acid
**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
Discuss methodologies for uric acid measurement
- 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
Discuss renal disease in terms of uric acid measurement
Abnormally increased uric acid concentration because filtration and secretion are impaired.
39
Discuss gout in terms of uric acid measurement
Abnormally increased uric acid concentration due to presence of MSU crystals
40
Discuss increased cell turnover in terms of uric acid measurment
Abnormally increased uric acid concentration due to patients on chemotherapy for overproliferative diseases as leukemia, lymphoma, multiple myeloma, and polycythemia.
41
Gout occurs in what demographic mainly?
- Men - Onset 30-50 years old
42
What is Lesch-Nyhan Syndrome?
- Self-mutilating behavior apparent in 85% of males affected with LNS - Purine catabolism disorder - X-linked genetic disorder
43
What is Fanconi's Syndrome?
Proximal tubular function of kidney is impaired -> hypouricemia
44
Describe hypouricemia
- 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
Explain the chemical structure, synthesis, and mode of excretion of ammonia
**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
Explain ammonia toxicity
Free ammonia is toxic, but it's present in plasma at low concentrations
47
What is the most common cause of abnormal ammonia levels and why?
**Severe liver disease** because ammonia is not removed from circulation. Elevated ammonia levels are neurotoxic and often associated with encephalopathy and coma
48
Specimen collection requirements of ammonia?
- Cold chain (on ice) - Stable for 30 min after collection - False elevation if tube cap off
49
What is Reye's Syndrome?
- Most common in children - High ammonia levels and fatty liver - Often preceded by viral infection treated with aspirin - Encephalopathy
50
What is ammonia used to diagnose?
Inherited deficiencies of urea cycle enzymes
51
Analytic methods of ammonia measurement?
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)