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CC1 LEC > NPN > Flashcards

NPN Flashcards

1
Q

UREA

Enzymatic Method
Chemical Method

A

GLDH coupled enzyme
Indicator dye
Conductimetric (ISE)

Fearon’s reaction

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2
Q

UREA

First step

A

Urea + 2 H2O –Urease 2 NH4+ + CO3 2-

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3
Q

GLDH coupled enzyme disappearance of NADH at ___

NH4+ + 2-oxoglutarate + NADH + H+ _____ glutamate + NAD+ + H2O

A

340 nm

NH4+ + 2-oxoglutarate + NADH + H+  GLDH  glutamate + NAD+ + H2O

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4
Q

Indicator dye

A

NH4+ + pH Indicator  color change
Nessler’s reaction (HgI2/KI)
Berthelot’s reaction (Alk. hypochlorite)

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5
Q

Conductimetric (ISE)

A

Conversion of unionized urea to NH4+ and CO32- results in increased conductivity

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6
Q

Fearon’s reaction

Urea + DAM (____.)  ____ (Diazine dirivative)

A

Urea + DAM (Diacetyl Monoxime Mtd.)  Yellow solution (Diazine dirivative)

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7
Q

Plasma or serum

Urine, 24 hour

A

6 – 20 mg/dL - 2.1-7.1 mmol/L

12-20 g/day - 11.5-4.4 mmol urea/day

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8
Q

Specimen Considerations

A
  1. Use fasting blood
  2. Avoid fluoride or citrate anticoagulants
  3. Refrigerate Samples
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9
Q

(↑ urea in the blood)

A

Azotemia

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10
Q

Azotemia 3

A

Prerenal
Renal (Uremia)
Postrenal

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11
Q

Reduce blood flow or ↑ protein catabolism

A

Prerenal

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12
Q

Damage of nephrons (Renal failure/disease)

A

Renal (Uremia)

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13
Q

Urinary tract obstruction (calculi, tumors)

A

Postrenal

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14
Q

Azotemia

4 Decreased Concentration

A

Low protein intake
Severe vomiting and diarrhea
Liver disease
Pregnancy

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15
Q

URIC ACID

1. Physiology

A

Major end-product of purine catabolism.

Present as monosodium urates in plasma (98-100% reabsorbed)

May precipitate in tissues (blood pH ≈ 7 ; BUA > 6.8 mg/dL )

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16
Q

URIC ACID

2. Clinical Application

A 
Inherited disorders of purine metabolism
Gout
Renal calculi
Uric acid nephropathy (chemotheraphy)
Kidney dysfunction
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17
Q

URIC ACID

Enzymatic Methods
Chemical Method

A

Spectrophotometric
(Blauch and Koch)

Coupled enzyme (I) 
Catalase
Coupled enzyme (II) 
Peroxidase

Phosphotungstic acid
(Caraway method)

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18
Q

URIC ACID
First step
Uric Acid + O2 +2 H2O –____ ____ + CO2 + ____

A

Uric Acid + O2 +2 H2O –Uricase allantoin + CO2 + H2O2

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19
Q

Spectrophotometric
(Blauch and Koch)
↓ absorbance at ___

A

↓ absorbance at 293 nm

Uric acid v. allantoin

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20
Q

Coupled enzyme (I)
Catalase
H2O2 + reagent –____ colored compound

A

H2O2 + reagent –Catalase colored compound

21
Q 
Coupled enzyme (II) Peroxidase
H2O2  + indicator dye –\_\_\_\_\_ - \_\_\_\_
A

H2O2 + indicator dye –Peroxidase Red dye

22
Q

Phosphotungstic acid
(Caraway method)
Uric Acid + H3PW12O4o + O2
- ______ allantoin + ____ + CO2

A

Uric Acid + H3PW12O4o + O2
- Na2CO3/OH- 
allantoin + tungsten blue + CO2

23
Q

Specimen Considerations

urea 3

A
  1. Heparinized plasma, serum or urine
  2. Lipemia, bilirubin, hemolysis (↓ UA)
  3. Salicylates and thiazides (↑ UA)
24
Q

Hyperuricemia (Enzyme deficiencies)

A

1) Lesch-Nyhan syndrome
2) Glycogen storage disease type 1
3) Fructose intolerance
4) Hemolytic and proliferative process
5) Treatment of myeloproliferative disease w/ cytotoxic drugs
6) Chronic renal disease
7) Toxemia of pregnancy and lactic acidosis
8) Purine-rich diet

25
Q

Lesch-Nyhan syndrome

A

↓ HGPRT

↓ reutilization of purine, ↑ synthesis of purine

26
Q

Glycogen storage disease type 1

A

↓ G-6-P

↑ triglycerides, ↓ renal urate excretion

27
Q

Fructose intolerance

A

↓ F1PA

↑ lactate, ↓ renal urate excretion

28
Q

Hypouricemia

5

A 
↓ PRPP Synthetase
Liver disease
Fanconi sydrome
Chemotheraphy with azathioprine or 6-mercaptopurine
Overtreatment with allopurinol
29
Q

↓ PRPP Synthetase

A

↓ de novo purine synthesis

30
Q

Liver disease

A

↓ uric acid synthesis

31
Q

Fanconi sydrome

A

Defective tubular reabsorption

32
Q

Chemotheraphy with azathioprine or 6-mercaptopurine

A

↓ de novo purine synthesis

33
Q

Overtreatment with allopurinol

A

↓ XO, ↓ de novo purine synthesis

34
Q

CREATININE

Physiology

A

Chief product of muscle metabolism

Not affected by protein diet

35
Q

CREATININE

2. Clinical Application

A

Sufficiency of kidney function
Severity of kidney damage
Progression of kidney disease
Completeness of 24-hour urine

36
Q

Volume of plasma filtered (V) by the glomeruli per unit of time (mL/minute)

A

Glomerular filtration rate (Creatinine clearance)

37
Q

GFR = V/t

A

GFR = UCrVu
———— x 1.73/A
PCrt

38
Q

CREATININE

Chemical Method

A

Jaffe Reaction
Jaffe-kinetic
Jaffe with adsorbent

39
Q

CREATININE

Principle

A

Creatinine + picrate  Red-orange complex

40
Q

CREATININE

Jaffe-kinetic

A

Rate of change of absorbance(color formation)

41
Q

Principle

Jaffe with adsorbent

A

PFF is adsorbed first onto Fuller’s earth (aluminum magnesium silicate)

42
Q

CREATININE
6
Falsely ↑

A 
Glucose
α-ketoacids
Ascorbate
Uric Acid
Cephalosporins
Dopamine
43
Q

CREATININE
3
Falsely ↓

A
  1. Bilirubin
  2. Hemoglobin
  3. Lipemic specimens
44
Q

CREATININE

Increased Concentration

A 
Renal failure (glomerular function)
↑ Plasma Concentration = ↓ GFR
45
Q

AMMONIA

1. Physiology

A

By product of amino acid deamination.

Converted to urea in the liver.

46
Q

AMMONIA

2. Clinical Application

A

Hepatic failure and hepatic coma
Reye’s syndrome
Inherited deficiencies of urea cycle

47
Q

AMMONIA

Chemical Method

Enzymatic Method

A

Ion-selective electrode
Spectrophotometric

GLDH
↓ absorbance (340 nm)

48
Q

Chemical Method
Principle

-Ion-selective electrode
Diffusion of ___ through selective membrane into ___ causing pH change.

-Spectrophotometric

-Enzymatic Method
GLDH

NH4+ + 2-oxoglutarate + ____ + H+ ____ Glutamate + NADP+ + H2O

A

NH3
NH4Cl

NH3 + bromphenol blue  blue dye

NH4+ + 2-oxoglutarate + NADPH + H+ GLDH Glutamate + NADP+ + H2O

49
Q

AMMONIA

Specimen Considerations

A
  1. Heparinized and EDTA tubes
  2. Samples is centrifuged at 0-4°C within 20 mins. of collection and the plasma/serum removed
  3. Avoid cigarette smoking for several hours

CC1 LEC (10 decks)

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