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Clinical Chemistry 1 > C - Chapter VIII: NPN > Flashcards

C - Chapter VIII: NPN Flashcards

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1
Q

FUNCTIONS of the KIDNEYS:
1. Elimination of (?)
2. Elimination of (?) (urea and creatinine)
3. Elimination of (?)like drugs
4. Retention of substances necessary for (?) (proteins & amino acids, glucose)
5. Regulation of (?) of the body fluids)
6. (?) function:

A

excess body water
waste products of metabolism
foreign substances
normal body function
electrolyte balance and osmotic pressure
Endocrine

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2
Q

Primary:

A

production of rennin, prostaglandin and erythropoietin

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3
Q

Secondary:

A

degradation of insulin, glucagon and aldosterone

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4
Q

Clinically Significant NPN compounds:

A
  1. urea – 45%
  2. amino acids – 20%
  3. uric acid – 20%
  4. creatinine – 5 %
  5. creatine – 1-2 %
  6. ammonia – 0.2%
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5
Q

TOTAL NPN METHODOLOGY: TWO STEPS:

A
  1. KJELDAHL DIGESTION
  2. MEASUREMENT OF AMMONIA FORMED
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6
Q

MEASUREMENT OF AMMONIA FORMED

A

A. NESSLERIZATION
B. BERTHELOT METHOD
C. MONITORING CONSUMPTION OF AMMONIA (Kaplan, Manoukian – Fawaz; Kallet – Cook Reaction)

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7
Q

 The nitrogen in a pff of the specimen is converted to ammonia using hot conc. H2SO4 with copper sulfate, mercuric sulfate or selenium oxide as the catalysts.

A

KJELDAHL DIGESTION

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8
Q

NPN + H2SO4 NH4HSO4

A

KJELDAHL DIGESTION

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9
Q

NH4HSO4 + NaOH Na2SO4 + NH3 + H2O

A

KJELDAHL DIGESTION

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10
Q

Nessler’s reagent

A

double iodide salt of potassium & mercury

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11
Q

– colloidal stabilizer

A

Gum ghatti

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12
Q

– yellow to orange brown product

A

Dimercuric ammonium iodide

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13
Q

NH3 + HgI2.2KI NH2Hg2I2 + KI + NH4I

A

NESSLERIZATION

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14
Q

Reagent: phenol and alkaline hypochlorite

A

BERTHELOT METHOD

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15
Q

Catalyst: sodium nitroprusside

A

BERTHELOT METHOD

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16
Q

Product: indophenol blue

A

BERTHELOT METHOD

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17
Q

NH3 + NaOCl + Phenol Indophenol + NaCl + H2O

A

BERTHELOT METHOD

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18
Q

NH3 + α – ketoglutarate + NADH + H Glutamate + NAD

A

MONITORING CONSUMPTION OF AMMONIA (Kaplan, Manoukian – Fawaz; Kallet – Cook Reaction)

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19
Q

Catalyst: Glutamate dehydrogenase

A

MONITORING CONSUMPTION OF AMMONIA (Kaplan, Manoukian – Fawaz; Kallet – Cook Reaction)

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20
Q

Measure a decrease in the absorbance at 340 nm

A

Glutamate dehydrogenase

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21
Q
  • most abundant NPN compound in plasma
A

UREA

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22
Q
  • major excretory product of protein metabolism
A

UREA

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23
Q
  • synthesized in the liver from CO2 and ammonia that arises from the deamination of amino acids in the reaction of the urea cycle
A

UREA

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24
Q

UREA STRUCTURE

A
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25
Q

UREA MW

A

60 g/mole

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26
Q

UREA
MW = 60 g/mole

C =
H =
O =
N =

A

C = 1 x 12 = 12
H = 4 x 1 = 4
O = 1 x 16 = 16
N = 2 x 14 = 28

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27
Q

From urea mass units to urea nitrogen (28/60) =

A

0.467

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28
Q

From urea nitrogen to urea mass units (60/28) =

A

2.14

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29
Q
  • [?] excreted through the kidneys
A

90%

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30
Q
  • excreted through the skin and GIT
A

10%

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31
Q
  • [?] reabsorbed in the renal tubules by passive diffusion
A

40 – 70%

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32
Q

Urea concentration depends on the following :

A
  1. renal function and perfusion
  2. protein content of the diet
  3. amount of protein catabolism
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33
Q

METHODS FOR UREA DETERMINATION

A

I. INDIRECT METHOD / ENZYMATIC
II. DIRECT METHODS

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34
Q

INDIRECT METHOD / ENZYMATIC

A
  1. Berthelot reaction
  2. Nessler’s reaction
  3. GLDH-coupled enzymatic method (Dupont ACA Analyzer)
  4. Conductimetric method: Beckman BUN Analyzer
  5. Urograph or Urastrat strip
  6. Indicator dye (uriol): Kodak Ectachem Analyzer
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35
Q

DIRECT METHODS

A
  1. Diacetyl Monoxime (Fearon)
  2. ortho – phthaldehyde: adapted by automated methods
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36
Q

measures Blood Urea Nitrogen

A

INDIRECT METHOD / ENZYMATIC

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37
Q

Based on the preliminary hydrolysis of urea with urease followed by some process that quantitates the ammonium ion

A

INDIRECT METHOD / ENZYMATIC

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38
Q

Decrease in absorbance of NAD at 340 nm

A
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39
Q

➢ Based on the measurement of the conductivity generated from the reaction of urease on urea producing ammonium ions & bicarbonates

A

Conductimetric method: Beckman BUN Analyzer

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40
Q

➢ Physical principle: based on chromatography

A

Urograph or Urastrat strip

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41
Q

➢ Chemical principle: Conway Microdiffusion method

A

Urograph or Urastrat strip

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42
Q

➢ Dye is added to NH4 ions from urea hydrolysis & the color change is measured

A

Indicator dye (uriol): Kodak Ectachem Analyzer

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43
Q

➢ Used in multilayer film reagents, dry reagent strips and automated systems

A

Indicator dye (uriol): Kodak Ectachem Analyzer

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44
Q

➢ Direct condensation reaction

A

DIRECT METHODS

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45
Q

➢ Diacetyl – very toxic

A

DIRECT METHODS

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46
Q

Urea + OP Isoindoline

A

ortho – phthaldehyde: adapted by automated methods

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47
Q

Isoindoline + Naphthylethylenediamine colored compound

A

ortho – phthaldehyde: adapted by automated methods

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48
Q

– a biochemical abnormality pertaining to increase NPN compounds especially creatinine and urea defining GFR defect

A

Azotemia

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49
Q

– due to reduced renal blood flow

A

a. prerenal

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50
Q

– decreased renal function

A

b. renal

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51
Q

– obstruction of urine flow

A

c. postrenal

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52
Q

Azotemia Three categories:

A

a. prerenal
b. renal
c. postrenal

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53
Q

> calculi, tumors of bladder or prostate

A

c. postrenal

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54
Q

> kidney diseases: glomerular nephritis

A

b. renal

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55
Q

> hemorrhage, dehydration, increased protein catabolism

A

a. prerenal

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56
Q

– a clinical syndrome characterized by increased BUN accompanying renal failure seen in metabolic acidosis, hyperkalemia and edema

A

Uremia/ Uremic syndrome

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57
Q

Decreased Urea: -

A

decreased protein intake, severe vomiting and diarrhea

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58
Q

Specimen Requirements and Interfering Substances
1. plasma, [?], or [?]
2. plasma : [?] and high concentrations of [?] and [?] must be avoided
3. [?] is acceptable
4. [?] is recommended
5. urine sample guarded against bacterial decomposition of [?]

A

serum or urine
ammonium ions; sodium citrate and sodium fluoride
non fasting sample
nonhemolyzed sample
urea

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59
Q

Reference Interval:
− adult serum/plasma

A

6-20 mg/dL 2.1-7.1 mmol/L

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60
Q

Reference Interval:
− conversion factor

mg/dL —> mmol/L :

A

0.357

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61
Q

Reference Interval:
- urine, 24hr

A

12-20 g/day 0.43-0.71 mol/day

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62
Q
  • principal waste product of muscle metabolism derived mainly from Creatine (alphamethylguanidinoacetate
A

CREATININE

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63
Q

Creatine is produced from two enzymatic processes:

A

o transamination of arginine & lysine forming guanidinoacetic acid in the kidneys, small intestines, pancreas and probably the liver
o methylation of guanidinoacetic acid in the liver

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64
Q

is the muscles’ energy source

A

Creatine PO4

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65
Q

RENAL HANDLING of CREATININE:
1. Glomerular filtration
2. Excreted without being reabsorbed. Thus, excretion is relatively constant. Creatinine output is sometimes used to measure the completeness of a 24-hour urine sample collection
3. When serum creatinine is elevated, it is secreted in the renal tubules

A
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66
Q

ANALYTICAL METHODS

A
  1. DIRECT METHOD: JAFFE REACTION
  2. INDIRECT / ENZYMATIC METHODS
  3. Yatzidis method
  4. High Performance Liquid Chromatography (HPLC)
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67
Q

Creatinine + alkaline picrate Creatinine picrate (red orange/yellow) 510 nm

A

DIRECT METHOD: JAFFE REACTION

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68
Q

Alkaline picrate:

A

1 part 10% NaOH and 5 parts sat. picric acid (2,4,6 trinitrophenol)

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69
Q

lacks specificity

A

Jaffe reaction

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70
Q

Non-creatinine Jaffe-reacting chromogens:

A
  • Proteins
  • Glucose
  • Ascorbic acid
  • Guanidine
  • Acetone
  • Cephalosporins
  • α-ketoacids (acetoacetate and pyruvate)
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71
Q

INDIRECT / ENZYMATIC METHODS

A

a. F. Lim – Creatininase or creatinine iminohydrolase
b. G.A. Moss – Creatinine Amidohydrolase

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72
Q

Creatinine —————-→ N-methylhydantoin + NH3 (Creatininase)

A

F. Lim – Creatininase or creatinine iminohydrolase

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73
Q

NH3 + α-ketoglutarate + NADH —————–→ glutamate + NAD + H+ (Glutamate DH)

A

F. Lim – Creatininase or creatinine iminohydrolase

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74
Q

Creatinine ———————————–→ Creatine (Creatinine amidohydrolase)

A

G.A. Moss – Creatinine Amidohydrolase

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75
Q

Creatine + ATP ——————→ CreatinePO4 + ADP (Creatine kinase)

A

G.A. Moss – Creatinine Amidohydrolase

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76
Q

ADP + PEP ——————→ Pyruvate + ATP (Pyruvate kinase)

A

G.A. Moss – Creatinine Amidohydrolase

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77
Q

Pyruvate + NADH + H+ —————→ Lactate + NAD (Lactate DH)

A

G.A. Moss – Creatinine Amidohydrolase

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78
Q

Creatinine reacts with alkaline picrate at two different pH levels

A

Yatzidis method

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79
Q

: protein & other interfering materials will reacts w/ picrate but creatinine does not

A

pH 10

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80
Q

: both creatinine & proteins react

A

pH 11

81
Q

High Performance Liquid Chromatography (HPLC)
Sources of error :

A
  1. ascorbate, glucose, alpha keto acids and uric acid
  2. drugs
82
Q

false increase

A

ascorbate, glucose, alpha keto acids and uric acid
cephalosporin and dopamine intake
lidocaine intake

83
Q

CREATININE
Specimen Requirements and Interfering Substances
3. plasma, [?]
4. avoid [?] especially for the Jaffe reaction
5. [?] cause errors
6. [?] acceptable
7. [?] may transiently elevate serum concentrations
8. [?] : refrigerated after collection or frozen if longer storage than 4 days is required

A

serum or urine
hemolyzed and icteric sample
lipemic samples
non-fasting sample
high protein ingestion
urine

84
Q
  1. overestimates but gives a reasonable approximation of glomerular filtration rate
A

Creatinine Clearance

85
Q

expressed in mL/minute

A

Creatinine Clearance

86
Q

plasma concentration of creatinine is inversely proportional to creatinine clearance (elevated creatinine clearance = decreased GFR)

A

Creatinine Clearance

87
Q

insensitive marker: >50% renal dysfunction = abnormal plasma creatinine

A

Creatinine Clearance

88
Q

Creatinine Clearance =

A

U x V / P

89
Q

− used in the diagnosis of muscle diseases

A

Creatine kinase

90
Q

: CREATININE RATIO

A

BUN

91
Q

NORMAL CREATININE RATIO :

A

10–20:1

92
Q

a. Acute tubular necrosis

A

BUN:CREA ratio <10:1

93
Q

b. Low protein intake; starvation

A

BUN:CREA ratio <10:1

94
Q

c. Severe liver disease

A

BUN:CREA ratio <10:1

95
Q

d. Repeated dialysis

A

BUN:CREA ratio <10:1

96
Q

e. Severe vomitting or diarrhea

A

BUN:CREA ratio <10:1

97
Q

a. Catabolic states w/ tissue breakdown

A

BUN:CREA ratio >10:1 with normal creatinine

98
Q

b. Pre-renal azotemia

A

BUN:CREA ratio >10:1 with normal creatinine

99
Q

c. High protein intake

A

BUN:CREA ratio >10:1 with normal creatinine

100
Q

d. After GIT hemorrhage

A

BUN:CREA ratio >10:1 with normal creatinine

101
Q

High ratio with elevated creatinine levels

A

✓ Post-renal obstruction
✓ Pre-renal azotemia superimposed on renal disease

102
Q

is MORE SPECIFIC for the diagnosis of renal disease

A

Creatinine determination

103
Q

is MORE SENSITIVE for the diagnosis of renal disease

A

BUN determination

104
Q

ASSOCIATED MYOPATHIES:

A

− muscular dystrophy
− familial periodic paralysis
− myasthenia gravis
− dermatomycosis

105
Q

Reference Interval
(1) plasma/serum
5. Jaffe: adult female

A

0.6-1.1 mg/dL (53-97 µmol/L)

106
Q

Reference Interval
(1) plasma/serum
5. Jaffe: adult male

A

0.9-1.3 mg/dL (80-115 µmol/L)

107
Q

Reference Interval
(2) 24h urine
adult female

A

600-1800 mg/day 5.3-15.9 mmol/day

108
Q

Reference Interval
(2) 24h urine
adult male

A

800-2000 mg/day 7.1-17.7 mmol/day

109
Q

Reference Interval
(1) plasma/serum
6. Enzymatic: adult male

A

0.6-1.1 mg/dL (53-97 µmol/L)

110
Q

Reference Interval
(1) plasma/serum
6. Enzymatic: adult female

A

0.5-0.8 mg/dL (44-71 µmol/L)

111
Q

− major product of the catabolism of purine nucleosides: adenosine & guanosine

A

URIC ACID

112
Q

− formed in the liver & intestinal mucosa from xanthine

A

URIC ACID

113
Q

− The bulk of purines ultimately excreted as uric acid in the urine arises from degradation of endogenous nucleic acids.

A

URIC ACID

114
Q

− Reutilization of the major purine bases (adenine, hypoxanthine and guanine) is achieved through “salvage” pathways

A

URIC ACID

115
Q

[?] of the free bases causes re-synthesis of the respective nucleotide monophosphates

A

Phosphoribosylation

116
Q

• 75% is excreted through the urine

A

URIC ACID

117
Q

The remainder is secreted into the GIT, where it is degraded to allantoin & other compounds by bacterial enzymes.

A

− Glomerular filtration ‘
− Tubular reabsorption in the PCT: 98 – 100%
− Active secretion
− Reabsorption in the DCT
− Net excretion: 10%

118
Q

RENAL HANDLING of URIC ACID FACTORS
1. Diet: [?]
2. Age & gender: increase w/ age; higher in [?]
3. 2x greater concentration in [?] than in plasma 4. Avoid the use of [?] because it forms salts that cause turbidity
5. UA is stable in [?] for several days at RT and longer at ref. temp.
6. [?] increases its stability

A

legumes, seeds, internal organs
males
RBC
K oxalate
serum
Thymol

119
Q

Uric Acid + PTA ——- OH——– Allantoin + CO2 + Tungsten blue (710 nm)

A

DIRECT METHOD: Phosphotungstic Acid (PTA)

120
Q

DIRECT METHOD: Phosphotungstic Acid (PTA)

Alkaline solution:

NaCN: Folin
Na2CO3: Caraway
Brown Henry Benedict Archibald Newton

A
121
Q

Uric Acid Allantoin + CO2

A

Blaunch and Koch (UV test with uricase)

122
Q

The decrease in the UA concentration is determined by measuring the absorbance in the range of 290 – 300 nm

A

Blaunch and Koch (UV test with uricase)

123
Q

Uric Acid + O2 + 2H2O Allantoin + CO2 + H2O2

A

Trinder – Uricase method

124
Q

H2O2 + DHBS + PAP Quinoneimine derivative (480 – 550 nm)

A

Trinder – Uricase method

125
Q

DHBS: 3,5 – dichloro – 2- dihydroxy benzene sulfonic acid

A

Trinder – Uricase method

126
Q

PAP: 4 – aminophenazone

A

Trinder – Uricase method

127
Q

Uric Acid Allantoin + CO2 + H2O2

A

Uricase – catalase system

128
Q

H2O2 + methanol —————→ formaldehyde + H2O (Catalase)

A

Uricase – catalase system

129
Q

Formaldehyde + acetylacetone + NH3 3H2O + 3,5-diacetyl-1,4- dihydrolutidine (410 nm)

A

Uricase – catalase system

130
Q

H2O2 + ethanol —————→ Acetaldehyde + H2O (Catalase)

A

Uricase – catalase system

131
Q

Acetaldehyde + NAD —————→ Acetate + NADH (increase in Abs at 340 nm) (Aldehyde DH)

A

Uricase – catalase system

132
Q

Cupric ions —–UA—→ Cuprous ions

A

Bittner method

133
Q

Cuprous ions + neocuproine copper neocuproine complex (yellow to orange)

A

Bittner method

134
Q

Ferric ions —–UA—→ Ferrous ions

A
135
Q

Ferrous ions + TPTZ blue colored complex (590 nm)

A

TPTZ Method by Morin

136
Q

TPTZ : 2,4,6- tripyridyl – 5 – triazine

A

TPTZ Method by Morin

136
Q

TPTZ : 2,4,6- tripyridyl – 5 – triazine

A

TPTZ Method by Morin

137
Q

OTHER METHODS:

A

A. HPLC
B. Amperometric Principle: Polarographic method

138
Q

URIC ACID DISEASE CORRELATIONS:

A

(1) HYPERURICEMIA
(2) HYPOURICEMIA

139
Q

HYPERURICEMIA
A. Increased Formation
Primary:

A
  • Idiopathic
  • Inherited metabolic disorders
140
Q

HYPERURICEMIA
A. Increased Formation
Secondary:

A
  • Excess dietary purine intake
  • Increased nuclear breakdown (e.g. Leukemia)
  • Psoriasis
  • Altered ATP metabolism
  • Tissue hypoxia
  • Pre-eclampsia
  • Alcohol
141
Q

HYPERURICEMIA
B. Decreased Formation
Primary:

A
  • Idiopathic
142
Q

HYPERURICEMIA
B. Decreased Formation
Secondary:

A
  • Renal failure
  • Drug therapy: salicylate
  • Poisons: heavy metal
  • Pre-eclampsia
  • Organic acids
  • Trisomy 21 (Down syndrome)
143
Q

Hereditary Hyperuricemia:

A

 Lesch-Nyhan syndrome
 Abnormal phosphoribosyl pyroPO4 synthetase

144
Q

: x-linked genetic disorder; deficiency of hypoxanthine guanine phosphoribosyl transferase (muricase)

A

Lesch-Nyhan syndrome

145
Q

: prevents reutilization of purine bases in the nucleotide salvage pathway

A

Abnormal phosphoribosyl pyroPO4 synthetase

146
Q

: monosodium urate precipitates from supersaturated body fluids

A

GOUT

147
Q

: o Atrophy of the liver

A

HYPOURICEMIA

148
Q

Specimen Requirements and
Interfering Substances
− heparinized plasma, serum or urine
− immediate separation from red cells to prevent dilution by intracellular contents
− non-fasting sample acceptable
− gross lipemia should be avoided
− high bilirubin may cause false decrease
− significant hemolysis will lower results
− drugs : salicylates and thiazides : false increase

A
149
Q

Reference Interval (uricase method)
Adult female
plasma or serum

A

2.6-6.0 mg/dL (0.16-0.36 mmol/L)

150
Q

Reference Interval (uricase method)
Adult male
urine, 24h

A

250-750 mg/day (1.48-4.43 mmol/day)

151
Q

Reference Interval (uricase method)
Child
plasma or serum

A

2.0-5.5 mg/dL (0.12-0.33 mmol/L)

152
Q

Reference Interval (uricase method)
Conversion factor:

A

0.059

153
Q

Reference Interval (uricase method)
Adult male
plasma or serum

A

2.5-7.2 mg/dL (0.21-0.43 mmol/L)

154
Q

− from deamination of amino acids thru the action of digestive and bacterial enzymes on proteins in the GIT

A

AMMONIA

155
Q

− used in the liver for urea production

A

AMMONIA

156
Q

− level in circulation is extremely low (15 – 45 µg/dL)

A

AMMONIA

157
Q

− increased in concentration in the blood in cases of severe liver damage

A

AMMONIA

158
Q

− most ammonia in the blood exists as ammonium ion

A

AMMONIA

159
Q

− concentration is not dependent on renal function

A

AMMONIA

160
Q

− high ammonia :

A

neurotoxic — encephalopathy

161
Q

METHODS for AMMONIA DETERMINATION:

A
  1. Conway and Cook Diffusion Method
  2. Forman’s Resin Absorption Method
  3. Kunahashi, Ishihora and Euhera Method
  4. Van Anken Enzymatic Method
  5. Ion Selective Electrode
162
Q

SOURCES OF AMMONIA CONTAMINATION:

A
  1. Smoking
  2. Laboratory atmosphere
  3. Poor venipuncture technique
  4. Metabolism of nitrogenous constituents
163
Q

• specimen is alkalinized to convert NH4 ions to NH3

A

Conway and Cook Diffusion Method

164
Q

• NH3 is trapped in acid medium of diffusion cell

A

Conway and Cook Diffusion Method

165
Q

• Quantitated by titration or colorimetry

A

Conway and Cook Diffusion Method

166
Q

• Time consuming with poor accuracy and precision

A

Conway and Cook Diffusion Method

167
Q

• Uses cation-exchange resin

A

Forman’s Resin Absorption Method

168
Q

• NH3 absorbed by the resin and eluted

A

Forman’s Resin Absorption Method

169
Q

• Quantitated by Berthelot reaction or by Nesslerization

A

Forman’s Resin Absorption Method

170
Q

Forman’s Resin Absorption Method N.V.:

A

16 – 33 µmol/L

171
Q

• NH3 is obtained through the use of a Dowax column

A

Kunahashi, Ishihora and Euhera Method

172
Q

• Assayed using the Berthelot method

A

Kunahashi, Ishihora and Euhera Method

173
Q

2-oxoglutarate + NH4+ + NADPH Glutamate + NADP + H2O

A

Van Anken Enzymatic Method

174
Q

Van Anken Enzymatic Method N.V.:

A

11 – 35 µmol/L

175
Q

• Based on the diffusion of NH3 through a selective membrane into NH4 chloride causing pH change which is determined potentiometrically

A

Ion Selective Electrode

176
Q

• Good precision and accuracy

A

Ion Selective Electrode

177
Q

SOURCES OF AMMONIA CONTAMINATION:

A
  1. Smoking
  2. Laboratory atmosphere
  3. Poor venipuncture technique
  4. Metabolism of nitrogenous constituents
178
Q

Metabolism of nitrogenous constituents

Minimized by:

A

o placing the specimen in ice water
o centrifuging w/o delay
o performing the assay immediately

179
Q

 Use of heparin lock

A

Poor venipuncture technique

180
Q

 Probing for a vein

A

Poor venipuncture technique

181
Q

 Partial fill of the evacuated tube

A

Poor venipuncture technique

182
Q

 Drawing blood into a syringe & transferring it into an anti-coagulated tube

A

Poor venipuncture technique

183
Q

 Blood collection & NH3 analysis must be done in a lab w/ restricted traffic

A

Laboratory atmosphere

184
Q

 Glassware: soaked in hypochlorite solution (52.5g/L)

A

Laboratory atmosphere

185
Q

AMMONIA CLINICAL SIGNIFICANCE

A

I. PRIMARY OR INHERITED HYPERAMMONEMIA
II. ACQUIRED HYPERAMMONEMIA

186
Q

A. Enzyme defects in the Kreb’s Henseleit Cycle

A

PRIMARY OR INHERITED HYPERAMMONEMIA

187
Q

B. Defects in the metabolism of amino acids: Lysine & Ornithine

A

PRIMARY OR INHERITED HYPERAMMONEMIA

188
Q

C. Defects in the metabolism of:
Propionic acid
Methylmalonic acid
Isovaleric acid

A

PRIMARY OR INHERITED HYPERAMMONEMIA

189
Q

A. Severe liver disease

A

ACQUIRED HYPERAMMONEMIA

190
Q

B. Impaired venous drainage (from intestine to liver by portal vein)

A

ACQUIRED HYPERAMMONEMIA

191
Q

C. Impaired renal excretion

A

ACQUIRED HYPERAMMONEMIA

192
Q

Severe liver disease:
o Acute –
o Chronic –

A

toxic or fulminant viral hepatitis & Reye’s syndrome

cirrhosis

193
Q

from intestine to liver by portal vein

A

Impaired venous drainage

194
Q

Impaired renal excretion

Decreased (?)
Increased (?)
increased excretion of (?) into intestines converted to (?)

A

urine output
BUN reabsorbed
urea; ammonia

195
Q

AMMONIA
Reference Interval
adult plasma

A

19-60 ug/dL 11-35 umol/L

196
Q

AMMONIA
Reference Interval
adult urine,24h

A

140-1500 mg N/day 10-107 mmol N/day

197
Q

Reference Interval
child
10days to 2y

A

68-136 ug/dL 40-80 umol

Clinical Chemistry 1 (10 decks)

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