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Clinical Chemistry 1 > B - Chapter VI: Carbohydrates > Flashcards

B - Chapter VI: Carbohydrates Flashcards

1
Q

use (?)

A

serum, plasma or whole blood

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2
Q

whole blood values (?) lower than serum or plasma

A

10 - 15%

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3
Q

erum or plasma should be refrigerated and separated from the cells (?) to prevent substantial loss thru glycolysis

A

within1 hour

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4
Q

separated unhemolyzed serum at rm temperature is stable for

A

8 hr; ref temperature for 48 - 72 hr

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5
Q

preferred additive :

A

sodium fluoride (gray top)

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6
Q

: approximately 8 - 10 hr fast (not >16 hr)

A

FBS

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7
Q

: immediate processing to prevent bacterial utilization of glucose

A

CSF glucose

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8
Q

: only for monitoring of diabetics and not for diagnosis

A

urine sugar

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9
Q

Chemical methods − done in an

A

alkaline medium

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10
Q

− glucose + boiling water —-> (?) (enol anion form) : reduce metallic ions

A

eneidol

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11
Q

Alkaline Copper reduction Tests

A

Folin-Wu
Nelson-Somogyi
Neocuproine

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12
Q

total reducing substances (true reducing substances and saccharoids) measured

A

Folin-Wu

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13
Q

barium sulfate enables measurement of true reducing substances only

A

Nelson-Somogyi

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14
Q

Campbell and King method

A

Neocuproine

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15
Q

neocuproine (7,9- dimethyl-1,10-phenanthroline) —> cuprous-neocuproine complex (yellow-orange)

A

Neocuproine

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16
Q

arsenomolybdic acid —> arsenomolybdenum blue

A

Nelson-Somogyi

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17
Q

phosphomolybdic acid —> phosphomolybdenum blue

A

Nelson-Somogyi

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18
Q

Alkaline Ferric reduction tests

A
  1. Johnson method
  2. Folin/ Prussian blue method
  3. Hagedorn-Jensen method
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19
Q

− reverse colorimetric method
− more specific than copper reduction

A

Alkaline Ferric reduction

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20
Q

− ferricyanide —> ferrocyanide

A

Alkaline Ferric reduction

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21
Q

Condensation methods

A

(a) with aromatic amines
(b) with phenols

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22
Q

Ortho-toluidine method by Dubowski (reference method)

A

Condensation methods with aromatic amines

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23
Q

based on the ability of carbohydrates to form Schiff bases with aromatic amines

A

Condensation methods with aromatic amines

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24
Q

glucose + ortho-toluidine —-> N-glycosylamine: Schiff base (green) 630 nm

A

Condensation methods with aromatic amines

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25
Q

Condensation methods with aromatic amines interfering substances:

A

galactose, mannose and aldopentose

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26
Q

glucose —> water + hydroxymethylfurfural (HMF)

A

Condensation methods with phenols

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27
Q

HMF + anthrone —> green colored compound

A

Condensation methods with phenols

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28
Q

Enzymatic methods

A

(a) Glucose Oxidase method
(b) Hexokinase method
(c) Glucose Dehydrogenase (GDH)

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29
Q

most specific enzyme reacting with only β-D-glucose

A

Glucose Oxidase method

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30
Q

glucose + O2 + H2O — GOD —> gluconic acid + H2O2

A

Glucose Oxidase method

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31
Q

H2O2 + reduced chromogen — POD—> oxidized chromogen + H2O

A

Glucose Oxidase method

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32
Q

mutarotase : added to convert alpha to beta glucose

A

Glucose Oxidase method

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33
Q

Methods to quantify H2O2 :

A
  1. Gochman and Schmitz
  2. Trinder
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34
Q

3-methyl-2-benzathiazolinone hydrazone + N,N-dimethylaniline —> indamine dye (590-66- nm)

A

Gochman and Schmitz

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35
Q

p-aminophenazone + phenol —-> purple product (quinoneimine)

A

Trinder

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36
Q

2,2-azine-di(3-ethyl bezothiazoline-(6)-sulfonic acid —> colored chromogen

A

Miskieweis

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37
Q
  • measures the amount of oxygen consumed in the glucose oxidase method
A

POLAROGRAPHIC OXYGEN ELECTRODE

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38
Q

POLAROGRAPHIC OXYGEN ELECTRODE

To prevent the formation of oxygen from H2O2 (by catalase present in some GOD preparations), it is removed by inclusion of two additional reactions:

A

❖ H2O2 + ethanol —– catalase—— Acetaldehyde + H2O
❖ H2O2 + H+ + 2I- — molybdate —- I2 + 2H2O

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39
Q
  • recommended for type 1 diabetics
A

Self-Monitoring of Blood Glucose: point of care device

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40
Q
  • to maintain levels as close to normal as possible
A

Self-Monitoring of Blood Glucose: point of care device

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41
Q
  • whole blood glucose testing using capillary blood as sample
A

Self-Monitoring of Blood Glucose: point of care device

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42
Q
  • more accurate, less interferences than glucose oxidase methods (REFERENCE method)
A

Hexokinase method

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43
Q
  • not affected by uric acid and ascorbic acid
A

Hexokinase method

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44
Q
  • false decrease: hemolyzed sample and elevated bilirubin levels
A

Hexokinase method

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45
Q
  • can also be used for urine, CSF and serous fluids
A

Hexokinase method

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46
Q

− glucose + ATP —hexokinase —> glu-6-phosphate + ADP

A

Hexokinase method

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47
Q

− glu-6-phosphate + NADP —G-6-PD —> NADPH + H + 6-phosphogluconate (340 nm)

A

Hexokinase method

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48
Q

Glucose + NAD —— GDH —– Gluconolactone + NADH + H+

A

Glucose Dehydrogenase (GDH)

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49
Q

Coenzyme I: NAD
Coenzyme II: NADP

A

Glucose Dehydrogenase (GDH)

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50
Q

− increased plasma glucose levels

A

HYPERGLYCEMIA

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51
Q

− caused by imbalance of hormones

A

HYPERGLYCEMIA

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52
Q

− normally : insulin is secreted : enhance entry of glucose into the liver, muscle and adipose and alters glucose metabolic pathways

A

HYPERGLYCEMIA

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53
Q

Laboratory Findings in Hyperglycemia

A
  1. increased glucose in plasma and urine
  2. increased urine specific gravity
  3. increased serum and urine osmolality
  4. ketonemia and ketonuria
  5. decreased blood and urine pH (acidosis)
  6. electrolyte imbalance
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54
Q

CLASSIFICATION of DIABETES MELLITUS:

A
  1. Type 1 DM
  2. Type 2 DM
  3. Gestational diabetes mellitus (GDM)
  4. Due to other causes:
    - monogenic diabetes syndromes
    - diseases of the exocrine pancreas
    - drug- or chemical-induced diabetes
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55
Q

due to autoimmune β-cell destruction, usually leading to absolute insulin deficiency

A

Type 1 DM

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56
Q

due to a progressive loss of β-cell insulin secretion frequently on the background of insulin resistance

A

Type 2 DM

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57
Q

diabetes diagnosed in the 2nd or 3rd trimester of pregnancy that was not clearly overt diabetes prior to gestation

A

Gestational diabetes mellitus (GDM)

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58
Q

e.g. neonatal diabetes & maturity-onset diabetes of the young [MODY]

A

monogenic diabetes syndromes

59
Q

e.g. cystic fibrosis

A

exocrine pancreas

60
Q

e.g. with glucocorticoid use

A

drug- or chemical-induced diabetes

61
Q

Fasting is defined as no caloric intake for at least 8 hours

A

FPG ≥ 126 mg/dL (7.0 mmol/L)

62
Q

The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.

A

2-H PG ≥ 200 mg/dL (11.1 mmol/L) during an OGTT.

63
Q

The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay

A

A1C ≥ 6.5% (48 mmol/mol).

64
Q

In a patient with classic symptom of hyperglycemia or hyperglycemic crisis

A

random plasma glucose ≥200 mg/dL (11.1 mmol/L)

65
Q

Frequency 5-10%

A
66
Q

Frequency 90-95%

A
67
Q

Age of onset

Any; most common in children and young adults

A
68
Q

Age of onset

More common in advancing age; can occur in children and adolescents

A
69
Q

Risk factors
Genetic (HLA-DR/DQ on chr 6)
Autoimmune
Environmental

A
70
Q

Risk factors
Genetic
Obesity (BMI)
Sedentary lifestyle
Race/ethnicity

A
71
Q

Pathogenesis:
Destruction of beta cells usually autoimmune

A
72
Q

Pathogenesis:
No autoimmunity
Insulin resistance
Progressive insulin deficiency

A
73
Q

C peptide:
Very low or undetectable

A
74
Q

C peptide:
Detectable

A
75
Q

Pre-diabetes:
Autoantibodies (GAD65,ICA512,IAA) may be present
GAD glutamic acid decarboxylase
ICA islet cell antigen
IAA insulin autoantibodies

A
76
Q

Pre-diabetes:
Autoantibodies absent (testing not indicated)

A
77
Q

Medication therapy:
Insulin

A
78
Q

Medication therapy:
Oral hypoglycemic agents

A
79
Q

Therapy to prevent or delay onset of diabetes:
None known

A
80
Q

Therapy to prevent or delay onset of diabetes:
Lifestyle change Oral hypoglycemic agents (metformin and acarbose)

A
81
Q

TOLERANCE TESTS PATIENT PREPARATION:
1. [?] of unrestricted diet
2. Avoid [?] that will interfere with the test
3. No [?]
4. No alcohol / no [?]
5. (?) fast

A

3 days
medications
beverages
cigarettes
Overnight 8 – 14 hour

82
Q

2-hour Postprandial Test Dose:

A

a gram / kg body wt.

83
Q

2-hour Postprandial Test Normal: peak value in [?]; back to normal in [?]

A

30 mins. (~150 mgs%)
2 hrs

84
Q

5-hour Postprandial Test Dose:

A

75 grams (WHO 1985)

85
Q

5-hour Postprandial Test Normal: back to normal in [?]

A

5 hours

86
Q

5-hour Postprandial Test

 Done only if value of 2-hr PPT is [?]

A

> 140 – 160 mgs%

87
Q

Indications:
 Poor absorption of ingested CHO
 History of GIT surgery

A

Intravenous Glucose Tolerance Test (IVGTT)

88
Q

Intravenous Glucose Tolerance Test (IVGTT) Dose: [?] ([?] solution given intravenously)

A

0.5g/kg
25 g/dL

89
Q

Insulin tolerance test Dose:

A

0.1 unit / kg

90
Q

Insulin tolerance test Normal:

In [?], [?] decrease in FBS level; back to normal on [?].

A

30 mins
50%
2nd hr

91
Q

❖ Delayed decrease in BGL

A

Insulin Resistance

92
Q

❖ DM, hyperadrenalism, Acromegaly

A

Insulin Resistance

93
Q

❖ Normal fall of BGL but delay in regaining normal value

A

Hypoglycemic Unresponsiveness

94
Q

❖ Addison’s disease, hypofunction of anterior PG, hyperinsulinism, Von Gierke’s disease

A

Hypoglycemic Unresponsiveness

95
Q

 Stimulates pancreas to produce insulin

A

Orinase or Tolbutamide

96
Q

 Evaluates hypoglycemia caused by insulinoma

A

Orinase or Tolbutamide

97
Q

Tolbutamide Tolerance Test

In [?], [?] decrease in FBS level; back to normal on [?].

A

30 mins
50%
2nd hr

98
Q

 Serves as an index of the quantity & availability of glycogen

A

Epinephrine tolerance test

99
Q

 Interpretation: Peak value after 30 mins.; normal within 2 hours

A

Epinephrine tolerance test

100
Q

 35 – 45 mgs% increase in conc. between 45 – 60 mins.

A

Epinephrine tolerance test

101
Q

 Detects the presence of mucosal lactase

A

Lactose tolerance test

102
Q

Causes of Lactose Intolerance:

A

 Deficiency of lactase
 Inhibition to lactase activity (e.g. intestinal disorders)

103
Q

− Defined as any degree of glucose intolerance that was first recognized during pregnancy, regardless of whether the condition may have predated the pregnancy or persisted after the pregnancy

A

GESTATIONAL DIABETES MELLITUS

104
Q
  • results from an imbalance between glucose utilization and production
A

HYPOGLYCEMIA

105
Q
  • observable symptoms appear at about 50-55 mg/Dl
A

HYPOGLYCEMIA

106
Q
  • triggered by the ANS
A

Neurogenic

107
Q
  • tremulousness, palpitations, anxiety
A

Neurogenic

108
Q
  • diaphoresis, hunger, paresthesias
A

Neurogenic

109
Q
  • CNS hypoglycemia
A

Neuroglycopenic

110
Q
  • dizziness, tingling, difficulty concentrating, blurred vision
A

Neuroglycopenic

111
Q
  • confusion, behavioral changes, seizure, coma
A

Neuroglycopenic

112
Q

historically : postabsorptive (?) and postprandial (?) hypoglycemia

A

(fasting)
(reactive)

113
Q

Measure glycosylated hemoglobin (HbA1c) every (?)

A

3-6 months

114
Q

(?) + (?) = ketoamine

A

glucose
amino group of hemoglobin

115
Q

rate of formation is directly proportional to

A

plasma glucose concentration

116
Q

provides an index of average BGL over the past 2-4 months

A

Measure glycosylated hemoglobin (HbA1c) every 3-6 months

117
Q

Values for total HbA1 & HbA1c have a high degree of correlation

A

EDTA whole blood sample

118
Q

TESTS FOR MONITORING DIABETIC PATIENTS

A

A. Measure glycosylated hemoglobin (HbA1c)
B. Microalbuminuria
C. C peptide

119
Q

METHODS for MEASUREMENT of Hemoglobin A1C:

A
  1. ION-EXCHANGE CHROMATOGRAPHY
  2. HPLC
  3. COLORIMETRY
  4. RADIOIMMUNOASSAY (RIA)
  5. ELECTROPHORESIS
  6. ISOELECTRIC FOCUSING
  7. AFFINITY CHROMATOGRAPHY
120
Q

 Cation-exchange resin or carboxymethyl cellulose resin

A

ION-EXCHANGE CHROMATOGRAPHY

121
Q

Reference method

A

HPLC

122
Q

 Hb A1c — acid — 5-HMF

A

COLORIMETRY

123
Q

 Antibodies against Hb A1c (sheep antiserum)

A

RADIOIMMUNOASSAY (RIA)

124
Q

 Citrate agar electrophoresis (pH 6.0-6.2)

A

ELECTROPHORESIS

125
Q

 Good resolution of Hb A & Hb A1

A

ELECTROPHORESIS

126
Q

 Scanned on high-resolution microdensitometer

A

ISOELECTRIC FOCUSING

127
Q

 Hb A1c is adequately resolved from HbA1a, A1b, S and F

A

ISOELECTRIC FOCUSING

128
Q

 Use of affinity gel columns

A

AFFINITY CHROMATOGRAPHY

129
Q
  • useful to assist in diagnosis at an early stage and before the development of proteinuria (> 0.5g/day)
A

Microalbuminuria

130
Q
  • reflects pancreatic secretion of insulin
A

C peptide

131
Q
  • proinsulin cleaved to give C peptide and insulin
A

C peptide

132
Q
  • reflects endogenous insulin production if patient is taking insulin
A

C peptide

133
Q

: produced by the liver thru the metabolism of fatty acids to provide a ready energy source from stored lipids at times of low carbohydrate availability

A

ketone bodies

134
Q

3 types of ketone bodies :

A

acetone (2%), acetoacetic acid (20%) and 3-beta-hydroxybutyric acid (78%)

135
Q

Ketone measurement diseases

A

ketonemia and ketonuria

136
Q

type 1 DM :

A

acute illness, stress, pregnancy, hyperglycemia of >300mg/dL or with signs of ketoacidosis

137
Q

serious and potentially fatal hyperglycemic condition

A

DKA

138
Q

nausea, vomiting, abdominal pain, electrolyte disturbances and severe dehydration

A

DKA

139
Q

specimen considerations :

A

− fresh serum or urine − tightly stoppered and assayed ASAP

140
Q

Ketone measurement lab methods :

A

a. Gerhardt’s
b. acetoacetic acid + sodium nitroprusside —-> purple color
c. enzymatic method

141
Q

a. Gerhardt’s : acetoacetic acid + ferric chloride —> red color

A
142
Q

b. acetoacetic acid + sodium nitroprusside —->

A

purple color

143
Q

acetoacetic acid + NADH + H —β-HBDH—> NAD + beta-hydroxybutyric acid

A

c. enzymatic method

Clinical Chemistry 1 (10 decks)

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