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CC1 > CARBOHYDRATES&GLUCOSE TESTING > Flashcards

CARBOHYDRATES&GLUCOSE TESTING Flashcards

1
Q

are organic compounds composed of
carbon, hydrogen and oxygen

A

Carbohydrates

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2
Q

Carbohydrates Chemical composition:

A

Cn(H2O)n

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3
Q
  • carbonyl group in the middle linked to 2 other carbon atoms
A

Ketose

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3
Q

Two forms of CHO

A

aldose
ketones

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4
Q
  • terminal carbonyl group called aldehyde group
A

Aldose

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5
Q

are the major constituents of physiologic
system: brain, erythrocyte, and retinal cells in humans.They
are also the major source of energy.

A

Carbohydrates

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6
Q

-simple sugars that cannot be hydrolyzed to a simpler form
- can contain 3 or more carbon atoms

A

Monosaccharides

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6
Q

types of Monosaccharides

A

-Glucose
-Fructose
-Galactose

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7
Q

is directly used as energy source and or stored as
glycogen in the liver or muscles.

A

Glucose

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8
Q

most important CHO; major metabolic fuel

A

Glucose

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9
Q

two monosaccharides are joined by a glycosidic linkage

A

Disaccharides

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10
Q

types of Disaccharides

A

Sucrose
Lactose
Maltose

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10
Q

Fructose + Glucose

A

Maltose

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11
Q

Glucose + Glucose

A

Maltose

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11
Q

Galactose + Glucose

A

Lactose

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11
Q

-linkage of many monosaccharide units

-on hydrolysis, will yield more than 10 monosaccharides

A

Polysaccharides

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11
Q

types of Polysaccharides

A

starch
glycogen
chitin

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12
Q

storage form of glucose in the body

A

Glycogen

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13
Q

fibrous substances consisting of polysaccharides
and forming the major constituent in the exoskeleton of
arthropods and the cell wall of fungi

A

Chitin

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14
Q

As food enters the mouth and oral cavity, food begins to be
broken down by _____, an enzyme produced by the parotid gland that helps in the initial metabolism of food

A

ptyalin

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15
Q

When food reaches the stomach, the acidity inactivates ptyalin and acid hydrolysis occurs. There is no carbohydrate digestion in the stomach, but protein digestion happens
through the enzyme _______.

A

pepsin

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16
Q

When food reaches the intestines, _______, an enzyme produced by the pancreas, further degrades the food and
convert polysaccharides into monosaccharides.

A

amylopsin

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17
Q

After 2 hours glucose levels go

A

back to normal

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17
Q

After 30 min glucose levels

A

rise

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18
Q

After 1 hour glucose levels

A

peak

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19
Q

What are the Glucose Metabolic Pathway

A

Embden-Meyerhoff Pathway
Hexose- Monophosphate Shunt
Glycogenesis

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19
Q

a Glucose Metabolic Pathway that can be aerobic and anaerobic

A

Embden-Meyerhoff Pathway

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20
Q

a pathway that provides energy for the body

A

Embden-Meyerhoff Pathway

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21
Q

glucose to pyruvate

A

Aerobic

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22
Q

glucose to lactate

A

Anaerobic

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23
Q

a pathway for production of reduced
NADPH and ribose-5-phosphate

A

Hexose- Monophosphate Shunt

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24
Q

glucose to pyruvate or lactate to produce
energy

A

Glycolysis

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25
Q

– formation of glucose-6-phosphate from
non-carbohydrate sources

A

Gluconeogenesis

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25
Q

– breakdown of glycogen to glucose for
energy

A

Glycogenolysis

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26
Q

– glucose to glycogen for storage

A

Glycogenesis

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27
Q

– conversion of carbohydrates to fatty acids

A

Lipogenesis

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27
Q

– Decomposition of fat

A

Lipolysis

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28
Q
  • produced by the β cells of the islets of Langerhans in the
    pancreas
  • only hormone that decreases glucose
  • promotes glycolysis, glycogenesis, lipogenesis
A

Insulin

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29
Q
  • produced by the α cells of the islets of Langerhans in the
    pancreas
  • primary hormone that decreases glucose for increasing
    glucose levels
  • promotes glycogenolysis and gluconeogenesis
A

Glucagon

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29
Q

immediate precursor of insulin

A

proinsulin

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30
Q

test that is based on the presence of proinsulin
that helps in the differential diagnosis of Type 1 from type 2
Diabetes Mellitus and the diagnosis of insulinomas

A

c peptide

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31
Q
  • produced by the δ cells of the islets of Langerhans in the
    pancreas
  • inhibition of pancreatic hormone release of insulin and
    glucagon
  • inhibition of gastric acid secretion
A

Somatostatin

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32
Q
  • produced by the zona fasciculata of the adrenal cortex
  • promotes hepatic gluconeogenesis and lipolysis
A

Cortisol

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32
Q
  • produced by the chromaffin cells of the adrenal medulla
  • inhibits insulin secretion and promotes glycogenolysis
A

Catecholamines

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33
Q
  • produced by the anterior pituitary gland
  • promotes glycogenolysis and gluconeogenesis
A

Adenocorticotropic Hormone

33
Q
  • produced by the anterior pituitary gland
  • promotes glycogenolysis and lipolysis
A

Growth Hormone

34
Q
  • produced by the thyroid gland
  • promotes glycogenolysis and intestinal absorption of
    glucose
A

Thyroid hormones

35
Q
  • low blood glucose levels

-May be due to insulinoma or diabetic shock

A

Hypoglycemia

36
Q

value when glucagon and other glycemic factors start to
increase

A

65-70 mg/dL

37
Q

value observable symptoms; strongly suggest hypoglycemia

38
Q

panic value

38
Q

value for severe CNS dysfunction

A

20-30 mg/dL

39
Q

high blood glucose levels
(FBS >126mg/dL)

A

Hyperglycemia

39
Q

Values greater than _____ may result to multiple organ
failure (nephropathy, neuropathy, retinopathy)

40
Q
  1. Symptoms present
  2. Low blood glucose
  3. Relief of symptoms when glucose is raised to normal
A

Whipple’s Triad

41
Q

is the most common type of hyperglycemia that can either be due to insufficient/complete
absence level of insulin or insulin resistance

A

Diabetes Mellitus

42
Q

Diabetes MellitusClinical signs and symptoms include

A

Polyuria
Polydipsia
Polyphagia

43
Q
  • excessive thirst
A

Polydipsia

44
Q
  • excessive urination
45
Q

is the presence of glucose in the urine

A

Glucosuria

45
Q
  • increased food intake
A

Polyphagia

46
Q

is the slight increase of albumin in the
urine that is due to the kidneys leaking out small amounts of
albumin passed through the urine

A

Microalbuminuria

47
Q

DM Non-diabetic___ mg/dL

48
Q

DM Pre-diabetes ______mg/dL

49
Q

DM RBS = _____mg/dL

50
Q

DM OGTT =_____mg/dL

51
Q

DM HbA1c ____

52
Q

-also known as Insulin dependent DM, Brittle diabetes,
Juvenile onset DM

-caused by the cellular-mediated autoimmune destruction of
the beta cells of the islets of Langerhans in the pancreas

A

Type I Diabetes Mellitus

53
Q

-signs and symptoms: Weight gain, milder symptoms than
Type I DM

-Not prone to ketoacidosis

-C-peptide: detectable/high

-Management: Healthy lifestyle

A

Type II Diabetes Mellitus

53
Q
  • signs and symptoms: Rapid weight loss, hyperventilation,
    mental confusion, possible loss of consciousness

-Prone to ketoacidosis

-C-peptide: Undetectable to very low

-Treatment or management include Exogenous Insulin
Therapy

A

Type I Diabetes Mellitus

54
Q

-also known as Non-insulin dependent DM, Stable
diabetes, Adult onset DM

  • caused by insulin receptor defect leading to insulin resistance
A

Type II Diabetes Mellitus

55
Q

-pregnancy onset usually in the second trimester due to
hormonal imbalance

-Occurs during pregnancy and should disappear after delivery

  • May lead to Type 2 DM after 5-10 years if not treated
A

Gestational Diabetes Mellitus

55
Q

Infants born to diabetic mothers are at increased risk for
respiratory distress syndrome, hypocalcemia, and
hyperbiliruninemia

A

Gestational Diabetes Mellitus

56
Q

Screening should be performed between ___
weeks of gestation (1-hr Glucose Challenge Test using 50g
glucose load)

A

24th and 28th

57
Q

can be used as specimens for glucose testing

A

Whole blood, serum, plasma, CSF, urine, synovial fluid

58
Q

Glucose is metabolized at a rate of:

A

7 mg/dL /hr at Room Temp 2 mg/dL /hr at 4°C

59
Q

Whole blood glucose levels are lower than serum
blood glucose levels

60
Q
  • screening test for DM
  • detect elevation of blood glucose
  • 8-10 hours fasting is required; not more than 16hrs
  • produced by the β cells of the islets of Langerhans in the
    pancreas
A

Fasting Blood Sugar (FBS)

60
Q

Categories of fasting plasma glucose
- Normal = ____ mg/dL
- Impaired fasting glucose = ______ mg/dL
- Provisional Diabetes dx = _____mg/dL

A

<110
>110- <126
>126

61
Q
  • sugar determination of randomly collected blood
  • requested during insulin shock or hyperglycemic ketonic
    coma
A

Random Blood Sugar (RBS)

62
Q
  • FBS is first performed
  • Patient is then given a glucose load (75g)
  • plasma glucose is determined after 2hrs
  • NORMAL: blood glucose will return within reference limits
    after 2 hours
A

2-hr Postprandial Blood Sugar

63
Q
  • series of glucose testing
  • FBS is first performed
  • Patient is then given a glucose load
  • collect blood specimen after 30 min, 1 hr and 2 hrs after
    glucose load intake
A

Oral Glucose Tolerance Test (OGTT)

64
Q
  • detects impaired glycogenolysis or severe liver damage
A

Galactose Tolerate Test

64
Q
  • for those who cannot take large carbohyrate intake, altered
    gastric physiology, undergone operation in intestine,
    chronic malabsorption syndrome
A

Intravenous Tolerance Test (IVTT)

64
Q

glucose load: ___ for adult; _____ for pregnant; ____for children

A

75g, 100g, 1.75g/kg wt

65
Q
  • evaluates sensitivity to insulin
  • glucose is administered orally 30min after insulin
A

Insulin Tolerance Test (ITT)

65
Q
  • used for children suffering from hypoglycemic episodes
A

Leucine Tolerance Test

65
Q

FBS is measured before giving the glucose load
*if FBS ____ mg/dL = stop test; if ____ mg/dL, proceed

A

> 140, < 140

66
Q
  • Hba1c is formed by attachment of glucose to the beta
    chains of Hemoglobin A1
  • Long term monitoring of glucose
  • Detects glucose levels in the average of 2-3 months since
    the RBC lifespan in the circulation is 120 days
  • Not suitable for patients with RBC lifespan disorders
A

Glycosylated haemoglobin (HbA1c)

66
Q
  • to evaluate the hypoglycemic effects by insulinomas
A

Tolbutamide Tolerance Test

67
Q

Glycosylated haemoglobin (HbA1c) Specimen: ______
- Normal value: ____
- (______ =prediabetes)

A

Whole blood EDTA
< 6.5%
5.7-6.4%

68
Q
  • is formed by attachment of glucose to
    albumin
  • Short term monitoring of glucose
  • Detects glucose levels in the average of 2-3 weeks since
    the lifespan of albumin in the circulation is 20 days
  • Not suitable for patients with hypoalbuminemia
A

Fructosamine

69
Q

(oldest method)
- Principle: glucose in a hot alkaline solution readily reduces cupric ions to cuprous ions

A

Copper Reduction Methods

70
Q

Fructosamine Normal value: ____

A

205-285 µmol/L

70
Q

Fructosamine specimen:

70
Q

Cuprous + phosphomolybdate = phosphomolybdenum blue
- Disadv: non-glucose reducing sugars are not precipitated
during process

A

Folin Wu Method

71
Q

Cuprous+arsenomolybdate = arsenomolybdenum blue
- Adv: non-glucose reducing sugars are adsorbed by barium
sulfate

A

Nelson Somogyi Method

72
Q

Cuprous + Neocuproine reagent = yellow-orange complex

A

Neocuproine Method

72
Q

Cuprous + Iodine + Acidic solution = colorless complex
- excess iodine is titrated with thiosulfate

A

Shaffer-Hartman Somogyi Method

73
Q

Copper sulfate (blue) + glucose + heat = brick red
precipitate

A

Benedict’s Method (modified Folin Wu method)

74
Q

Ferricyanide (yellow) + glucose = ferrocyanide (colorless)
- inverse colorimetry; measured at 420 nm

A

Hagedorn-Jensen Method

74
Q

defect in glycogen metabolism

A

GLYCOGENOSES

75
Q

glucose + 0-toluidine + acetic acid + heat = green complex
(630 nm)
- most specific non-enzymatic method for glucose

A

Dubowski Method (o-Toluidine Method)

76
Q

defect Glucose-6-phosphatase

A

Von Gierke disease

77
Q

defect in Glycogen debranching
enzyme

A

Anderson’s disease

77
Q

defect Lysosomal acid α-glucosidase

A

Pompe disease

78
Q

defect in Muscle phosphorylase

A

McArdle disease

79
Q

defect in Glycogen phosphorylase
(liver)

A

Hers disease

80
Q

defect in Phosphofructokinase

A

Tarui disease

81
Q

defect in GLUT 2

A

Fanconi-Bickel
disease

CC1 (4 decks)

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