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
After 1 hour glucose levels
peak
19
What are the Glucose Metabolic Pathway
Embden-Meyerhoff Pathway Hexose- Monophosphate Shunt Glycogenesis
19
a Glucose Metabolic Pathway that can be aerobic and anaerobic
Embden-Meyerhoff Pathway
20
a pathway that provides energy for the body
Embden-Meyerhoff Pathway
21
glucose to pyruvate
Aerobic
22
glucose to lactate
Anaerobic
23
a pathway for production of reduced NADPH and ribose-5-phosphate
Hexose- Monophosphate Shunt
24
glucose to pyruvate or lactate to produce energy
Glycolysis
25
– formation of glucose-6-phosphate from non-carbohydrate sources
Gluconeogenesis
25
– breakdown of glycogen to glucose for energy
Glycogenolysis
26
– glucose to glycogen for storage
Glycogenesis
27
– conversion of carbohydrates to fatty acids
Lipogenesis
27
– Decomposition of fat
Lipolysis
28
- produced by the β cells of the islets of Langerhans in the pancreas - only hormone that decreases glucose - promotes glycolysis, glycogenesis, lipogenesis
Insulin
29
- 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
Glucagon
29
immediate precursor of insulin
proinsulin
30
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
c peptide
31
- 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
Somatostatin
32
- produced by the zona fasciculata of the adrenal cortex - promotes hepatic gluconeogenesis and lipolysis
Cortisol
32
- produced by the chromaffin cells of the adrenal medulla - inhibits insulin secretion and promotes glycogenolysis
Catecholamines
33
- produced by the anterior pituitary gland - promotes glycogenolysis and gluconeogenesis
Adenocorticotropic Hormone
33
- produced by the anterior pituitary gland - promotes glycogenolysis and lipolysis
Growth Hormone
34
- produced by the thyroid gland - promotes glycogenolysis and intestinal absorption of glucose
Thyroid hormones
35
- low blood glucose levels -May be due to insulinoma or diabetic shock
Hypoglycemia
36
value when glucagon and other glycemic factors start to increase
65-70 mg/dL
37
value observable symptoms; strongly suggest hypoglycemia
55 mg/dL
38
panic value
<40 mg/dL
38
value for severe CNS dysfunction
20-30 mg/dL
39
high blood glucose levels (FBS >126mg/dL)
Hyperglycemia
39
Values greater than _____ may result to multiple organ failure (nephropathy, neuropathy, retinopathy)
500 mg/dL
40
1. Symptoms present 2. Low blood glucose 3. Relief of symptoms when glucose is raised to normal
Whipple’s Triad
41
is the most common type of hyperglycemia that can either be due to insufficient/complete absence level of insulin or insulin resistance
Diabetes Mellitus
42
Diabetes MellitusClinical signs and symptoms include
Polyuria Polydipsia Polyphagia
43
- excessive thirst
Polydipsia
44
- excessive urination
Polyuria
45
is the presence of glucose in the urine
Glucosuria
45
- increased food intake
Polyphagia
46
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
Microalbuminuria
47
DM Non-diabetic___ mg/dL
< 100
48
DM Pre-diabetes ______mg/dL
100-125
49
DM RBS = _____mg/dL
≥ 200
50
DM OGTT =_____mg/dL
≥ 200
51
DM HbA1c ____
≥ 6.5%
52
-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
Type I Diabetes Mellitus
53
-signs and symptoms: Weight gain, milder symptoms than Type I DM -Not prone to ketoacidosis -C-peptide: detectable/high -Management: Healthy lifestyle
Type II Diabetes Mellitus
53
- 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
Type I Diabetes Mellitus
54
-also known as Non-insulin dependent DM, Stable diabetes, Adult onset DM - caused by insulin receptor defect leading to insulin resistance
Type II Diabetes Mellitus
55
-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
Gestational Diabetes Mellitus
55
Infants born to diabetic mothers are at increased risk for respiratory distress syndrome, hypocalcemia, and hyperbiliruninemia
Gestational Diabetes Mellitus
56
Screening should be performed between ___ weeks of gestation (1-hr Glucose Challenge Test using 50g glucose load)
24th and 28th
57
can be used as specimens for glucose testing
Whole blood, serum, plasma, CSF, urine, synovial fluid
58
Glucose is metabolized at a rate of:
7 mg/dL /hr at Room Temp 2 mg/dL /hr at 4°C
59
Whole blood glucose levels are lower than serum blood glucose levels
10-15%
60
- 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
Fasting Blood Sugar (FBS)
60
Categories of fasting plasma glucose - Normal = ____ mg/dL - Impaired fasting glucose = ______ mg/dL - Provisional Diabetes dx = _____mg/dL
<110 >110- <126 >126
61
- sugar determination of randomly collected blood - requested during insulin shock or hyperglycemic ketonic coma
Random Blood Sugar (RBS)
62
- 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
2-hr Postprandial Blood Sugar
63
- 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
Oral Glucose Tolerance Test (OGTT)
64
- detects impaired glycogenolysis or severe liver damage
Galactose Tolerate Test
64
- for those who cannot take large carbohyrate intake, altered gastric physiology, undergone operation in intestine, chronic malabsorption syndrome
Intravenous Tolerance Test (IVTT)
64
glucose load: ___ for adult; _____ for pregnant; ____for children
75g, 100g, 1.75g/kg wt
65
- evaluates sensitivity to insulin - glucose is administered orally 30min after insulin
Insulin Tolerance Test (ITT)
65
- used for children suffering from hypoglycemic episodes
Leucine Tolerance Test
65
FBS is measured before giving the glucose load *if FBS ____ mg/dL = stop test; if ____ mg/dL, proceed
>140, < 140
66
- 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
Glycosylated haemoglobin (HbA1c)
66
- to evaluate the hypoglycemic effects by insulinomas
Tolbutamide Tolerance Test
67
Glycosylated haemoglobin (HbA1c) Specimen: ______ - Normal value: ____ - (______ =prediabetes)
Whole blood EDTA < 6.5% 5.7-6.4%
68
- 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
Fructosamine
69
(oldest method) - Principle: glucose in a hot alkaline solution readily reduces cupric ions to cuprous ions
Copper Reduction Methods
70
Fructosamine Normal value: ____
205-285 µmol/L
70
Fructosamine specimen:
Serum
70
Cuprous + phosphomolybdate = phosphomolybdenum blue - Disadv: non-glucose reducing sugars are not precipitated during process
Folin Wu Method
71
Cuprous+arsenomolybdate = arsenomolybdenum blue - Adv: non-glucose reducing sugars are adsorbed by barium sulfate
Nelson Somogyi Method
72
Cuprous + Neocuproine reagent = yellow-orange complex
Neocuproine Method
72
Cuprous + Iodine + Acidic solution = colorless complex - excess iodine is titrated with thiosulfate
Shaffer-Hartman Somogyi Method
73
Copper sulfate (blue) + glucose + heat = brick red precipitate
Benedict’s Method (modified Folin Wu method)
74
Ferricyanide (yellow) + glucose = ferrocyanide (colorless) - inverse colorimetry; measured at 420 nm
Hagedorn-Jensen Method
74
defect in glycogen metabolism
GLYCOGENOSES
75
glucose + 0-toluidine + acetic acid + heat = green complex (630 nm) - most specific non-enzymatic method for glucose
Dubowski Method (o-Toluidine Method)
76
defect Glucose-6-phosphatase
Von Gierke disease
77
defect in Glycogen debranching enzyme
Anderson’s disease
77
defect Lysosomal acid α-glucosidase
Pompe disease
78
defect in Muscle phosphorylase
McArdle disease
79
defect in Glycogen phosphorylase (liver)
Hers disease
80
defect in Phosphofructokinase
Tarui disease
81
defect in GLUT 2
Fanconi-Bickel disease