3. Carbohydrates Flashcards

1
Q

Carbohydrates: Function

A

Need ATP for:
Molecular Synthesis
Muscle Contraction
Active Transport of Nutrients into Cells

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2
Q

What happens when the daily dietary energy intake exceeds daily expenditure?

A

The excess is converted to fat and is stored in adipose tissue

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3
Q

Dietary Sources: Starches

A
  • Wheat
  • Rice
  • Potatoes
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4
Q

Dietary Sources: Glucose/Fructose

A
  • Molasses
  • Fruits
  • Honey
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5
Q

Dietary Sources: Lactose

A

Milk products

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6
Q

What is the storage form of glucose in animals? What is its primary storage site?

A

Glycogen is stored primarily in the liver; stored glycogen can be used to raise blood glucose levels

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7
Q

Muscle Glycogen

A
  • Muscle glycogen makes up 2/3 of glycogen mass

- Can’t be used to raise blood glucose levels because muscle lacks the enzyme: Glucose-6-phosphatase

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8
Q

Classification of Carbohydrates: First Classification

A

Based on the number of sugar units in a chain

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9
Q

Monosaccharides

A
  • Simple sugars that can’t be hydrolyzed to a simpler form
  • Subunits from which the other groups are formed
  • Sugars containing 3, 4, 5, 6 or more carbon atoms
  • Colorless, crystalline solids that are water-soluble
    e. g. glucose, galactose, fructose, mannose
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10
Q

Notation of Monosaccharides

A

Carbohydrates are hydrates of either an aldehyde or a ketone group
Glyceraldehyde
- Aldose
- Carbonyl Group is at the end of the chain

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11
Q

Fischer Projection Model: D-Glucose

A

e. g. D-Glucose
* * Look at the OH group on the highest numbered symmetrical carbon
* * If on the right, it is the D Form.

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12
Q

Fischer Projection Model: L-Glucose

A

L-Glucose

    • The OH group on the highest asymmetrical carbon is on the Left Side
    • It is the L Form
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13
Q

Stereoisomers: Definition

A

These are compounds that are identical in composition and differ only in spatial configuration
- D Glucose is the most common form

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14
Q

Beta vs. Alpha

A

Look at the Carbonyl Group:
If it is on the Left, we call it Beta
If it is on the Right, we call it alpha

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15
Q

Haworth Projection Model

A

Most Monosaccharides with 5 or more carbons usually occur in aqueous solutions as cyclic or ring structures in which the carbonyl group has formed a covalent bond with the oxygen of the hydroxyl group along the chain

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16
Q

When converting from the Fischer model to the Haworth model the following rules apply:

A
  • All groups to the right in the Fischer Model will be written downward.
  • All groups on the left in the Fischer Model will be written upward.
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17
Q

Chemical Properties of Monosaccharides: Oxidation vs. Reduction

A

Monosaccharides can be oxidized by Ferric (Fe3+) or Cupric (Cu2+) ions.

    • To be oxidized is to lose an electron
    • To be reduced is to gain an electron
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18
Q

Reducing Sugars: Defintion

A

Sugars capable of “reducing” (gaining electrons) Ferric or Cupric ions

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19
Q

Disaccharides

A

Two monosaccharides joined together

e.g. maltose = glucose + glucose

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20
Q

Formation of Disaccharides: Condensation Reaction

A
  • Two monosaccharides are joined together when the hydroxyl group on one sugar reacts with the carbonyl carbon of the other
  • Referred to as a condensation reaction because water is generated
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21
Q

Hydrolysis: Definition

A

When Disaccharides are broken down, Hydrolysis Occurs (Loss of Water)

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22
Q

Why are some sugars not considered reducing sugars?

A

When the carbonyl carbon is part of the glycosidic bond, it cannot be oxidized

The end of the chain that has the free carbonyl carbon is the reducing end

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23
Q

What does it mean when both Carbonyl carbons are involved in the bond?

A

If both Carbonyl carbons are involved in the bond, the sugar cannot be a reducing agent

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24
Q

Polysaccharides: Definition

A

Linkage of many monosaccharide units together

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25
Q

Amylose: Linkage

A

Only alpha 1,4, linkages

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26
Q

Amylopectin: Linkage

A

Alpha 1, 6 Linkage branch every 25 glucose units

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27
Q

Glycogen (animal storage): Linkage

A

Alpha 1,6 Linkage branch every 8-12 glucose units

** More compact than starch types

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28
Q

Metabolism of Glucose: Salivary Amylase

A

Salivary Amylase hydrolyzes these nonabsorbable forms into Dextrins and Disaccharides

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29
Q

What happens after salivary amylase is produced?

A

These products now go to the stomach

The stomach pH inhibits Salivary Amylase

Pancreatic Amylase in the small intestines will hydrolyze these products into maltose, sucrose, and lactose

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30
Q

Digestive Enzymes will be released by the..

A

Intestinal Mucosa

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31
Q

Digestive Enzymes: Maltase

A

Breaks down Maltose into two glucose monosaccharides

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32
Q

Digestive Enzymes: Sucrase

A

Breaks down Sucrose into glucose and fructose

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33
Q

Digestive Enzymes: Lactase

A

Breaks down Lactose into glucose and galactose monosaccharides

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34
Q

Glucose, Galactose, and Fructose are absorbed into the blood supply and taken to the..

A

LIVER

  • Glucose is the only one that can be used directly for energy or storage
  • Galactose and Fructose must be converted into glucose before they can be used
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35
Q

Glucose can be:

A
  • Stored in the liver as glycogen
  • Metabolized to CO2 + H2O for immediate energy within a cell
  • Converted to Keto Acids or Amino Acids
  • Converted to Fat and stored in adipose tissue
  • Released into circulation
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36
Q

Steps of Glycolysis

A

Glucose –> Hexokinase –> Glucose-6-P

Glucose-6-Phosphate –> Fructose-6-P

Fructose-6-Phosphate- -> Fructose1, 6 Diphosphate

Glyceraldehyde-3P and Dihydroxyacetone-P are produced

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37
Q

Glycolysis: Where does it take place? How many ATP are produced?

A

Formation of Pyruvate from Glucose

  • Made a total of 4 ATP molecules
  • Used 2 ATP molecules
  • Net gain of 2 ATP molecules per molecule of glucose
  • Glycolysis takes place in the cytoplasm of the cell
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38
Q

What happens when ATP is high?

A

When ATP is high, the rate Acetyl CoA enters the citric acid cycle decreases and the synthesis of Fatty Acids increase

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39
Q

Glycolysis: End Results

A

Produces 4 pairs of electrons (in the form of NADH and FADH2)

These electrons pass through the respiratory chain which ultimately drives the synthesis of ATP

Net Effect: 38 Molecules* of ATP are generated from the glycolysis of glucose

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40
Q

Other names for Citric Acid Cycle (Aerobic Process)

A
  • Tricarboxylic Acid

- Krebs Cycle

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41
Q

Galactose Feeder Pathway

A

Galactose must be converted into glucose to be utilized

Galactose

Galactose-1-Phosphate

Glucose-1-Phosphate

Glucose- 6-Phosphate –> Glycolysis

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42
Q

Gluconeogenesis: Definition & Purpose

A
  • Formation of Glucose from non-carbohydrate sources
  • Maintains glucose levels during starvation and/or vigorous exercise
  • Occurs primarily in the Liver
  • Use Amino Acids from the break-down of Protein or Glycerol from the break-down of fat
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43
Q

How many ATP molecules are used to make glucose?

A

Have to spend 6 molecules of ATP to make Glucose

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44
Q

Source of Carbohydrate Fasting Individual

A
  1. Liver Glycogen
  2. Carbohydrate found in Plasma: Glucose
  3. Fast lasts longer than one day (Gluconeogenesis)
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45
Q

Glucose –6-Phosphatase

A

Converts Glucose -6 Phosphate back into glucose; Found in Liver but not in muscle

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46
Q

Hexokinase

A

Converts Glucose to Glucose-6-Phosphate

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47
Q

Glycogen Phosphorylase

A

Degrades glycogen by breaking the alpha 1,4 linkages to release glucose units. Also adds a phosphate group that keeps glucose from diffusing out of the cell

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48
Q

Pancreas: Insulin

A
  • Synthesized by the β Cells of the Islet of Langerhans
  • Stimulates movement of glucose into cells
  • Increased glucose utilization (glycolysis)
  • Increases hepatic and muscle glycogenesis
  • Increases Lipogenesis (Fat)
  • Inhibits gluconeogenesis
  • Inhibits glycogenolysis
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49
Q

Name the only hormone that decreases blood glucose levels, hypoglycemic agent

A

Insulin

50
Q

Glucagon

A
  • Primary hormone responsible for increasing blood glucose levels
  • Hyperglycemic agent
  • Synthesized by the alpha cells of the islets of Langerhans
  • Stimulates glycogenolysis in the liver increases Lipolysis and Gluconeogenesis
51
Q

Somatostatin

A
  • Produced by the Delta (δ) Cells of the islets of Langerhans
  • Inhibits the secretion of Insulin and Glucagon,
  • Helps modulate the reciprocal relationship between the two hormones
  • Increases plasma glucose
52
Q

Anterior Pituitary Gland

A
  • Growth Hormone
  • Inhibits the uptake of glucose by cells
  • Insulin inhibitor
53
Q

ACTH (Adrenocorticotropic Hormone)

A
Causes the release of Cortisol from the adrenal cortex which:
	increases glycogenolysis in the liver
	increases gluconeogenesis
	Lipolysis
Net Effect: Increase Plasma Glucose
54
Q

Adrenal Medulla: Epinephrine

A
  • Secreted in the time of stress
  • Stimulates glycogenolysis and lipolysis
  • Inhibits insulin secretion
    Net Effect: Increases Plasma Glucose
55
Q

Thyroid Gland

A

Thyroxine (T4)
- Stimulates glycogenolysis, gluconeogenesis.
- Increases intestinal absorption of glucose
Net Effect: increases plasma glucose

56
Q

Hyperglycemia

A

Abnormally high levels of glucose

- associated with Diabetes Mellitus

57
Q

Type I Diabetes

A

Insulin Dependent Diabetes Mellitus

  • Absolute Deficiency of Insulin
  • Makes up 10-20% of all patients with Diabetes Mellitus
  • Primarily diagnosed in childhood and adolescence
  • Autoimmune destruction of the Beta Cells of the Pancreas
  • 85-90% of patients demonstrate autoantibodies to islets cells or Insulin
  • Usually requires Insulin therapy
  • Associated with ketoacidosis
58
Q

Type I Diabetes: Complications

A
  • neuropathies
  • cataracts
  • nephropathies
  • atherosclerosis
  • vascular insufficiency
59
Q

Type I Diabetes: Symptoms

A

(1) polydipsia: excessive thirst
(2) polyphagia: increased food intake
(3) polyuria: excessive urine production rapid weight loss

60
Q

Type II Diabetes Mellitus

A
  • Non-Insulin Dependent Diabetes Mellitus
  • Most common form of Diabetes Mellitus
  • 80-90% of patients with Diabetes Mellitus
    Diagnosed usually after 40 years old.
  • Insulin levels are higher than normal.
  • There is a resistance to insulin due to a decrease in insulin receptor sites in the obese patient
  • Usually not associated with Ketoacidosis
61
Q

Type II Diabetes: Treatment

A

(1st) Weight Reduction for Obese patients
(2nd) Dietary Restrictions
(3rd) Tolbutamide (oral hypoglycemic agent)
(4th) Small doses of Insulin

62
Q

Gestational Diabetes Mellitus

A
  • Abnormal Glucose concentration during pregnancy
  • Patients frequently return to normal after delivery
  • 30% probability that women with GDM will develop Diabetes Mellitus within 20 years
  • Greater risk if delivered a baby greater than 9 lbs.
  • Infants born to GDM mothers have an increased risk of respiratory distress syndrome, hypocalcemia, and hyperbilirubinemia
63
Q

Secondary Causes of Diabetes Mellitus

A
  • Chronic Pancreatitis
  • Drugs/ Chemical Induced Diabetes (Dilantin)
  • Endocrinopathies
    • Hyperthyroidism
    • Hyper-pituitarism
64
Q

When any one of the following criteria are met and confirmed on a subsequent day, the diagnosis of Diabetes is confirmed:

A
  1. Random plasma glucose >200 mg/dL and symptoms of diabetes
  2. Fasting plasma glucose >126 mg/dL
  3. Two hour plasma glucose > 200 mg/dL during an OGTT
  4. Hgb A1C: > 6.5% (certified method)

** American Diabetes Association (ADA) recommends a Fasting Blood Sugar or Hgb A1C test for everyone over the age of 45 years old every 3 years. People in high risk groups are recommended to have it more often.

65
Q

Relative Hypoglycemia

A
  • Normal fasting glucose level

- Occurs in relationship to a meal

66
Q

Functional Hypoglycemia

A
  • Common in adults

- Occurs 2-4 hours after eating a meal

67
Q

Prediabetic or Diabetic Hypoglycemia

A

Insulin response is delayed and exaggerated

68
Q

Alimentary Hypoglycemia

A
  • Patients who have had G.I. surgery

- Accelerated absorption of glucose- yields an exaggerated insulin response

69
Q

Drug-Induced Hypoglycemia

A

Fasting glucose is low

(1) Alcohol: Has a negative effect on glycogen storage; glycolysis
(2) Insulin
(3) Tolbutamide or oral hypoglycemic agents

70
Q

Insulinoma

A

Beta Cell Tumors

  • 80% are benign
  • 10% are malignant
  • 10% are multiple tumors
71
Q

Endocrinopathies

A
  • Hypothyroidism
  • Hypopituitarism
  • Addisons Disease
      • Adrenal Cortical Insufficiency: decreased Cortisol
72
Q

Massive Liver Disease: Definition

A

Glycogen Storage Disease

  • Deficiency in Glucose-6-Phosphatase, therefore cannot convert glycogen to glucose
  • Also called Von Gierke Disease
  • Enlarged liver due to increased glycogen stores
  • Severe hyperlipidemia
  • Capillary Blood: higher than venous blood
73
Q

Massive Liver Disease: Reference Ranges

A
Plasma: <100 mg/dL
Whole Blood:	65 – 95 mg/dL
CSF: 40 – 70 mg/dL
	*Approximately 60% of Plasma Glucose  
	 Levels
	*When blood glucose levels change, it takes 2 hours for CSF/blood glucose equilibrium to occur
74
Q

Specimens

A

Stability

  • Serum on Cells: decreased glucose (5 –7% per hour)
  • Plasma should be separated from cells within 1 hour
  • 8 hours at room temperature
  • 72 hours at 4C
75
Q

Preservatives

A
  • Sodium Fluoride/ Iodoacetate gives Plasma
  • Prevents RBCs, WBCs, and PLTs from metabolizing glucose (inhibits glycolytic enzymes)
  • Stable for 3 days at room temperature
76
Q

Glucose Oxidase: What does it measure?

A

Polarographic Oxygen Electrode Method (CX3)

    • The electrode measures the Rate of Oxygen Consumption after the addition of the glucose sample to a buffered solution containing glucose oxidase reagent
    • The greater the glucose concentration in the sample - the faster the Rate of Oxygen Consumption
77
Q

Glucose Oxidase Method- Chromogenic (Trinder Method)

A

This method uses the same initial reaction as above with the addition of a chromogen which is oxidized by peroxidase to give a colored reaction

    • The amount of colored product formed (oxidized chromogen) is proportional to the glucose concentration in the sample
    • The Glucose Oxidase method is specific for B-D-Glucose
    • Mutarotase can be added to convert -D-Glucose (36% of glucose) into B-D-Glucose
    • The incubation time will be longer for the test
78
Q

Chromogenic (Trinder Method): Interferences

A
  • Chromogen can be influenced by uric acid, ascorbic acid, and bilirubin.
  • These substances are oxidized by peroxidase and will decrease the amount of chromogen oxidized giving a falsely low glucose result
  • Bleach can oxidize the chromogen and give a falsely elevated glucose result
  • Urine samples cannot be used for this method due to the presence of enzyme inhibitors in urine
79
Q

Hexokinase Method

A

Glucose + ATP = Glucose-6-Phosphate + ADP (G-6-P)

80
Q

G-6-PD: Yeast vs. Bacteria Sources

A

G-6-PD from yeast sources use NADP+ as the co-factor
G-6-PD from bacteria sources use NAD+ as the co-factor

** Not affected by interferences like Glucose Oxidase

81
Q

Whole Blood Test Strip Methods

A
  • Glucometers are Reflectance Meters that use Glucose Oxidase-Peroxidase Chromogen test strips
  • Reflectance Meter: The colored reaction produced by the test is measured by light that is reflected as compared to reflected light from a reference surface
  • This is not a linear reaction like the spectrophotometer. There is a microprocessor that uses math algorithms to calculate the concentration of glucose
  • Whole blood glucose levels are 11% less than serum or plasma values
  • These methods are primarily used by diabetic patients to monitor their own blood glucose levels for insulin therapy-3-4 timers per day
82
Q

2 –Hour Post Prandial Test

A
  • Patient is given a 75 gram dose of glucose
  • Two hours later, blood is drawn
  • If the level is > 200 mg/dL, and is confirmed on another day, the patient is diagnosed with Diabetes Mellitus
  • Less than 140 mg/dL is considered normal
83
Q

Oral Glucose Tolerance Test

A
  • Not recommended for routine use as the first screening test
  • The serial measurement of plasma glucose before and after glucose is given orally
84
Q

When a OGTT is ordered, the following

conditions must be met:

A
  • Diet containing >150 g of carbohydrates for 3 days prior to the test
  • Fasting 10-16 hours before the test
  • Fasting specimen must be below 126 mg/dL before the Glucola can be given
  • The oral glucose load is 75 grams for adults and 1.75 g/kg, up to 75 grams maximum for children
  • Should be ingested over 5 minutes
  • The Glucose Tolerance Test would measure Plasma glucose at fasting, and then every 30 minutes for 2 hours
85
Q

Interfering Substances

A

Drugs and Medications:

  • Oral contraceptives
  • Salicylates
  • Nicotinic acid (cigarettes, cigars, etc)
  • Diuretics (caffeine)
  • Hypoglycemic Agents (Insulin, etc)
  • Anticonvulsants (Dilantin)
  • Corticosteroids
86
Q

Time of Day

A

Morning due to diurnal variation in glucose values

87
Q

The OGTT test is best used to assess:

A
  • Borderline Fasting glucose levels
  • Risk counseling (High Risk for developing Diabetes)
  • Diagnosis of Gestational Diabetes
88
Q

Universal Screening for Gestational Diabetes Mellitus:

A
  • High Risk Patients should be screened for GDM.
  • Risk Factors include:
      • Older than 25 years of age
      • Overweight
      • Family History of Diabetes
      • Glycosuria
89
Q

One-Step Glucose Tolerance

A
  • 2 hour OGTT using a 75 g Glucose Load
  • Gestational Diabetes if:
      • Fasting: >92 mg/dL
      • 1 Hour: > 180 mg/dL
      • 2 Hour: > 153 mg/dL
90
Q

2-Step Glucose Tolerance: STEP 1

A

Step 1:
50 g Glucose Load is given.
If > 140 mg/dL after one hour then proceed to Step 2

91
Q

2-Step Glucose Tolerance: STEP 2

A

Step 2:

  • 100 g Glucose Load
  • 3 hour OGTT
  • Gestational Diabetes if:
    • *Fasting: >92 mg/dL
    • *1 Hour: > 180 mg/dL
    • *2 Hour: > 153 mg/dL
    • *3 Hour: > 140 mg/dL
92
Q

All who are positive for Gestational Diabetes will be:

A
  • Screened again 6-12 weeks postpartum

- Life Long screen every 3 years

93
Q

Glycosylated Hemoglobin

A
  • Want to maintain control over glucose levels when managing Diabetes.
  • `By measuring Glycosylated Hemoglobin, the physician can see long term compliance with monitoring and achieving blood glucose level control
94
Q

Normal Adult Type Hemoglobin

A
Hemoglobin:  A1	97%  
- 2 alpha chains; 2 beta chains
Hemoglobin:  A2	2.5%	
- 2 alpha chains; 2 delta chains
Hemoglobin F:		0.5%	
- 2 alpha chains; 2 gamma chains
95
Q

Circulating normal adult Hemoglobin A1 is made up of

A

A number of minor hemoglobins- Hgb A1a, Hgb A1b, Hgb A1c and are referred to as the glycohemoglobins

96
Q

Hgb A1c

A
  • Makes up 80% of Hemoglobin A1
  • Glucose molecule attaches to one or both ends (N-terminal Valine) of the Beta chain of normal adult Hemoglobin
  • Nonenzymatic reaction
97
Q

The rate of formation is proportional to:

A

The amount of plasma glucose concentration

98
Q

Irreversible, so because the average red cell lives 120 days, the Glycosylated Hemoglobin level reflects:

A

Plasma glucose levels over the previous 2-3 months unrelated to short-term fluctuations in plasma glucose levels

  • Normal Values: 3.0 – 6.0%
  • Estimated Average Glucose (EAG) can be calculated:
    1. 7 X A1c – 46.7
  • Recommended that A1c be reported out with a mean glucose level
  • Goal is to maintain levels of Hemoglobin A1c around 7.0% for Diabetics
99
Q

Interferences: Red Blood Cell Life Span decreased due

to disease such as..

A

(1) Hemoglobinopathies
(2) Hemolytic anemia, etc;
* * The hemoglobin will have less time to become glycosylated and levels will be falsely decreased
* * Longer Life span of Red Cells (post-splenectomy) may have increased levels

100
Q

Abnormal Hemoglobins in Homozygous State

A

If there is no Hemoglobin A1 present, there cannot be Hgb A1c
HOWEVER:
Variant Hemoglobin’s can be glycosylated—but are NOT linked to certified methods and cannot be correlated in the same way!

  • Hemoglobin’s S and C have substitutions closer to the N-terminal of the beta chain, therefore interfere in some methods
  • Hemoglobin’s E and D have substitutions further away –so are less likely to interfere in some methods
101
Q

Methods for A1C

A

(1) Based on charge differences between glycosylated and non-glycosylated hemoglobin’s
e. g. Cation-Exchange High Pressure Liquid Chromatography (HPLC), Electrophoresis

(2) Those based on structural differences between glyco-groups
e. g. Immunoassays, Affinity Chromatography

102
Q

High Pressure Liquid Chromatography Cation Exchange

A
  • Bio-Rad Variant II Turbo

- Hemoglobin’s are separated based upon their charge in a cation-exchange column.

103
Q

Stationary Phase

A
  • The sample is injected into a cartridge which contains negatively charged binding sites (Stationary Phase)
  • Positively charged hemoglobins will bind to those sites
  • Some hemoglobin variants have more “positively charged” sites and will bind tighter than other hemoglobin variants
104
Q

Mobile Phase

A

Three Phosphate buffers of increasing ionic strength are used to elute the individual components which are read on a spectrophotometer at 415 and 690 nm (Mobile Phase)

105
Q

Interferences with this method:

A

(1) Temperature Dependent

(2) Hemoglobin F >25%

106
Q

Immunoassay

A
  • Siemens Advia 1650
  • Roche Cobas is similar only turbidimetric
  • Latex Agglutination inhibition
  • Normally, the agglutinator (synthetic Hb A1c) will bind to reagent antibody (Anti-Hb A1c) that is attached to a latex bead
107
Q

Agglutination produces an increase in..

A

Scattered light which is read by the instrument

108
Q

Patient Hb A1c when present, will compete for the binding sites on the antibody..

A

Preventing the agglutinator from binding

  • Produces decreased light scattering
  • Patient Hb A1c has an inversely proportional relationship with light scattering
109
Q

Affinity Chromatography

A
  • Glycosylated Hemoglobin attaches to the resin but non-glycosylated hemoglobin does not
  • The glycosylated hemoglobin is then removed from the resin bed using a buffer
  • Not affected by Temperature
110
Q

Specimen Requirement for A1c

A
EDTA Whole Blood Specimen
	Hemolysate is prepared
Patients should have this test:
	Twice a year:  Controlled Diabetics
	Quarterly:	  Treatment Changes
				  Uncontrolled Diabetics
111
Q

Fructosamine (Plasma Protein Ketoamine)

A
  • Glycated Albumin and Protein
  • Albumin has a half-life of 2-3 weeks
  • Glucose Control over 2-3 weeks
  • Responds more quickly to changes in therapy
  • Fructosamine reduces Nitro-Blue Tetrazolium to Formazan
  • (Colorimetric at 530 nm)
112
Q

Microalbuminuria

A
  • Useful in the diagnosis of early kidney disease in diabetic patients
  • Type I Diabetics are typically screened annually beginning 5 years after diagnosis
  • Type 2 Diabetics screened annually from diagnosis
113
Q

How is microalbuminuria assessed?

A

Microalbuminuria is assessed by using the Albumin to Creatinine Ratio
Present when the Albumin – Creatinine Ratio:
30 – 299 mg of Albumin to 1 gm of Creatinine

114
Q

Specimen Requirement for Microalbumin

A
  • Random Urine (Most Common)

- Positive result in 2 out of 3 urine samples collected within a period of 3 -6 months as recommended by the ADA

115
Q

False Increases in Urinary Albumin

A
  • Exercise within 24-hour period
  • Infection
  • Fever
  • Congestive Heart Failure
  • High Blood Pressure
116
Q

C-Peptide

A

Part of the Proinsulin Molecule

117
Q

What removes the C-peptide during purifiation? What is this process useful for?

A
  • Commercial insulin removes the C-peptide during purification
  • Useful in distinguishing between endogenous and exogenous insulin
  • Helps diagnose Insulinomas
  • An Insulinoma is an insulin- secreting tumor; Most are benign.
118
Q

Urinary Sugars: How and why is it examined?

A

Urine is examined routinely to detect the presence or determine the amount of glucose
Glucose Renal Threshold: 170 mg/dL

119
Q

Urinary Sugars: Definition

A

The plasma concentration of glucose above which glucose cannot be reabsorbed by the renal tubules and thus is excreted into the urine

120
Q

Galactosemia: Definition

A

Inability to metabolize galactose

Deficiency: Galactose-1-Phosphate Uridylyl Transferase; Type 1 GALT Gene Mutation

121
Q

Galactosemia: Complications

A
  • Liver disease
  • Cataracts
  • Mental Retardation
  • Ecoli or other gram negative sepsis
122
Q

Lactose Intolerance Testing: Hydrogen Breath Test

A
  • Normally have very little Hydrogen or Methane in breath
  • If unable to break down lactose, it will be fermented in the colon by bacteria releasing hydrogen and methane gases
  • Patient takes a baseline breath test
  • Drink a liquid that contains a source of lactose
  • Takes Breath samples at 15 minute intervals over 2-3 hours
  • The breath is measured for Hydrogen, Methane, and Carbon Dioxide