Lesson 5: Carbohydrates

• They are organic compounds, because they have carbon.

• There are so many.carbon compounds kasi yung carbon, they can create stable bonds and
lies two carbon versatility in creating stable bonds.

STRUCTURE
• Carbohydrates are composed of carbon, hydrogen and
oxygen
• All contain C=0 and -ОН functional groups
• General molecular formula:
(HO), where n = 3 or some
higher number
• Includes polyhydroxy aldehyde or ketone and their derivatives
• Aldehyde - has C=0 group at the end of the carbon chain
• Ketone - has C=O group on an internal carbon atom
- saccharide = sakcharon=sugar
Sucrose - table sugar
Chitin - exoskeleton of crustaceans
Cellulose - plant cell wall
Ribose - RNA
- Carbohydrates contain carbonyl and hydroxyl functional groups
Functional groups- reactive groups of molecules, site that chemical reactions occur
Aldehyde and Ketone - simplest carbonyl group
Aldehyde - if yung carbonyl is nasal end ng carbon chain.
Ketone- internal carbon atom.

CLASSIFICATION
Prefix - # of carbon atoms in a chain and structure
Suffix - ose
3 - triose
4 - Tetrose
5 - pentose
6 - hexose

Aldose - carbonyl group is an aldehyde.

Ketone - carbonyl group is ketone.
Aldohexose - 6 carbon sugar - carbonyl is aldehyde.

Based on 4 different properties

1. Size of the base carbon chain > triose, tetrose, etc.
2. Location of the carbonyl functional group.
3. No. of sugar units > mono, di, oligo, poly, (saccharide)
4. Stereochemistry of the compound > D or L sugars

MONOSACCHARIDES - 3-7 carbon atoms

• Simplest sugars; cannot be hydrolyzed to simpler carbohydrates
• Most contain three to seven carbon atoms: trioses, tetroses, pentoses, hexoses, and
heptoses
• Most notable monosaccharides: pentoses and hexoses
Pentoses
• Ribose and deoxyribose
Hydrolysis - breakdown of larger molecule into smaller molecules by adding water, to
breakdown the chemical bonds.
MONOSACCHARIDES
Hexoses
• Predominant type of monosaccharide in the body
1. Glucose - central pivotal point of carbohydrate metabolism
2. Galactose - must be converted to glucose before it can be used by the body
3. Fructose - the key intermediate in the utilization of monosaccharides
• They are structural isomers
Isomers - same number of atoms and kind of groups but they have different arrangement of
groups around the carbon atom. (Different in structural formula)
Epimers - they vary in one position for the placement of hydroxyl groups.

Asymmetric or Chiral Carbon

• Carbon atom bonded to four different atoms or group of atoms

D and L sugars
• For sugars with more than one chiral center, D or L refers to the asymmetric carbon that is the
farthest from the aldehyde or keto group
• D sugar - the -OH group on the more distal asymmetric carbon is on the right
Dextro - right
• L sugar - the -OH group is on the left.
Levo - left
• The D and L forms of glucose are mirror images (optical isomers)
• Most naturally occurring sugars in the body are D sugars

Ring (Hemiacetal & Hemiketal) Formation

• Formed when the functional group (ketone/aldehyde) reacts with an alcohol group on the
same sugar (intramolecular reactions)
• When the bond is formed, the carbon of the C=O group becomes asymmetric and is called an
anomeric carbon
Aldehyde - hemiacetal
Ketone - hemiketal
Ring - reaction between C=O and the highest numbered chiral carbon (hemiacetal and
hemiketal.

DISACCHARIDES
Composed of 2 monosaccharides -
• General formula: Cn(H20)n-1
• Covalently linked together by a condensation reaction (dehydration synthesis) where one
molecule of water is removed/produced = glycosidic bond
• Frequently formed between the -OH group of one sugar and a -OH group located on an
anomeric carbon of an adjacent sugar molecule
• In naming such bonds, the projection of the hydroxyl group on the anomeric carbon forming
the bond is designated (a or B), and the numbers of those carbon atoms that participate in the
bond are indicated
• simplest and most common oligosaccharides
• Condensation reaction - kapag maglilink ng 2 sugar units (water is removed)
• Hydrolysis - kapag maghihiwalay (water is addded).
• Alpha - hydroxyl bond (bottom)
• Beta - Hydroxyl bond (top)
Reducing Sugars
• Glycosidic bond is formed involving the hydroxyl group of only one anomeric carbon,
causing the sugar to have a free carbony! group
• Can oxidize or reduce other compounds
Non-Reducing Sugars
• Glycosidic bond is formed involving the hydroxyl group of both anomeric carbons, causing
the sugar to have no free carbony! group (no active ketone/aldehyde group)
• Cannot oxidize or reduce other compounds

Maltose
• Reducing sugar
• 2 glucose units
• Present in cereals, wheat and malt products
Lactose
• Reducing sugar
• 1 galactose unit
• 1 glucose unit AKA milk sugar
• Present in dairy products such as milk and cheese
Sucrose
• Non-reducing sugar
• 1 glucose unit
• 1 fructose unit
• AKA table/cane sugar
• Best known disaccharide
• Provides a major portion of the av carbohydrate intake of many individuals
• Present in beets, sugar cane, etc.
• Table sugar
-Biochemical markers for certain CHO malabsorption disorder.

POLYSACCHARIDES
Oligosaccharides
• Yield 2-10 monosaccharide unit upon hydrolysis
Polysaccharides
• Formed by the condensation of large numbers of monosaccharide units
• Yield more than 10 monosaccharide unit upon hydrolysis
• Most notable:
• Starch
• Cellulose
• Glycogen

1. Starch
• Primary carbohydrate in the diet; present in most plants
• Composed of amylose and amylopectin
• Amylose is a linear polymer and its glucose units are joined by a (1-4)
glycosidic bonds
• Amylopectin is a branched polymer and are joined also by a (1-4) glycosidic bonds, with a
(1-6) glycosidic bonds forming the branch points
• polymer of alpha, gamma-D-glucose
• Glycogen - sa animal
• Storage of carbohydrates in plants.
• Partial hydrolysis produces - disaccharides & dextrins
2. Cellulose
• Forms the cell walls and other supporting tissues of plants
• Cannot be digested by humans but provide bulk necessary for intestinal function
• Linkage between the glucose units is composed of B (1-4) glycosidic bonds
• termites, ruminants - digest and utilize cellulose.
• Roughage - other term for dietary fiber
• iodine in starch - dark blue color

3. Glycogen
• Carbohydrate storage form in the body of human and animal tissue
• Principally found in the liver (up to 10% of its net weight), also found in skeletal muscles (1-2%
of net weight)
• Branched polymer of thousand glucose units
• Similar to amylopectin, but with more frequent branch points, which permits rapid release of
glucose, which is essential in humans and animals
• Described to have a tree-like shape
• animal starch
• used to maintain blood sugar level between meals
• Liver - totally depleted of glycogen after 12 to 18 hours fasting.

METABOLISM
Bloodstream -carbohydrates, amino acids, fatty acids
Brain - only use glucose
2/3 glucose utilization - occurs in the CNS

DIGESTION

Starch and Disaccharides

• Only types of carbohydrates that contribute to human nutrition
• Must be broken down to monosaccharides before they can be absorbed by the intestinal
mucosal cells
Amylase Food
• Enzyme responsible for the breakdown of starch
1. Salivary amylase/ptyalin - active in mouth
2. Pancreatic amylase/amylopsin - duodenum
Enzymes: salivary amylase, pancreatic amylase, dextrinase
Anabolism - building
Catabolism - breaking down
Duodenum - after stomach

Disaccharidases
• Located on the microvilli of the intestine
1. Maltase -degrade maltose (Glucose+Glucose)
2. Lactase - degrade lactose (Glucose+Galactose)
3. Sucrase - degrade sucrose (Glucose+Fructose)

ABSORPTION

• Digested carbohydrates (monosaccharides) are absorbed by both active transport and simple
diffusion through the intestinal wall and into the blood stream.
• These monosaccharides are then transported to the liver via the
portal vein.
• In the liver, the monosaccharides may then be:
• Used for energy (glucose only)
• Converted to glycogen for storage
• Converted to carbohydrate derivatives or pentose sugars
• Converted to fat
• Converted to amino acids
Hepatic glycogen - liver
Muscle glycogen - muscle

METABOLISM
• Glycogenesis - conversion of glucose to glycogen for storage
• Glycogenolysis - conversion of glycogen to glucose and other intermediate products for
energy production
• Gluconeogenesis - conversion of noncarbohydrates le.g.. fasting stat proteins, amino acids,
fats, glycerol, lactic acid to glucose
• Glycolysis - the metabolism of glucose and other hexoses into lactate or pyruvate for energy
production
• Lipogenesis - formation of fat from carbohydrate
• Lypolysis - breakdown of fat and the release of fatty acids from fat cells into the blood
Galactose (Leloir Pathway) - Galactose to Glucose-6-phosphate
Galactosemia - lack one of the necessary enzymes

Glucose Metabolism
1. Embden-Meyerhof Pathway (EMP) / Glycosis - aerobic/anaerobic
2. Hexose Monophosphate Shunt/Pathway (HMP/HMS) - anaerobic
3. Glycogenesis Pathway - Glucose storage
• The first step for all three pathways require glucose to be converted to glucose-6-phosphate
(G6P) using the high energy molecule, ATP. This reaction is catalyzed by the enzyme,
hexokinase.
Lactic acid - anaerobic
Pyruvate - aerobic
Glycolysis - 30-32 ATP
Krebs cycle - occurs in mitochondria

Q: What happens when glucose supply is low (glucose crisis)?

• The liver will use the following to elevate blood glucose concentration:
• Glycogen
• Glycerol
• Lactic acid
• Amino acids
Glucose/Dextrose - fuel of brain
-Sweetness is one of the basic flavors that human can taste together with sour,bitter,salty, and
umami.
-Carbohydrates - major fuel for most organism
Toxics that can’t be eaten: nitrobenzene and ethylene glycol.

REGULATION OF CARBOHYDRATE METABOLISM

7 types of hormones that increase serum glucose (GAG CHET)
Glucagon.
ACTH
Growth hormone
Cortisol
Human placental lactogen
REGULATION OF CARBOHYDRATE METABOLISM
7 types of hormones that increase serum glucose (GAG CHET)
Glucagon.
ACTH
Growth hormone
Cortisol
Human placental lactogen
Epinephrine
T3 and T4

Hormones
• Produced by the endocrine glands/system
• Chemicals released into the bloodstream in response to changes taking place somewhere in
the body
• Discharged into the bloodstream after an appropriate stimulus and transported to its site of
action

1. Insulin
* the only hormore that decreases glucose level
• AKA hypoglycemic agent
• Synthesized by the beta cells of the islets of Langerhans of the pancreas as proinsulin when
there is an increase in body glucose
• Proinsulin is cleaved by enzymes to insulin and G-peptide biocherical actinty
• Decreases plasma glucose levels by:
• Increasing transport entry of glucose into cell receptor
• Dependent on insulin and insulin cell receptor
• Cell receptor is integral in glucose transport and metabolism process
• Increasing glycogenesis,
• Certain tissues need not insulin for glucose transport across cell membrane
•Increasing glycogenesis, lipogenesis, and glycolysis
• Inhibiting glycogenolysis

2. Glucagon
• AKA hyperglycemic agent blood glucose
• Synthesized by the alpha cells of the islets of Langerhans of the pancreas
• Has a specific target tissue
• Stimuli: stress and fasting states
• Increases plasma glucose levels by:
• Increasing glycogenolysis in the liver and gluconeogenesis

3. Catecholamines: Epinephrine (Adrenaline) and

Norepinephrine (Noradrenaline)
• Released from the chromaffin cells of the adrenal medulla
• Stimuli: Physical/emotional stress
• Overall effect to plasma glucose : increase plasma glucose level
• Inhibits insulin release and provokes glucagon release
• Stimulates glycogenolysis and lipolysis
• Pheochromocytoma (tumor of the adrenal medulla)
• produces epinephrine and causes hyperglycemia
4. Glucocorticoids: Cortisol and Cortisone
• Released from the adrenal cortex upon stimulation of the adrenocorticotropic hormone
(ACTH)
• Stimuli: Physical/emotional stress
• Overall effect to plasma glucose: increase plasma glucose level
• Decrease entry into the cell
• Increase gluconeogenesis, glycogenolysis and lipolysis
• Decrease muscle and adipose tissue response to insulin-stimulated glucose uptake
antagonistic effect to insulin.
• Cushing's syndrome (tumor/hyperplasia of the adrenal cortex
• produces glucocorticoids and causes hyperglycemia

5. Adrenocorticotropic Hormone (ACTH)

• Released from the anterior pituitary gland
• Stimuli: Decreased cortisol levels
• Overall effect to plasma glucose: increase plasma glucose level
• Stimulates the release of cortisol

6. Thyroxine / Tetralodothyronine (T4)

• Released from the thyroid gland in response to TSH
• Overall effect to plasma glucose: increase plasma glucose level
• Increase gluconeogenesis and glycogenolysis
• Increased intestinal absorption of glucose.
Hyperthyroidism (e.g., thyrotoxicosis)
• May show symptoms of mild diabetes and almost complete absence of liver glycogen

7. Growth Hormone (GH)

• Released from the anterior pituitary gland
• Overall effect to plasma glucose: increase plasma glucose level
• Decreasing the entry of glucose into the cells
• Increase glycolysis
Acromegaly (disease caused by increased GH)
• May be hyperglycemic

8. Somatostatins
• Released from the delta cells of the islets of Langerhans of the pancreas. as well as the
hypothalamus and GI tract.
• Inhibit pituitary (GH and TSH), gastrointestinal (gastrin, secretin, vaso-intestinal peptide) and
pancreatic (insulin, glucagon) hormones
• Possess nonendocrine functions
• Inhibition of gastric acid secretion, gastric emplying time
• Pancreatic enzyme release

Clinical Conditions Involving Glucose Absorption

1. Hyperinsulinism - increased secretion ofinsulin.
2. Insulinoma - tumor of the pancreas resulting to increased insulin
3. Hypo-insulinism - decreased secretion of insulin hormone
4. Hyperglycemia - increased blood glucose level
5. Hypoglycemia - decreased blood glucose level
CLINICAL SIGNIFICANCE

HYPOGLYCEMIA (low blood sugar)

Glucose Levels
• ≤60 mg/dL (3.3 mmol/L) - strongly suggestive of hypoglycemia (series of random/fasting
serums specimens)
• ≤55 mg/dL (3.0 mmol/L) + hypoglycemic symptoms in individuals not receiving medications for
diabetes diagnostic assessment
• ≤50 mg/dL (2.8 mmol/L) in infants → diagnostic assessment
Diagnosis (Whipple's Triad) (Allen Whipple)
• Symptoms:
• Neurogenic: tremors, palpitations, anxiety, diaphoresis
• Neuroglycopenic: increased hunger, cold sweat, dizziness, nausea, vomiting, nervousness,
shaking, blurring of speech and sight, mental confusion, behavioral changes/irritability, tingling,
fast heartbeat, weakness, fatigue.
• Decreased plasma glucose concentration
• Relief of symptoms after giving corrective measures
Insulinoma - excessive insulin
Normal blood glucose level: 70-110 mg/dL
Glucagon and glycemic factors: 65-70 mg/dL
Strongly suggestive of hypoglycemia: ≤60 mg/dL
Observable symptoms: 50-55 mg/dL

Causes
• Drug administration: Excessive insulin or oral hypoglycemic agents
• Others: alcohol, salicylates, sulfonamides, pentamidine
• Organ problems and critical illnesses
• Liver disorders (hepatis, cirhosis) and hepatic failure loss of liver tissue
• Renal failure or cardiac failure
• Gastrointestinal/alimentary disorders/surgery
• Others: Malnutrition* and sepsis -7 renal / liver failure
• Hormonal deficiency: impaired response to hypoglycemia (glucagon, etc.)
• Cancer: insulinoma, mesotheliomas, adrenocortical tumors, leukemia, hepatoma, lymphoma
• Childhood hypoglycemia: galactosemia, Reye's syndrome, GSDs
• Autoimmune hypoglycemia
• Idiopathic/functional postprandial hypoglycemia

HYPERGLYCEMIA (high blood sugar)

• Glucose level of ≥126 mg/dL (7.0 mmol/L) usually caused by imbalance of hormones
• Toxic to beta cell function and impairs insulin secretion
Symptoms
• 3Ps: polyuria, polydiosia, polyphagia
• Others: blurred vision, nausea, drowsiness, dry skin, fatigue
Long-Term Effects
• Weight loss
• Increase in bacterial and yeast infections
• Women: vaginal infections and cessation of menstruation
• Men: impotence
• Nephropathy and retinopathy
Laboratory Findings
• Increased glucose in plasma and urine type I patients
• Increased urine specific gravity
• Increased serum and urine osmolality
• Ketonemia and ketonuria
• Decreased blood and urine pH (acidosis)
• Electrolyte imbalance
Kussmaul-lien respiration - deep respiration/rapid

Causes
• Diabetes mellitus
• Pancreatic disorders / pancreatectomy
• Endocrine disorders: Cushing's syndrome, pheochromocytoma, acromegaly, hyperthyroidism,
PCOS
• Exocrine disorders: cystic fibrosis, neoplasia, hemochromatosis
• Drugs or chemical inducers of f cell dysfunction (dilantin and pentamidine) and impair insulin
action (thiazides, glucocorticoids)
• Genetic syndromes: Down, Klinefelter's, Huntington's chorea, Turner, Leprechaunism,
Rabson-Mendegall syndrome

DIABETES MELLITUS

• Group of metabolic disorders characterized by hyperglycemia resulting from defects in insulin

secretion, insulin action, or both
• Type 1 vs Type 2: See separate table
Predisposing Factors
• History of impaired fasting glucose (110-126 mg/dL) or impaired 2-hr glucose tolerance
(140-200 mg/dL.)
• History of diabetes in a first-degree relative
• History of GDM or delivering a baby >9 Ibs or 4.1 kgs - magloroon ang babae ng GDM
• Obesity - 120% of the desirable body weight or BMI
• Hypertension
• Abnormal lipoprotein levels (TAG, total C, HDL, LDL)
• High-risk minority population: African-American, Hispanic-American,
Native America, Asian-American
DM 1- Kahit anong diet walang epekto, insulin ang kailangan

Diagnostic Criteria
• Any one of the following is considered diagnostic for DM:
• Classic symptoms of diabetes + RPG of ≥200 mg/dL (11.1 mmol/L)
• Fasting plasma glucose of ≥ 126 mg/dL (7.0 mmol/L)
• 2-hr post-glucose load of ≥ 200 mg/dL (7.0 mmol/L)
• HbA1c of ≥6.5%

GESTATIONAL DIABETES MELLITUS

• Disorder characterized by impaired ability to metabolize glucose commonly caused by insulin
deficiency, metabolic changes, or hormonal changes
• Occurs during pregnancy and disappears after delivery, but in some cases, returns years later
Mechanism
• The placenta produces certain hormones that promotes insulin resistance → the body makes
three times more insulin than normal to maintain normal blood glucose level
• 5% of pregnant women cannot produce enough insulin to maintain normal blood glucose
level, ending up with GDM at around the 20th to 24th week of gestation
Screening GDM: 24th - 28th weeks of gestation
Predisposing Factors
• 25 years of age or more
• Above normal BMI
• History of diabetes in a first-degree relative (mama or papa)
• High-risk minority population: African-American, Hispanic-American,
Native America, Asian-American

Maternal Complications
• Increased rate of caesarean delivery
• Chronic hypertension
• 30-40% will develop DM type 2 within 10 years

Infant Complications
• Respiratory distress syndrome
• Hypocalcemia
• Hyperbilirubinemia
• Severe hypoglycemia after delivery
Fetal insulin secretion is stimulated due to high maternal hyperglycemia upon delivering of the
umbilical cord, the oversupply of glucose is terminated and infant insulin remains high.

KETONEMIA AND KETONURIA

• Seen in cases of carbohydrate deprivation or decreased carbohydrate use:
• Diabetes mellitus
• Starvation
• High-fat diet
• Prolonged vomiting
• Glycogen storage diseases
• Results from lipolysis which engenders the following ketone bodies as end-products into the
blood:
• Acetone - 2%
• Acetoacetic acid (AAA) - 20%
• 3-B-hydroxybutyric acid - 78%

Ketone Determination
• Recommended in patients with:
• DM Type 1 (during acute illness)
• Stress
• Pregnancy
• Hyperglycemia (≥300 mg/dL)
• Signs/symptoms of ketoacidosis
• Specimen: fresh serum or urine, tightly stoppered and analyzed immediately
• Methods:
• Gerhardt's ferric chlorde test
• Sodium nitroprusside test
• Acetest tablets and Ketostix
• KetoSite test
• Decreased lactase level → inability of the small intestines to breakdown lactose → lactose
accumulation in the small intestines → lactose breakdown by gut bacteria → cramping,
diarrhea, malabsorption, GI discomfort

Lactose Tolerance Test

• Fasting plasma glucose is determined
• 50 g lactose load in 200-300 mL water is given to the patient (for adults)
• Blood sample is collected every 30 minutes for 2 hours
• Result:
• Glucose rise of ≥25 mg/dL above the fasting level = normal lactose tolerance
• Glucose rise of <20 mg/dL above the fasting level = lactose intolerance

GALACTOSEMIA
• Increased level of galactose in the blood due to a congenital deficiency of one the three
enzymes for galactose metabolism:
1. Galactose-1-phosphate uridyl transferase
2. Galactokinase
3. UDP-galactose-4-phosphate epimerase
• Galactose must be removed from the diet to prevent the development of complications:
• hepatomegaly, jaundice, kidney damage, mental retardation, cataracts

Laboratory Findings
• Galactose accumulation in blood, tissue and urine following milk ingestion
• Hypoglycemia
• Hyperbilirubinemia

OTHER DISORDERS
Essential Fructosuria
• Fructokinase deficiency
• Inability to convert fructose to fructose to fructose-1-phosphate
Hereditary Fructose Intolerance (HFI)
• Fructose-1,6-biphosphate aldolase B deficiency
• Inability to cleave fructose-1,6-phosphate into glyceraldehy-3-phosphate and
dihydroxyacetone phosphate
Glycogen Storage Disease (GSD)
• Caused by the deficiency of a specific enzyme needed in glycogenesis
• Lab Test: plasma glucose response to 0.5mg IM glucagon
• See separate table for types of GSD

CSF GLUCOSE
• 40-60% of blood plasma glucose level
• Reference Range: 40-70 mg/d (adults); 60-80 mg/dL (child)
• Changes in the blood sugar is refected in the CSF -one hour later because of the lag in CSF
glucose equilibrium time
• For comparison, a blood glucose specimen should be collected at least 1 hour before the
lumbar puncture
• Increased in diabetes mellitus
• Decreased in bacterial, tubercular, fungal and amebic meningitis, subarachnoid hemorrhage,
systemic hypoglycemia
LABORATORY TESTING

FASTING BLOOD SUGAR

• AKA fasting plasma glucose
• A measure of overall glucose homeostasis
• Resire 6-8 hour overnight non-per-orem (NOyfasting prior to
• Reference Ranges: 70-110 mg/dL
• Conversion Factor to SI units (mmol/L): 0.055555

RANDOM BLOOD SUGAR

• AKA random blood glucose
• Sometimes equated to capillary blood glucose
• May be used to monitor sugar levels in diabetic patients
• One of the first tests to be measured in code blue
• Requested during insulin shock and hyperglycemic ketonic coma
• Reference Ranges: <200 mg/dL
• 160-199 mg/dL - borderline; must do follow up testing

2-HOUR POSTPRANDIAL BLOOD GLUCOSE

• 2HPPBG or 2PPBG or 2PPBS
• Measures how well the body metabolizes glucose
• Glucose testing 2 hours after meal
• Variation: 75 g standardized load of solution instead of a meal
• Reference Ranges: 60-200 mg/dL *140 mg/dL

ORAL GLUCOSE TOLERANCE TEST

• Measures how well the body metabolizes glucose
• Used to diagnose DM, especially in patients with impaired FBS
Principle
• After testing for FBS, patient is given a standard glucose load and the ability of the patient to
handle the glucose load is monitored by measuring blood over a 3-hour period
Glucose Load
• 50 grams - screening program of DM
• 100 grams - confirmatory of DM
• 75 grams - adult patients
• 1.75 g/kg body weight (maximum of 75g) - children

Patient Considerations
• Should be administered only to ambulatory patient
• At least 3 days prior should eat normal meals
• Interfering substances should be avoided 3 days prior to the test
• Drugs like salicylates, diuretics, anticonvulsants, oral contraceptives, and corticosteroids
• Before the test is performed, the patient should have fasted for 8-12 hrs
• Should be performed in the morning because of the hormonal diurnal-effect on glucose
• No smoking and alcohol drinking
• Patient must remain seated, limited walking is allowed
• Patient may drink water before and during the test
• Conditions that may affect results: GI problems (e.g. malabsorption), GI surgery, vomiting,
endocrine dysfunctions
Testing
• FBS is obtained and the glucose load is given
• Glucose load must be consumed within 5 minutes
• Blood samples are collected at 30-minute interval for two hours
• Note:
• If possible, venous blood should be collected
• Urine for glucose testing may be collected together with each blood samples
Results
• 30 minutes: FBS + 30-60 mg/dL
• 1-hour: FBS + 20-50 mg/dL
• 2-hour: FBS + 5-15 mg/dL
• 3-hour: FBS level or below

TESTS FOR GESTATIONAL DIABETES MELLITUS

Screening (O'Sullivan's Test)
• Performed between 24th and 28th week of gestation to high-risk patients
• 50 grams of oral glucose load given
• Time of the day and time of the last meal is not taken into consideration
• Venous plasma glucose is tested after an hour
• Reference Range: <140 mg/dL
Diagnosis (3-hr OGTT using 100g glucose)
• Performed in the morning after 8-12 hours overnight fasting
• FBS is measured and the 100g glucose load is given orally
• Plasma glucose is measured hourly for 3 hours
• Diagnostic for GDM: at least two values among the following::
• FBS: >105 mg/dL
• 1-hour: >190 mg/dL
• 2-hour: >165 mg/dL
• 3-hour: >145 mg/dL

POINT-OF-CARE GLUCOSE TESTING

• May be done by a health care professional, a patient's company or the patient himself/herself
• DM Type 1: 3-4 times a day is recommended
• Most monitors employ glucose oxidase method; others utilize hexokinase method
• Uses whole blood: 12-15% lower than plasma determinations

HEMOGLOBIN A1C
• AKA glycated hemoglobin, glycohemoglobin, glycosylated hemoglobin, fast hemoglobin
• Refers to the compound of hemoglobin formed when glucose reacts with the amino group of
hemoglobin
• Reflects the average blood glucose level over the previous 2-4 months.
• Reliable method of measuring long-term glucose level control compared to RBS and FBS
Factors affecting levels
• Average glucose concentration
• Red blood cell life span
*The rate of formation of glycated hemoglobin is directly proportional to the plasma glucose
concentration
Specimen Considerations
• Hemolysate from EDTA whole blood
• False decrease: hemolyzed sample, Hb C & Hb s
• False increase: Hb F

Methods
• Chromatography, electrophoresis, isoelectric focusing, immunoassay, spectrophotometry

Reference Ranges
• 4.5-5.7% - normal
• 5.7-6.4% - pre-diabetes
• 26.5% - DM
Older RBC > Iron deficiency anemia
Shorten RBC lifespan > Hemolytic anemia
For every 1% increase in HBA1C , there is 35mg/dL added to the plasma glucose.

FRUCTOSAMINE
- Refers to glycosylated albumin and other protein
- Gives clear picture of more short term glucose levels
2-3 weeks = albumin
2-3 days = other proteins