1 - CARBOHYDRATES

Glucose, fructose, galactose

Common Sugars

Monosaccharides (3)

Maltose, lactose, sucrose

Common Sugars

Disaccharides (3)

Glucose + Glucose

Common Sugars

Disaccharides

Maltose:

Glucose + Galactose

Common Sugars

Disaccharides

Lactose:

Glucose + Fructose

Common Sugars

Disaccharides

Sucrose:

Starch, glycogen

Common Sugars

Polysaccharides (2)

Starch

Common Sugars

Polysaccharides

Plant-based glucose polymer

Glycogen

Common Sugars

Polysaccharides

Animal-based glucose polymer

Reducing sugars

Common Sugars

Has a free aldehyde or ketone group that can be oxidized

Glucose, fructose, maltose, lactose, galactose

Common Sugars

Examples of reducing sugars (5)

Nonreducing sugars

Common Sugars

Lack a free aldehyde/ketone due to glycosidic bonding

Glucose

Common Sugars

Primary source of energy for humans

Glycogen

Common Sugars

Glucose storage form (liver and muscle)

1.5 to 2

Common Sugars

Glucose level returns to normal _ to _ hours after eating

Glycolysis

Glycogenesis

Lipogenesis

GLUCOSE METABOLISM
↓ Glucose	_	Glucose → Pyruvate
	_	Glucose → Glycogen
	_	Carbohydrates → Fats

Gluconeogenesis

Glycogenolysis

GLUCOSE METABOLISM
↑ Glucose	_	Noncarbohydrates → Glucose
	_	Glycogen → Glucose
	x	Fat → Carbohydrates

Embden-Meyerhof pathway (Glycolysis)

Hexose Monophosphate Shunt

Storage (Glycogenesis)

Glucose Metabolism

Once inside a cell, glucose-6-phosphate (phosphorylated glucose) enters into: (3)

Embden-Meyerhof pathway (Glycolysis)

Glucose Metabolism

2 ATP net gain

Hexose Monophosphate Shunt

Glucose Metabolism

NADPH for oxidative damage protection

Storage (Glycogenesis)

Glucose Metabolism

Glycogen

Insulin

Glucose Metabolism Regulation

Only hypoglycemic agent

For glucose uptake into cells

glycolysis, glycogenesis, lipogenesis

Glucose Metabolism Regulation

Insulin

Increases (3)

β-cells

Glucose Metabolism Regulation

Insulin

Synthesized by _ of islets of Langerhans in pancreas

Glucagon

Glucose Metabolism Regulation

Primary hyperglycemic agent

glycogenolysis, gluconeogenesis

Glucose Metabolism Regulation

Glucagon

Increases (2)

α-cells

Glucose Metabolism Regulation

Glucagon

Synthesized by _ of islets of Langerhans in pancreas

Somatostatin, GH, Cortisol, Epinephrine, T4

Glucose Metabolism Regulation

Other hyperglycemic agents (5)

Plasma/serum

Whole blood

Specimens for Glucose Measurement (2)

Plasma/serum

Specimens for Glucose Measurement

More preferred

30, 1

Specimens for Glucose Measurement

Plasma/serum

Must be separated within _ minutes/_ hour

11

Specimens for Glucose Measurement

Whole Blood

Glucose ~_% lower than plasma

gray

sodium fluoride

Specimens for Glucose Measurement

Considerations:

Use _-top tubes (_ _) to inhibit glycolysis

citrate

Specimens for Glucose Measurement

Considerations:

Sodium fluoride is now recognized to be ineffective; Less glycolysis was found in tubes w/ _ buffer, separated by gel barrier (Henry’s 24th)

7 mg/dL/hour

Specimens for Glucose Measurement

Considerations:

At RT, glycolysis decreases glucose by _ _ in uncentrifugated blood

2 mg/dL/hr

Specimens for Glucose Measurement

Considerations:

During refrigeration, glucose is metabolized by _ _

2 mg/dL/decade

4 mg/dL/decade

8-13 mg/dL/decade

Specimens for Glucose Measurement

Considerations:

Glucose increases with age:

Fasting: _

Postprandial: _

OGTT: _

Folin Wu

Nelson-Somogyi

Neocuproine

Glucose Measurement Methods

Obsolete Methods

Copper Reduction (3)

Folin Wu

Glucose Measurement Methods

Obsolete Methods

Copper Reduction

Copper + phosphomolybdate → Phosphomolybdenum blue

Nelson-Somogyi

Glucose Measurement Methods

Obsolete Methods

Copper Reduction

Copper + arsenomolybdate → Arsenomolybdenum blue

Neocuproine

Glucose Measurement Methods

Obsolete Methods

Copper Reduction

Copper + Neocuproine → _____________________________

Hagedorn-Jensen

Glucose Measurement Methods

Obsolete Methods

Ferric Reduction (1)

Hagedorn-Jensen

Glucose Measurement Methods

Obsolete Methods

Ferric Reduction

Yellow ferricyanide → Colorless (Inverse colorimetry)

O-toluidine (Dubowski)

Glucose Measurement Methods

Obsolete Methods

Condensation (1)

O-toluidine (Dubowski)

Glucose Measurement Methods

Obsolete Methods

Condensation

End result of a green Schiff’s base

Glucose Oxidase-Peroxidase (GOD-POD)

Hexokinase

Glucose Measurement Methods

Enzymatic Methods (2)

Glucose Oxidase-Peroxidase

Glucose Measurement Methods

Enzymatic Methods

Highly specific for glucose

polarographic

Trinder reaction

Glucose Measurement Methods

Enzymatic Methods

Glucose Oxidase-Peroxidase

Measures either oxygen consumption (_) or H2O2 (_ _)

decreased

increase

Glucose Measurement Methods

Enzymatic Methods

Glucose Oxidase-Peroxidase

Prone to interferences with uric acid, bilirubin, ascorbic acid (all causing false _ results), and bleach (causes false _)

Hexokinase

Glucose Measurement Methods

Enzymatic Methods

Reference Method

Gross hemolysis

bilirubin

Glucose Measurement Methods

Enzymatic Methods

Hexokinase

Highly specific, minimal interference (_ _ and extremely elevated _ may cause a false decrease)

340

Glucose Measurement Methods

Enzymatic Methods

Hexokinase

Measures NADPH formation at _ nm

>100 mg/dL

>140 mg/dL

Hyperglycemia: glucose _ (fasting) or _ (non-fasting)

Insulin

Hyperglycemia

Key Regulator

Hormonal imbalance, especially involving insulin

Hyperglycemia

Cause

insulin

Hyperglycemia

Diabetes Mellitus

Group of disorders characterized by:

Chronic hyperglycemia due to _ defects (secretion, action, or both)

>180 mg/dL

Hyperglycemia

Diabetes Mellitus

Group of disorders characterized by:

Glucosuria when plasma glucose _

Diabetic Ketoacidosis

Hyperglycemia

Diabetes Mellitus

Group of disorders characterized by:

_ _ (More common in type 1)

Nonketotic Hyperglycemic State

Hyperglycemia

Diabetes Mellitus

Group of disorders characterized by:

_ _ _ (More common in Type 2)

β-cell destruction

Insulin resistance

TYPE 1 VS TYPE 2 DIABETES MELLITUS
	Type 1	Type 2
Cause	_	_

Childhood/Teens

Advancing age

TYPE 1 VS TYPE 2 DIABETES MELLITUS
	Type 1	Type 2
Onset	_	_

5-10%

90-95%

TYPE 1 VS TYPE 2 DIABETES MELLITUS
	Type 1	Type 2
Incidence	_	_

Genetic, viral

Genetic, lifestyle, obesity

TYPE 1 VS TYPE 2 DIABETES MELLITUS
	Type 1	Type 2
Risk factors	_	_

Develop abruptly

Develop gradually

TYPE 1 VS TYPE 2 DIABETES MELLITUS
	Type 1	Type 2
Symptoms	_	_

Insulin absolute

Oral agents

TYPE 1 VS TYPE 2 DIABETES MELLITUS
	Type 1	Type 2
Treatment	_	_

Type 1.5 DM / Latent Autoimmune Diabetes in Adults (LADA)

Other Types of Diabetes Mellitus

Presence of GAD antibodies, like Type 1

Adult onset (usually >30 years), like type 2

Insulin dependence progresses more slowly than classic Type 1

Type 3c DM / Pancreatogenic Diabetes

Other Types of Diabetes Mellitus

Insulin & glucagon loss secondary to pancreatic disease or surgery

Common causes: Pancreatitis, pancreatic cancer, cystic fibrosis

No autoantibodies present

Maturity-Onset Diabetes of the Young (MODY)

Other Types of Diabetes Mellitus

Monogenic: caused by a single gene mutation

Onset before 25 years old but not neonatal

No autoantibodies present, asymptomatic, requires genetic testing

Neonatal Diabetes Mellitus (NDM)

Other Types of Diabetes Mellitus

Also monogenic: Occurs within the first 6 months of life

Gestational Diabetes Mellitus (GDM): in 2nd or 3rd trimester

Other Types of Diabetes Mellitus

Maternal risks: Later development of type 2 DM

Neonatal risks: Hypoglycemia, respiratory issues, macrosomia

Level 1 (<70 mg/dL)

Hypoglycemia

Classifications:

Glucose alert value

Level 2 (<54 mg/dL)

Hypoglycemia

Classifications:

Clinically significant hypoglycemia

Level 3

Hypoglycemia

Classifications:

Severe hypoglycemia with cognitive impairment

Postabsorptive (Fasting)

Hypoglycemia

Types:

Seen in insulinomas (pancreatic β-cell tumors)

Postprandial (Reactive)

Hypoglycemia

Types:

Occurs within 4 hours after eating

Alimentary

Hypoglycemia

Types:

Triggered by rapid gastric emptying (after GI surgery)

Drug-induced

Hypoglycemia

Types:

Diabetics taking insulin or insulin secretagogues

Alcohol-induced

Hypoglycemia

Types:

Usually occurs after binge drinking without food

Non-β Cell Tumor

Hypoglycemia

Types:

Paraneoplastic IGF-II ("big IGF-II") production

Von Gierke Disease (Type I Glycogen Storage Disease)

Hypoglycemia

Genetic Defects Causing Hypoglycemia

Most common congenital form of GSD

Deficiency: ________________________

Von Gierke Disease (Type I Glycogen Storage Disease)

Hypoglycemia

Genetic Defects Causing Hypoglycemia

With ↑ lactate, alanine, lipids, uric acid

Diagnosis: Liver biopsy via glycogen stain (PAS)

Pompe Disease (Type II Glycogen Storage Disease)

Hypoglycemia

Genetic Defects Causing Hypoglycemia

Deficiency: Lysosomal acid alpha glucosidase

Hallmark: Muscle weakness

Galactosemia

Hypoglycemia

Genetic Defects Causing Hypoglycemia

Deficiency: Galactose-1-phosphate uridyltransferase (most common)

Mechanism: Glycogenolysis inhibition

Galactosemia

Hypoglycemia

Genetic Defects Causing Hypoglycemia

With hyperbilirubinemia and galactose in blood/urine

Diagnosis: Erythrocyte enzyme activity

Fructose Intolerance

Hypoglycemia

Genetic Defects Causing Hypoglycemia

Deficiency: _______________________________

Triggers: Fructose ingestion → nausea, vomiting, hypoglycemia

≥126 mg/dL

≥200 mg/dL

≥200 mg/dL + symptoms

≥6.5%

Hypoglycemia

<50 mg/dL

glucose

DIAGNOSTIC CRITERIA
Type 1 and 2 DM	Hypoglycemia (Whipple’s Triad)
Fasting Blood Sugar _ 2-hour OGTT _ Random Sugar _ HbA1c _	_ symptoms Documented glucose _ Resolution by administering _

70-99

≤140

<5.7%

CATEGORIES OF GLUCOSE LEVELS
	FBS	2-hr PP & OGTT	HbA1c
Normal GT	_ mg/dL	_ mg/dL	_

100-125

140-199

5.7-6.4%

CATEGORIES OF GLUCOSE LEVELS
	FBS	2-hr PP & OGTT	HbA1c
Impaired GT	_ mg/dL	_ mg/dL	_

≥126

≥200

≥6.5%

CATEGORIES OF GLUCOSE LEVELS
	FBS	2-hr PP & OGTT	HbA1c
Provisional	_ mg/dL	_ mg/dL	_

0.0555

To convert mg/dL to mmol/L (glucose only) multiply the mg/dL value with _

Random Blood Sugar

Glucose Biomarkers

Requested during insulin shock and hyperglycemic ketonic coma

Collected anytime

Fasting Blood Sugar

Glucose Biomarkers

A measure of overall glucose homeostasis

8-10 hours (not over 16 hours) fasting required

Self-monitoring (POCT glucometers)

Glucose Biomarkers

If type 1 DM: 3-4x a day

If type 2 DM: Frequently individualized (unknown)

Oral Glucose Tolerance & 2-Hour Postprandial Glucose

Glucose Biomarkers

Measures the response of the body (glucose metabolism)

2-hour postprandial glucose

Glucose Biomarkers

Oral Glucose Tolerance & 2-Hour Postprandial Glucose

2 hours after a full meal (monitoring)

OGTT

Glucose Biomarkers

Oral Glucose Tolerance & 2-Hour Postprandial Glucose

after intaking a glucose load (especially in GDM diagnosis)

OGTT

Glucose Biomarkers

Oral Glucose Tolerance & 2-Hour Postprandial Glucose

after intaking a glucose load (especially in GDM diagnosis)

One Step (1 intake)

Oral Glucose Tolerance Test for GDM

1. Patient undergoes fasting

2. Patient’s blood is drawn

3. Patient intakes glucose load

4. 1hr after intake, blood drawn

5. 2hrs after intake, blood drawn

Two Step (2 intakes)

Oral Glucose Tolerance Test for GDM

1. Patient intakes glucose load

2. 1hr after intake, blood drawn

3. If glucose, ≥140 mg/dL, undergo

fasting, and come back tomorrow

4. Patient’s blood drawn next day

5. Patient intakes ____________

6. 1hr after intake, blood drawn

7. 2hrs after intake, blood drawn

8. 3hrs after intake, blood drawn

≥92

≥180

≥153

Oral Glucose Tolerance Test for GDM

One Step (1 intake)

Diagnostic if AT LEAST 1 was met:

 Fasting: _ mg/dL

 1h after intake: _ mg/dL

 2h after intake: _ mg/dL

≥95

≥180

≥155

≥140

Oral Glucose Tolerance Test for GDM

Two Step (2 intakes)

Diagnostic if AT LEAST 2 were met:

 Fasting: _ mg/dL

 1h after intake: _ mg/dL

 2h after intake: _ mg/dL

 3h after intake: _ mg/dL