Carbohydrates ( CC1 Lab)
Page 1: Carbohydrates
Primary source of energy for brain, erythrocytes, retinal cells
Major food source and energy supply for the body
Stored as Glycogen in the liver and muscle
Diseases: Hyperglycemia and Hypoglycemia
Carbohydrates are hydrates of aldehyde or ketone derivatives
Page 2: General description of carbohydrates
Carbohydrates contain CHO (Carbon, Hydrogen, Oxygen)
Classifications based on:
Number of carbons (Trioses, tetroses, pentoses, hexoses)
Properties (Size of the carbon, Location of the functional group, Number of sugar units, Stereochemistry of the compound)
Page 3: Classification of carbohydrates based on the number of sugar units
Monosaccharides: Simple sugars with more than 3 carbons (e.g., glucose, fructose, galactose)
Disaccharides: Two monosaccharides joined by Glycosidic linkages (e.g., maltose, sucrose, lactose)
Oligosaccharides: Chaining of 2 to 10 sugar units
Polysaccharides: Linkages of many monosaccharide units (e.g., starch and glycogen)
Page 5: Pathways in Glucose Metabolism
Glycolysis: Metabolism of glucose to pyruvate/lactate for energy production
Gluconeogenesis: Formation of glucose-6-phosphate (G6P) from non-carbohydrate sources
Glycogenolysis: Breakdown of glycogen to glucose
Glycogenesis: Conversion of glucose to glycogen
Lipogenesis: Conversion of carbohydrates to fatty acids
Lipolysis: Decomposition of fats
Page 7: INSULIN
Hypoglycemic agent
Hormone responsible for the entry of glucose into the cell
Synthesized by the cells of the Islet of Langerhans
Increases glycogenesis, lipogenesis, and glycolysis
Inhibits glycogenolysis
Page 8: Glucagon
Hyperglycemic agent
Primary hormone responsible for increasing glucose levels
Synthesized by the A cells of Islets of Langerhans
Released during stress and fasting
Promotes glycogenolysis and gluconeogenesis
Page 9: Hormones
Epinephrine: Increases plasma glucose by inhibiting insulin, promotes glycogenolysis and lipolysis
Cortisol: Increases plasma glucose by decreasing intestinal entry to the cell, increases gluconeogenesis and lipolysis
Growth hormone: Increases glucose by decreasing entry of glucose into the cell, increases glycolysis
ACTH: Conversion of glycogen to glucose, promoting gluconeogenesis
Thyroxine: Increases plasma glucose, increasing glycogenolysis and gluconeogenesis
Somatostatin: Inhibits insulin, glucagon, and growth hormone
Page 13: Conditions: HYPERGLYCEMIA
Increase in plasma glucose
Diabetes Mellitus: Metabolic disorder with a defect in insulin secretion or action
Types: Type I, Type II, Other specific types, Gestational DM
Page 14: Laboratory findings in Hyperglycemia
Increase in glucose in plasma and urine
Increase in specific gravity
Presence of ketones in serum and urine
Decrease in blood and urine pH
Electrolyte imbalance: Low sodium and bicarbonate, high potassium
Page 15: Type I Diabetes Mellitus
Pancreatic islet B cell destruction
Cellular-mediated autoimmune destruction of B cells, insulin secretion deficiency (insulinopenia)
Onset in childhood or adolescence
Initiated by environmental factors or infection
Abrupt onset
Insulin-dependent
Ketosis prone
Symptoms: Polydipsia, polyphagia, polyuria, weight loss, hyperventilation, mental confusion, loss of consciousness
Complications: Nephropathy, neuropathy, retinopathy, heart disease
Page 17: Type II Diabetes Mellitus
Due to insulin resistance with an insulin secretory defect
Common in obese individuals
Associated with age, obesity, and lack of exercise
Page 18: Other specific types of Diabetes Mellitus
Genetic defects: Down syndrome, Klinefelter syndrome
Pancreatic disease
Drugs and Chemicals: Dilantin and pentamidine, Thiazides and glucocorticoid
Maturity onset diabetes of youth: Rare form, inherited, autosomal dominant
Page 19: Gestational Diabetes Mellitus
Recognized during pregnancy (24 to 28 weeks of gestation)
Metabolic and hormonal changes
Complications for the baby: Respiratory distress, hypocalcemia, hyperbilirubinemia
Page 20: Idiopathic Type I Diabetes and Impaired fasting glucose
Idiopathic Type I Diabetes: No known etiology, strongly inherited
Impaired fasting glucose: Intermediate stage between normal and diabetes level
Page 21: Risk factors for Diabetes Mellitus
Glucosuria
Age: 45 years old, FBG every 3 years
BMI >25
Risk factors: Physically inactive, family history, high-risk population, history of GDM (Gestational DM), hypertension, high HDL (high-density lipoprotein)
Page 27: Hypoglycemia
Symptoms appear at 50 to 55 mg/dL
Diagnostic hypoglycemia at <50 mg/dL
Results from imbalance in glucose utilization and production
Symptoms: Increased hunger, sweating, nausea, vomiting, dizziness, nervousness, shaking, blurring of speech and sight, mental confusion
Page 28: Diagnostic criteria for Diabetes Mellitus
FPG (Fasting Plasma Glucose):
Pre-diabetes: <100 mg/dL
Impaired PG: 100-125 mg/dL
DM: >126 mg/dL
OGTT (Oral Glucose Tolerance Test):
Non/Normal: <140 mg/dL
Impaired GTT: 140-199 mg/dL
DM: >200 mg/dL
Page 29: Diagnostic criteria for Gestational Diabetes Mellitus
Age: >25 years old
Overweight
Family history
History of abnormal glucose metabolism
Glucosuria
PCOS (Polycystic Ovary Syndrome)
Ethnic group
Page 25: Impaired Fasting Glucose and Impaired Glucose Tolerance
Impaired Fasting Glucose: Fasting Blood Glucose (FBG) between 100-126 mg/dL
Impaired Glucose Tolerance: 2-hour Oral Glucose Tolerance Test (OGTT) between 140-199 mg/dL
Page 26: Diagnostic criteria for Gestational Diabetes Mellitus
Fasting: >95 mg/dL
1 hour: >180 mg/dL
2 hours: >155 mg/dL