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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

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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

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