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Published by: faats on Oct 07, 2010
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Carbohydrates source of energy for the human body aldehydes or ketones w/ 2 or more hydroxyl groups classified: monosaccharides, oligosaccharides, and polysaccharides D-glucose

D-Glucose  Principal and most exclusive CHO circulating in the blood  Blood glucose---derived from the hydrolysis of dietary starch, from conversion of other dietary hexose into glucose by the liver, and from the synthesis of glucose from AA, FA and lactate  Principal fuel for peripheral tissues  Maintained by metabolic processes and hormonal control HORMONAL REGULATION Epinephrine  Adrenaline  Increases glucose by: stimulating glycogenolysis and lipolysis while inhibiting the release of pancreatic insulin Thyroxine  Secreted by thyroid gland  Promotes glycogenolysis and can lead to a depletion of glycogen stores in the liver

Insulin *small peptide secreted by the beta cells of the pancreatic islets of Langerhans in respons to an blood glucose level  The only hormone that lowers the blood glucose  Increasing membrane permeability to glucose by binding to receptors on cell surface-entry into liver, muscle and adipose tissue  Enhancing the synthesis of glycogen, lipid and CHON  Blood glucose , insulin is secreted  Blood glucose , inhibits release of insulin

Glucagon  Polypeptide hormone secreted by the α cells of the pancreatic islets of Langerhans in response to a low blood glucose level  Principal hormone for producing a rapid increase in the concentration of glucose in the blood  Stimulates hepatic glycogenolysis and gluconeogenesis

Growth Hormone    Somatotropin, secreted by the anterior pituitary Inhibits glucose uptake by the tissues Stimulate liver glycogenolysis- raising glucose concentration 

Adrenocorticotropin ACTH Stimulates the release of cortisol from the adrenal glandincreasing glucose level

Cortisol  Stimulates gluconeogenesis ***Somatostatin, Somatomedins Disorders of Carbohydrates: increased plasma glucose concentration (hyperglycemia) decreased plasma glucose concentration (hypoglycemia) normal or decreased plasma glucose, often with the excretion of a nonglucose reducing sugar in the urine (inborn errors of carbohydrate metabolism) Hyperglycemia: Diabetes Mellitus

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 most important disease associated with hyperglycemia  characterized by: deficiency of insulin secretion or action resulting in hyperglycemia and the probable development of complications overtime Type I DM Laboratory Findings  severe form of DM  characterized by absolute deficiency of insulin (autoimmune destruction or degeneration of the pancreatic islet beta cells)  ciral or chemical, genetic  islet cell autoantibodies, insulin autoantibodies etc…  abrupt onset of symptoms, often following viral infection and proneness to ketosis  require insulin treatment to prevent ketosis and sustain life  history of rapid weight loss, polyphagia, polydipsia, polyuria  neurologic: confusion, disorientation and loss of consciousness Type II DM  Milder form of DM  Characterized by a relative deficiency of insulin activity due to insulin resistance (insulin level normal, but insufficient peripheral response to the insulin), and insulin secretory defect   amyloid deposition (starchlike-protein-carbohydrates complex) in tissues  Environmental factors: intake of excessive calories, lack of physical exercise  No relationship to viruses  Not prone to ketosis; usually do not require insulin   risk of developing vascular complication and hyperosmolar coma  Obese, after age 40 and progress slowly  Most common form of DM, accounts for 80 to 90% of patients IGT (impaired glucose tolerance)  Plasma glucose levels following an oral glucose load that are not normal yet not sufficiently abnormal to be classified as DM  Hyperglycemia ( blood glucose level)  Polyuria,  urine and serum osmolality,  specific gravity, ketonemia, ketonuria, acidosis, electrolyte imbalance *occur at any age, frequently juveniles 10% of all cases of DM Asian or African descent

Gestational DM  During pregnancy due to hormonal and metabolic changes  Family history of diabetes; history of recurrent monilial infections or reproductive history of large babies (>4000g) or infants w/ congenital anomalies  Maternal symptoms mild; on fetus can be devastating (congenital malformation and perinatal mortality)  After delivery-revert to normal or develop DM later in life

IFG(impaired fasting glucose)  Plasma glucose levels following an 8-hour fast that are greater than normal but not sufficiently elevated to be classified as DM

PATHOPHYSIOLOGY Type I Type 2  Low levels of insulin-entry of glucose into cells is impaired Hyperglycemis hyperosmolar nonketotic coma resulting in elevated blood glucose *leading to urinary losses of H2O, glucose and electrolytes (osmotic diuresis)  Elevated glucose exceed the renal reabsorptive capacity, glucose is without sufficient fluid replacement-dehydration-extremely high blood excreted in the urine-glycosuria or glucosuria glucose and finally coma  Since water is excreted w/ the glucose-thirst and hungrypolydipsia (intake of large volume of water) and polyphagia  Elderly patients (excessive desire for eating)  Increased level of glucagons  Glycolysis is inhibited---glycogenolysis, lipolysis and gluconeogenesis are stimulated  Catabolism of AA and FA-amounts of acetyl CoA-converted to holesterol or ketoacid, acetoacetic acid, beta-hydroxybutyric acid and acetone---KETOSIS o Ketonemia (ketones in blood) o Ketonuria (ketones in urine) o Sweet “organic” odor (acetone)  Overproduction of ketoacids-acidosis or lowered blood pHdecreasing bicarbonate concentration-to yield CO2 and H2O  Depletion of bicarbonate-metabolic acidosis  Respiratory center stimulated- rapid, deep breathing and increased excretion of CO2 by the lungs---coma may result TREATMENT  Dietary measures  Insulin or oral hypoglycemic agents *complication w/in 10 to 15 years Retinopathy-blindness Kidney failure (nephropathy) Neuropathy Microvascular/macrovascular disease Heart attacks and strokes due to vascular complications Arterisclerosis---diminish blood flow to the legs---gangrene Susceptibility to infection Casual (Random) plasma Fasting Plasma Glucose glucose  Collected irrespective of when  8 hours or more fasting the last meal was ingested or w/o any caloric intake time of the day  >126mg/L  >200mg/L (11.1 mmol/L)— (7.0mmol/L)---DM presumptive of DM       

LAB DIAGNOSIS  3 criteria: o Symptoms of DM + random plasma glucose >200mg?dL (11.1mmol/L) o Fasting plasma glucose : 126mg/L ( 7.0 mmol/L) o OGTT: 2 hours after oral glucose load >200mg/L (11.1mmol/L)

Urine Glucose  Glucose in urine 160 to 180 mg/L (8,9to 10 mmol/L)  Screening test

Two-hour postprandial plasma glucose  2 hours after patient consumes standard load of glucose (75g)  >200mg/L (11.1mmol/L)---DM

Oral Glucose Tolerance Test (OGTT) Glycated Hemoglobin  Unlimited physical activity and unrestricted diet 150g CHO for 3 days  Glycosylated hemoglobin; Hb A1c  Test perform in the morning after fasting 10 to 16 hours (only water  Useful in determining compliance with therapy; extent to which satisfactory is permitted) diabetic control has been achieved  Fasting glucose collected  More convenient than OGTT  Glucose for nonpregnant 75g in flavored solution (1.75 g/kg body  Requires only 1 blood sample weight---pedia; 100g for pregnant women Self-monitoring of blood glucose  Drink ingested 5 minutes  Plasma glucose measured every 30 minutes for 2 hours  Use capillary whole blood  Patient seated throughout the test  Serum/plasma glucose values higher than the capillary whole blood level  Samples collected in sodium fluoride; within 4 hours  normal: rise about 150mg/L (8.3mmol/L) or higher w/in 30 to 60 minutes---normal in 3 hours  diabetic: higher for longer period of time  gestational diabetic (2): fasting >105mg/L (5.8); 1-hour glucose >190mg/L (10.6); 2-hour >165mg/L (9.2); 3-hour >145mg/L (8.1)  factors affect OGTT: illness, trauma, stress, some drugs HYPOGLYCEMIA  Syndrome characterized by low glucose <50mg?L (2.8mmol/L)  Reactive hypoglycemia---excessive administration of insulin  Factitious hypoglycemia—other hypoglycemic agent  Ethanol ingestion—reduction of gluconeogenesis  Fasting or spontaneous hypoglycemia---uncommon ~rapid fall in plasma glucose: triggers the release of epinephrine and symptoms caused by epinephrine  Weakness, sweating, shakiness, trembling, nausea, lightheadedness, rapid pulse  Adrenergic symptoms ~gradual fall in plasma glucose: <20 or 30 mg?L (1.1 or 1.7 mmol/L)  Causes impairment of CNS function  Neuroglycopenia: headache, confusion, lethargy, unconsciouness Laboratory:  Samples drawn frequently every 4 hours

INBORN ERRORS OF CARBOHYDRATES Glycogen Storage Disease  Inheritable disorders that result from a deficiency of one or more enzymesinvolved in the metabolism of glycogen  Liver, heart or musculoskeletal system Type I (Von Gierke’s) Galactosemia Hereditary Fructose Intolerance  Deficiency of fructose-1phosphate aldolase  Vomiting, hypoglycemia, hepatomegaly, failure to thrive

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 More common type  Rare genetic disorder  Short stature and a huge abdomen (massive  Inability to metabolize enlargement of the liver) galactose  Severe hypoglycemia, inc plasma conc of lactic acid,  Develop vomiting, hyperlipidemia diarrhea, cirrhosis of the liver, cataracts and  Caused by deficiency or absence of the enzyme glucose mental retardation 6-phosphatase in the liver (needed for the final step in the formation of glucose from hepatic glycogen)i Mucopolysaccharide Storage Diseases Hurler’s Syndrome Structural components of cartilage, bone, skin, and other connective tissues  Severe progressive disorder characterized by corneal clouding and death (before age of 10) Mucopolysaccharidoses  Coarse facies, skeletal abnormalities, developmental delay, Hereditary disorders hepatosplenomegaly Glycosaminoglycans—accumulate in various tissues and excreted in the urine Dermatan sulfate, hepara sulfate nd keratin sulfate

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