320 likes | 684 Views
MLAB 2401: Clinical Chemistry Keri Brophy-Martinez. Diabetes and Other Carbohydrate Disorders. Hyperglycemia. Increase in plasma glucose levels due to hormone imbalance Healthy patients Insulin is secreted by the β cells of the pancreatic islets of Langerhans Reference Range
E N D
MLAB 2401: Clinical ChemistryKeri Brophy-Martinez Diabetes and Other Carbohydrate Disorders
Hyperglycemia • Increase in plasma glucose levels due to hormone imbalance • Healthy patients • Insulin is secreted by the β cells of the pancreatic islets of Langerhans • Reference Range • Increased plasma glucose: • > 110 mg / dl • Glucose reference range: • 74 - 106 mg / dl
Effects of Hyperglycemia • Immediate Effects • Increased extracellular osmotic pressure • The increased glucose in plasma pulls water out of cells • Results in dehydration • Acidosis - metabolic acidosis. • May result • If the patient’s cells are not able to take in glucose, they may begin to convert fats to fatty acids, which then become keto acids.
Effects of Hyperglycemia: Long term • Physiological • Heart attacks/strokes, Diabetic retinopathy(Blindness), kidney failure, neurologic defects, susceptibility to infections • Chemical • Glycosylated hemoglobin • the formation of glycosylated hemoglobin is the result of prolonged elevation of plasma glucose.
Diabetes • Characterized by hyperglycemia • Disorders differ in etiology, symptoms and consequences • Lab’s role • Assist in diagnosis of the disease • Identification of the disorder • Assessment of progression of tissue damage
Physiologic abnormalities of diabetes • Hyperglycemia • increase blood glucose. • Doesn’t matter how the glucose is derived - diet, fat metabolism, protein destruction/wasting • Ketosis • from fat metabolism, ketonemia, ketonuria • Hyperlipidemia -increase blood lipids from faulty glucose metabolism. • Decrease blood pH - metabolic acidosis • Urine abnormalities • Glycosuria– glucose present • Polyuria - increase in urine volume • Loss of electrolytes - washing out with the urine
Diabetes • World Health Organization (WHO) and American Diabetes Association (ADA) recommends four categories of diabetes: • Type 1 diabetes • Most severe and potentially lethal • Type 2 diabetes • Other (secondary diabetes) • Gestational diabetes mellitus (GDM)
Type 1 Diabetes • Insulin dependent diabetes mellitus ( IDDM ) • 5-10 % of diabetes cases • Demographics • Non-Hispanic Whites/ Non-Hispanic Blacks • Children & adolescents • Pathology • Disease triggered by viral illness or environmental factors that destroys beta cells in pancreas. • Absolute Insulin deficiency • Defect in secretion, production or action or all • Autoimmune destruction of islet beta – cells in pancreas • Auto-antibodies are present
Type 1 Diabetes • Clinical Symptoms • CLASSIC TRIAD • Polyphagia(increased food uptake) • Polydipsia (thirst) • Polyuria( increased urine production) • Other symptoms • Mental confusion • Rapid weight loss • Hyperventilation • Diabetic ketoacidosis
Laboratory Findings • Hyperglycemia- plasma levels > 110 mg/dL • Glucosuria- plasma glucose > 180 mg / dl • Decreased insulin • Increased glucagon • Stimulation causes • Gluconeogenesis • Lipolysis (breakdown of fat produces ketones) • Ketoacidosis • Decreased blood pH ( acidosis ) • Sodium … Potassium … CO2
Type II Diabetes • Non – Insulin Dependent Diabetes Mellitus( NIDDM ) • Most common form of diabetes • Demographics • Adult onset • Patients usually > 20 years old • American Indians and non-Hispanic blacks
Type II Diabetes: Pathology • Develops gradually • Disorder in insulin resistance and relative deficiency of insulin • Plasma glucose is unable to enter cells • Contributory factors • Obesity • Lack of exercise • Diet • Genetics • Drugs, such as diuretics, psychoactive drugs • Increases in hormones that inhibit/antagonize insulin (GH & cortisol)
Laboratory Findings • Hyperglycemia • Glucosuria • Insulin is present • Glucagon is notelevated • No lipolysis and noketoacidosis • Excess glucose is converted to triglycerides ( plasma triglycerides ) • Normal / Increased Na / K • Increased BUN & Creatinine ( Decreased renal function ) • Hyperosmolar plasma from hyperglycemia
Other (SecondaryDiabetes) • Genetic defects of beta cell function • Genetic defects in insulin action • Genetic syndromes • Pancreatic disease • Endocrinopathies • Drug or chemical induced
Gestational Diabetes • Glucose intolerance associated with pregnancy’s hormonal and metabolic changes • Mothers usually return to normal after pregnancy, but with increased risk for diabetes later on in life • Infants are at increased risk for respiratory complications and hypoglycemia after birth
Criteria for Diagnosis of Diabetes • Symptoms of diabetes plus random plasma glucose concentration > 200 mg/dL. Random is defined as any time of day without regard to time OR • Fasting plasma glucose > 126 mg/dL. Fasting is defined as no caloric intake for at least 8 hours. OR • 2-Hour postprandial glucose > 200 mg/dL during an oral glucose tolerance test OR 4. A HgbA1C > 6.5%, confirmed on repeat measurement • Side notes • Glucose tolerance testing ( GTT ) is considered to be of limited additional use in the diagnosis of diabetes and not recommended, do 2 hour pp test as stated above. • Urine glucose testing is also not recommended in diabetes diagnosis
Hypoglycemia • Plasma glucose level falls below 60 mg/dL • Glucagon is released when plasma glucose is < 70 mg / dL to inhibit insulin • Epinephrine, cortisol, and growth hormone released from adrenal gland to increase glucose metabolism and inhibit insulin • Treatment • Varies with cause. Generally, hypoglycemia is treated with small, frequent meals, (5-6 / day) low in carbohydrates, high in protein
Hypoglycemia Symptoms Lab Findings Decreased plasma glucose • Increased hunger • Sweating • Nausea • Vomiting • Dizziness • Shaking • Blurring of speech and sight • Mental confusion • Whipple’s Triad • Symptoms of hypoglycemia • Low plasma glucose at time of symptoms • Alleviation of symptoms with glucose ingestion
Hypoglycemia • Causes of: • Reactive • Insulin overdose in diabetics • Ethanol ingestion • Fasting • Insulin-producing tumors • Hepatic dysfunction • Sepsis
Galactosemia • Resulting from : • Galactose 1, phosphate uridyl transferase deficiency • enzyme that converts galactose to glucose, patients cannot change either galactose or lactose into glucose. • results in galactosemia (galactose in blood) • Effects: • Can lead to mental retardation, cataracts, death • check children < 3 yrs for reducing substances
References • Bishop, M., Fody, E., & Schoeff, l. (2010). Clinical Chemistry: Techniques, principles, Correlations. Baltimore: WoltersKluwer Lippincott Williams & Wilkins. • Centers for Disease Control. (2012). Diabetes Public Health Resource. Retrieved from http://www.cdc.gov/diabetes/pubs/factsheet11.htm • Sunheimer, R., & Graves, L. (2010). Clinical Laboratory Chemistry. Upper Saddle River: Pearson . • http://crossfitovercome.com/2011/12/29/diabetes-primer/