Anesthesia Pharmacology: Diabetes
Type II diabetes represents a group of milder forms of diabetes that occurs mainly in adults.
Endogenous insulin is sufficient to prevent ketoacidosis; however, abnormal insulin secretion and resistance to insuling action at tissues occur.
Obesity: common risk factor
NIDDM patients exhibit a deficiency in pancreatic B cell response to glucose.
The impaired response is worsened by hyperglycemia.
Plasma glucose: normal -- elevated insulin levels
Elevated insulin levels -- postprandial hypoglycemia
Insulin or systems to change -- reduced insulin secretion causes fasting hyperglycemia him (diabetes)
NIDDM: appears in middle age or later; mainly in overweight patients
Gradual onset of symptoms
Extreme hyperglycemia
Hyperosmolality
Volume depletion
CNS symptoms (ranging from clouded sensorium to coma)
Seizure activity (Jacksonian)
Transient hemiplegia
Infections: pneumonia and gram-negative sepsis (common, associated with very negative prognosis)
Patients with NIDDM usually do not develop ketoacidosis
Patients with NIDDM may develop hyperosmolar, nonketotic coma
Results from sustained hyperglycemia diuresis if patient cannot drink enough water to keep up with urinary fluid loss
Complete manifestation occurs when volume depletion decreases urine output
Hyperosmolar coma can occur in insulin-dependent diabetics if the insulin given is sufficient to prevent ketosis but not enough to control hyperglycemia.
Hyperosmolar coma can also be caused by:
Peritoneal/hemodialysis
Tube feeding of high-protein formulas
High-carbohydrate in fusion loads
Osmotic agents (mannitol and urea)
Mortality rate and hyperosmolar coma may be > 50%
Treatment of hyperosmolar coma states
large amounts of intravenous fluids (average fluid deficit: 10-11 liters.
Insulin: more rapid control hyperglycemia
Potassium salts (counteract intracellular shifted plasma K+)
Sodium bicarbonate (if lactic acidosis present)
Antibiotics
Type II diabetes treatment Overview
Diet
Weight reduction
Drugs other than insulin, if diet in weight reduction are inadequate.
Insulin may be required
Karam, J. H., Pancreatic Hormones and Antidiabetic Drugs, in Basic and Clinical Pharmacology, (Katzung, B. G., ed) Appleton-Lange, 1998, pp 684-703
Foster, D. W., Diabetes Mellitus, In Harrison's Principles of Internal Medicine 14th edition, (Isselbacher, K.J., Braunwald, E., Wilson, J.D., Martin, J.B., Fauci, A.S. and Kasper, D.L., eds) McGraw-Hill, Inc (Health Professions Division), 1998, pp 2060-2080
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