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Ch. 32 Pharm

Antidiabetic Drugs

Decribe two types of diabetes Type 1- Usually begins in childhood , Rapid onset Unknown cause Type 2-Adult Onset Diabetes Genetics, it’s in your family history, Over-weight/Obesity, Little or no exercise*, immune response
S/Sx of diabetes Elevated fasting blood glucose (higher than 126 mg/dL) Polyuria,Polydipsia,Polyphagia, Glycosuria,Unexplained weight loss, Fatigue, Hyperglycemia
Criteria for diagnosis for DM Symptoms + plasma glucose level less than or equal to 200 mg/dL OR Fasting plasma glucose higher than or equal to 126 mg/dL OR 2-hour postload glucose level higher than or equal to 200 mg/dL during an oral glucose tolerance test
what is type 1 DM Lack of insulin production or production of defective insulin Pts need exogenous insulin. Will starve. Fewer than 10% of all diabetes cases are type 1 Complications:Diabetic ketoacidosis (DKA), Hyperosmolar nonketotic syndrome
what is type 2 DM Most common type: 90% of all cases Insulin deficiency and insulin resistance, glucose does not go into cell. Many tissues are resistant to insulin Reduced number of insulin receptors Insulin receptors less responsive
Often known as metabolic syndrome or insulin resistance syndrome or syndrome X central obesity, high BP, high triglyderides, low HDL, insulin resistance
what is gestational diabetes hyperglycemia during preg. insulin given prevent birth defects, subsides after delivery, 30% dev. type 2 DM in 10-15 yrs
what are major long term complications of DM macrovascular (atherosclerotic plaque) coronary aa, cerebral aa, peripheral vessels
what are major long term complications of DM Microvascular (capillary damage) retinopathy, neuropathy, nephropathy
What indicates "prediabetes" Fasting plasma glucose (FPG) levels higher than or equal to 110 mg/dL but less than 126 mg/dL. Screening recommended every 3 years for all patients 45 years and older
Treatment for DM Type 1-Insulin therapy Type 2- Lifestyle changes, Oral drug therapy, Insulin when the above no longer provide glycemic control
how do insulins fx substitute for endogenous hormone, restores pt ability to metabolize carbs, fats, proteins, store glucose in liver, convert glycogen to fat stores
What are rapid acting insulins Most rapid onset of action (5 to 15 minutes), shorter duration Pt must eat after injection May be given SC or via continuous SC infusion pump (but not IV) Insulin lispro (Humalog) Insulin aspart (NovoLog) Insulin glulisine (Apidra)-Newest
What is short acting insulin Regular insulin (Humulin R) Onset 30 to 60 minutes The only insulin product that can be given by IV bolus, IV infusion, or even IM
what is intermediate acting insulin Isophane insulin suspension (also called NPH) - Cloudy appearance Slower in onset and more prolonged in duration than endogenous insulin
what is long acting insulin glargine (Lantus), detemir (Levemir) Clear, colorless solution Referred to as basal insulin
Common combined insulins Combination insulin products NPH 70% and regular insulin 30% (Humulin 70/30, Novolin 70/30, Novolog 70/30) NPH 50% and regular insulin 50% (Humulin 50/50)
How is a sliding scale insulin dose determined SC short-acting or regular insulin to blood glucose test hospitalized pts/TPN or enteral tube feedings Subcutaneous insulin ordered that incr as blood glucose incr. Disadv: delays insulin adm. til hyperglycemia occurs; lg swings in glucose control
when can you use oral antidiabetic drugs type 2 w/ lifestyle modifications ex: Biguanides: Glucophage Sulfonylureas: 1st gen-diabinese, Tolinase 2nd g- Amaryl, glucotrol, DiaBeta, Micronase
More oral antidiabetic drugs Glinides: Prandin, Starlix Thiazolidinediones: Actos, Avandia (glitazones) Alpha-glucosidase inhibitors: Precose, Glyset
what are some new antidiabetic drugs Amylin mimetics: Symlin Incretin mimetics: Byetta, Januvia
What is MOA of Biguanides Decrease production of glucose by the liver Decrease intestinal absorption of glucose Increase uptake of glucose by tissues Do not increase insulin secretion from the pancreas (does not cause hypoglycemia)
What is MOA of Sulfonylureas Stimulate insulin secretion from the beta cells of the pancreas, increasing insulin levels Beta cell function must be present Improve sensitivity to insulin in tissues Result in lower blood glucose levels First-generation drugs not used as frequently
What is MOA of Glinides Action similar to sulfonylureas Increase insulin secretion from the pancreas
What is MOA of Thiazolidinediones Decrease insulin resistance “Insulin sensitizing drugs” Increase glucose uptake and use in skeletal muscle Inhibit glucose and triglyceride production in the liver
What is MOA of alpha-glucosidase inhibitors Reversibly inhibit the enzyme alpha-glucosidase in the small intestine Result in delayed absorption of glucose Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)
what is MOA of Amylin mimetics Mimics the natural hormone amylin Slows gastric emptying Suppresses glucagon secretion, reducing hepatic glucose output Centrally modulates appetite and satiety Used when other drugs have not achieved adequate glucose control Subcutaneous injection
what is MOA of Incretin mimetics Mimics the incretin hormones Enhances glucose-driven insulin secretion from beta cells of the pancreas Only used for Type 2 diabetes Exenatide: Injection pen device
Adverse effects of Metformin Primarily affects GI tract: abdominal bloating, nausea, cramping, diarrhea, feeling of fullness, also metallic taste, red.vit. B12 levels Lactic acidosis is rare, lethal. No hypoglycemia Taken with meals, discontinued if pt studies with contrast dye
adverse effects of sulfonylureas Hypoglycemia, hematologic effects, nausea, epigastric fullness, heartburn, may interact w/ alcohol cause disulfiram type reaction
adverse effects of glinides Headache, hypoglycemic effects, dizziness, weight gain, joint pain, upper respiratory infection or flulike symptoms
adverse effects of thiazolidinediones Moderate weight gain, edema, mild anemia Hepatic toxicity—monitor ALT levels
adverse effects of alpha-glucosidase inhibitors Flatulence, diarrhea, abdominal pain Do not cause hypoglycemia, hyperinsulinemia, or weight gain
what is hypoglycemia Abnormally low blood glucose level (below 50 mg/dL) Mild cases can be treated with diet—higher intake of protein and lower intake of carbs—to prevent a rebound postprandial hypoglycemia
hypoglycemia ss/sx Early Confusion, irritability, tremor, sweating Later Hypothermia, seizures Coma and death will occur if not treated
glucose elevating drugs Oral forms of concentrated glucose Buccal tablets, semisolid gel 50% dextrose in water (D50W) Glucagon
if pt is NPO and on antidiabetic drug, what should you do before procedure contact Dr to clarify orders
When insulin is ordered, ensure: Correct route, Correct type of insulin, Timing of the dose, Correct dosage Second-checked with another nurse Check blood glucose level, Roll vials b/n hands no shake. ONLY use insulin syringes, calibrated in units, correct timing of dose with meals
When drawing up insulin which do you do first always withdraw the regular or rapid-acting insulin first
Pt. education wtih insulin self-administration of insulin injections, including timing of doses, monitoring blood glucoses, and injection site rotations
when giving oral antidiabetic meds when should you give 30 minutes before meals Alpha-glucosidase inhibitors are given with the first bite of each main meal
What should you give if hypoglycemia occurs conscious- oral form of glucose:glucose tablets or gel, corn syrup, honey, fruit juice, or nondiet soft drink, eat crackers or a half sandwich Unconscious- give D50W or glucagon, intravenously, monitor blood glucose levels
Created by: palmerag



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