1. Drug Therapy for Diabetes Mellitus
Chapter 41
Drug Therapy for Diabetes Mellitus

2. Diabetes Mellitus Classifications Type 1 Type 2
Characterized by hyperglycemia
Differ in
Onset, course
Pathology, treatment

3. Diabetes Mellitus (cont.)
Type 1
Common chronic disorder of childhood
Autoimmune disorder that destroys pancreatic beta cells difficult to control
Sudden onset between ages 4 and 20 years
High incidence of complications
Requires exogenous insulin administration

4. Diabetes Mellitus (cont.)
Type 2
Characterized by hyperglycemia and insulin resistance
Historically, onset after age 40 years
Increasing prevalence among children and teens
Gradual onset with less severe symptoms
90% of people with diabetes have type 2 disease

5. Diabetes Mellitus (cont.)
Type 2 (cont.)
Risk factors for development
Presence of metabolic syndrome (estimated greater than 50 million Americans)
Abdominal obesity low HDL
Hypertriglyceridemia
Hypertension and/or impaired fasting glucose

6. Diabetes Mellitus (cont.)
Type 2 (cont.)
Ethnicities at high risk for type 2 development
African Americans (13.3%)
Hispanics (greater than 13.9%)
Commonly undiagnosed
Native Americans/Alaskans (12.8%)
Caucasians (8.7%)

7. Diabetes Mellitus (cont.)
Chronic, systemic disease characterized by
Metabolic abnormalities
Vascular abnormalities
Major clinical manifestation of metabolic abnormalities
Hyperglycemia
Fasting blood glucose levels greater than 126 mg/dL

8. Diabetes Mellitus (cont.)
Major clinical manifestation of metabolic abnormalities (cont.)
Impaired fasting glucose (IFG) (i.e., prediabetes)
Fasting blood glucose levels between 100 and 125 mg/dL
Recommended blood glucose level for those with diabetes
80 to 120 mg/dL before a meal
100 to 140 mg/dL HS

9. Diabetes Mellitus (cont.)
Major clinical manifestation of metabolic abnormalities (cont.)
Macrovascular abnormalities
Hypertension
Myocardial infarction
Stroke
Peripheral vascular disease (PVD)

10. Diabetes Mellitus (cont.)
Major clinical manifestation of metabolic abnormalities (cont.)
Microvascular abnormalities
Retinopathy
Blindness
Nephropathy

11. Diabetes Mellitus (cont.)
Signs and symptoms
Hyperglycemia
Glycosuria
Polydipsia
Polyuria
Dehydration
Polyphagia

12. Diabetes Mellitus (cont.)
Complications
Myocardial infarction, stroke
Blindness
Leg amputation
Renal failure
Hyperosmolar hyperglycemic nonketotic coma (HHNC)

13. Question Is the following statement True or False?
Diabetes mellitus is a chronic, systemic disease characterized by metabolic abnormalities.

14. Answer
False
Rationale: Diabetes mellitus is a chronic, systemic disease characterized by metabolic and vascular abnormalities. While a major clinical manifestation of DM is hyperglycemia, vascular problems include atherosclerosis throughout the body, which results in hypertension, MI, stroke, and peripheral vascular disease (PVD).

15. Endogenous Insulin Protein hormone secreted by pancreas
Secretion levels increase after a meal
Secreted into portal circulation
Transported to liver (about ½)
Reaches systemic circulation (about ½)
Insulin binds with cellular receptors, allowing rapid entry of glucose into cells.
Affects cellular metabolism

16. Endogenous Insulin (cont.)
Clears from circulating blood in 10 to 15 minutes.
Insulin plays major role in metabolism.
Carbohydrates to glucose
Fats to lipids
Proteins to amino acids
Overall effect is to lower blood glucose levels.

17. Endogenous Insulin (cont.)
Regulation of insulin secretion
Glucose is a major stimulus.
Several hormones raise blood glucose levels.
Insulin secretion is inhibited.
Stimulation of specific adrenergic receptors
Stress conditions

18. Question Is the following statement True or False?
Insulin is a lipid hormone secreted by beta cells in the pancreas.

19. Answer
False
Rationale: Insulin is a protein hormone secreted by beta cells in the pancreas that allows rapid entry of glucose into cells.

20. Antidiabetic Medications
Insulins
Oral hypoglycemics
Amylin analogs
Incretin mimetics
Dipeptidyl peptidase 4 (DPP-4) inhibitors

21. Hypoglycemic Medications
Insulin
Human insulins only—in the United States
Synthetic product is identical to endogenous insulin.
Insulin analogs
Synthesized in laboratories by altering the type or sequence of amino acids

22. Hypoglycemic Medications (cont.)
Insulin (cont.)
Administration
Cannot be given orally
Most given sub-Q
Regular can also be administered IV
Differ in onset and duration of action

23. Hypoglycemic Medications (cont.)
Insulin (cont.)
Short acting
Rapid onset, short duration of action
Intermediate, long acting
Slower absorption, prolonged action
Several mixtures of intermediate and short acting are available and commonly used.

24. Hypoglycemic Medications (cont.)
Insulin (cont.)
Main insulin concentration is U-100.
In the United States
Measured with orange-tipped syringe
Sub-Q injection absorbed most rapidly
Abdomen
Followed by upper arm, thigh, buttocks

25. Hypoglycemic Medications (cont.)
Oral hypoglycemics
Sulfonylureas
Alpha-glucosidase inhibitors
Biguanide
Thiazolidinediones
Meglitinides

26. Question Is the following statement True or False?
Insulin plays a major role primarily in the metabolism of carbohydrate.

27. Answer
False
Rationale: Insulin plays a major role in the metabolism of carbohydrate, fat, and protein where the nutrients are broken down into simpler molecules (glucose, lipids, and amino acids, respectively).

28. Sulfonylureas Mechanism of action: increases secretion of insulin
Indications for use: elevated serum glucose
Adverse effects: hypoglycemia
Nursing process implications: contraindicated during pregnancy, with renal or hepatic impairment, and critical illness

29. Alpha-Glucosidase Inhibitors
Mechanism of action: delay digestion of complex carbohydrates
Indications for use: decrease in postprandial glucose
Adverse effects: hypoglycemia
Nursing process implications: contraindicated for patients with hepatic disease, inflammatory and malabsorptive disorders

30. Biguanide
Mechanism of action: increases use of glucose by muscle and fat cells, decreases hepatic glucose production, and decreases intestinal absorption of glucose
Indications for use: insulin resistance
Adverse effects: lactic acidosis
Nursing process implications: No hypoglycemia; monitor for potentially fatal lactic acidosis

31. Thiazolidinediones (Glitazones)
Mechanism of action: stimulate insulin receptors on muscle, fat, and liver cells
Indications for use: insulin resistance
Adverse effects: hepatotoxicity, congestive heart failure, weight gain
Nursing process implications: monitor liver function studies, and closely monitor patients for signs of heart failure

32. Meglitinides
Mechanism of action: stimulate pancreatic stimulation of insulin
Indications for use: elevated serum glucose
Adverse effects: hypoglycemia although less so than sulfonylureas
Nursing process implications: proper medication administration including holding the medication if a meal is held

33. Amylin Analogs
Mechanism of action: suppresses postprandial glucagon secretion
Indications for use: regulate the postprandial rise in blood glucose
Adverse effects: hypoglycemia
Nursing process implications: monitor blood sugars closely; this medication increases the sense of satiety, possibly reducing food intake and promoting weight loss

34. Incretin Mimetics
Mechanism of action: stimulating the pancreas to secrete the right amount of insulin based on the food that was just eaten
Indications for use: postprandial glucose elevations
Adverse effects: GI distress and nausea
Nursing process implications: proper medication administration; monitor for a rare but serious side effect in the development of acute pancreatitis

35. Dipeptidyl Peptidase 4 Inhibitors
Mechanism of action: balance the release of insulin and limit the release of additional glucose from the liver; it has also been linked to increased beta cell neogenesis, inhibition of beta cell apoptosis, inhibition of glucagon secretion, delayed gastric emptying, and induction of satiety.
Indications for use: elevated serum glucose.
Adverse effects: may complicate renal disease.
Nursing process implications: monitor for common side effects including upper respiratory tract infection, stuffy or runny nose, sore throat, and/or headache.

36. Angiotensin-converting Enzyme Inhibitors, Angiotensin II Receptor Blockers, and Statins
Pharmacokinetics
Pharmacodynamics
Pharmacotherapeutics

37. Goals of Antidiabetic Therapy
Blood glucose at normal or near-normal levels
Promote normal metabolism of
Carbohydrate, fat, protein
Prevent acute and long-term complications
Prevent hypoglycemic episodes

38. Nursing Interventions
Use nondrug measures to improve control of diabetes and to help prevent complications.
Assist the patient in maintaining the prescribed diet.
Assist the patient to develop and maintain a regular exercise program.

39. Nursing Interventions (cont.)
Perform and interpret blood tests for glucose accurately, and assist the patient and family members to do so.
Test urine for ketones when the patient is sick, when blood glucose levels are greater than 200 mg/dL, and when episodes of nocturnal hypoglycemia are suspected. Also teach patients and family members to test urine when indicated.

40. Nursing Interventions (cont.)
Promote early recognition and treatment of problems by observing for signs and symptoms of urinary tract infection, peripheral vascular disease, vision changes, ketoacidosis, hypoglycemia, and others. Teach patients and family members to observe for these conditions and report their occurrence.
Discuss the importance of regular visits to health care facilities for blood sugar measurements, weights, blood pressure measurements, and eye examinations.

41. Nursing Interventions (cont.)
Perform and teach correct foot care.
Help patients keep up with newer developments in diabetes care by providing information, sources of information, consultations with specialists, and other resources.
Provide appropriate patient teaching for any drug therapy and combination drug therapy for patients with type 2 diabetes mellitus.

42. Patients’ Adherence
Complications of diabetes mellitus can be life threatening.
Diabetes is the leading cause of myocardial infarction, stroke, blindness, leg amputation, and kidney failure.
Metabolic abnormalities lead to damage in blood vessels and other body tissues.