1. Agents Used to Treat Hyperglycemia and Hypoglycemia
Chapter 35
Agents Used to Treat Hyperglycemia and Hypoglycemia

2. Diabetes Mellitus
Disorder of the pancreas
Results in hyperglycemia
Treatment
Insulin
Oral hypoglycemics

3. Diabetes Mellitus Can precipitate - cardiovascular disease
- kidney damage
- nerve damage
- vision loss due to diabetic retinopathy

4. Diabetes Mellitus
Pancreatic beta cells
Excrete an insufficient amount of insulin, or no insulin at all
Flawed carbohydrate, fat, and protein metabolism

5. Diabetes Mellitus
Two types:
Type 1 (formerly known as insulin- dependent diabetes mellitus, IDDM)
Type 2 (formerly known as noninsulin- dependent diabetes mellitus, NIDDM)

6. Diabetes Mellitus
Type 1 diabetes mellitus
Treated with insulin subcutaneous injections
Type 2 diabetes mellitus
Treated with oral hypoglycemic agents

7. Symptoms of Diabetes Mellitus
Polyuria (increased urine output)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)

8. Treatment for Diabetes Mellitus
Dietary management
Close monitoring
Weight reduction
Insulin
Oral agents

9. Insulin
Promotes:
Glucose transport across cell membranes (think of this as an “escort service”!)
Conversion of glycogen into glucose
Utilizes fatty acids and inhibits lipolysis
Enhances protein synthesis and inhibits protein breakdown
Blood glucose rises as carbs are digested

10. Normal Physiology of Insulin Function
Release of insulin is triggered and promotes:
- transport of glucose across cell membranes
- conversion of glycogen to glucose
- utilization of fatty acids by cells
- inhibition of lipolysis (breakdown of fats to fatty
acids)
- amino acid utilization enhances synthesis of protein
- protein breakdown is inhibited

11. Insulin Function Continued release of insulin reduces blood glucose
Will eventually produce a hypoglycemic state
Insulin is inhibited and hormones are released
Glucose rises and evens out

12. Insulin Malfunction Blood glucose remains high after a meal
Blood glucose level >180 can cause glucose to spill into urine
Water is drawn into the urinary tract
Increased urination
Fluid depletion
Increased thirst
Glucose in urine is a medium for bacteria culture

13. Insulin Malfunction
Body is not utilizing circulating glucose
Other nutrients breakdown to provide fuel
Fatty acids are converted to ketones
Proteins breakdown to amino acids

14. Liver glycogen is broken down into glucose Development of ketoacidosis
Insulin Malfunction
(cont’d)
Liver glycogen is broken down into glucose
Development of ketoacidosis
Wasting muscle tissue
Higher blood glucose levels

15. Insulin malfunction Diabetic ketoacidosis
Inadequate or no insulin -> hyperglycemia
too much fat is being burned for fuel instead –
waste products from this fat builds up to toxic levels in the bloodstream  ketones or ketoacidosis

16. Regular insulin is the only insulin typically used IV
Insulin Therapy
Usually available in 100 units per milliliter
500 units per milliliter is also available
Prescription/insulin pumps/for patients requiring large daily doses
Regular insulin is the only insulin typically used IV

17. Insulin Therapy Insulin preparations differ by
(cont’d)
Insulin preparations differ by
- onset and duration of action
- degree of purity
- source (cow, pig, or human)
Human insulin most prevalent
Insulin is administered parenterally

18. Insulin Synthetic human insulin Produced either by:
Recombinant DNA synthesis of human insulin
Conversion of pig to human insulin
Human in origin
Humulin, Novolin, and Lispro
Older versions
Pig or cow in origin

19. Four Preparations of Insulin
Rapid-
Acting
Fast-
Intermediate-
Long-
Lispro
Aspart
Regular
Humulin-R
Novolin-R
NPH
Lente
Humulin-L
Ultralente
Humulin-U
Glargine- Lantus
Note the differences in onset, peak, and duration of action.

20. Adverse Effects of Insulin
Allergic reactions
Lipodystrophy
Insulin resistance

21. Nursing Implications
Several drugs antagonize the hypoglycemic effects of insulin.
Check your drug manual before administering any drug agent.
Type 2 diabetics (NIDDM) may still need insulin if NPO for surgery or illness

22. Hypoglycemia Blood glucose is low (< 40 mg/dL) Produced from
Skipped or irregularly scheduled meals
Excessive exercise
Insulin administration errors

23. Signs and Symptoms of Hypoglycemia
Sweating
Confusion
Tachycardia
Headache
Hunger
Weakness
Poor muscle control
Emotional instability
Coma and death

24. Hypoglycemia Treatment
Glucagon (intramuscular, intravenous, or subcutaneous)
IV dextrose 50%, also known as D50W

25. Treatment for Type 2 Diabetes
Oral antidiabetic agents
Sulfonylureas (oldest category)
First generation
Second generation
Biguanides
Meglitinides
Alpha-glucosidases
Thiazolidinediones

26. Oral Hypoglycemic Agents
Stimulates pancreatic beta cells to excrete insulin
May increase binding between insulin and insulin receptors
May increase number of receptors

27. Oral Hypoglycemic Agents
Need some pancreatic function
For Type 2 diabetics
Used when diet alone is not controlling blood glucose and patient does not want to take insulin

28. Oral Hypoglycemic Agents
May have a link to risk for cardiovascular death
Decline in popularity
Certain patients respond to oral agents better
- diagnosed after age 40
- not overweight
- would require less than 40 units per day of insulin

29. Sulfonylureas
Action: stimulate the beta cells of the pancreas to secrete more insulin
Glipizide (Glucotrol), glyburide (DiaBeta, Micronase,Glynase), glimepiride (Amaryl)

30. Biguanides
Action: inhibit hepatic glucose production and increase the sensitivity of peripheral tissue to insulin
May be given with sulfonylureas
Metformin Hcl (Glucophage)

31. Repaglinide (Prandin)
Meglitinide
Action
Stimulate the beta cells of the pancreas to secrete insulin
Minimal risk of hypoglycemia
More rapid onset than sulfonylureas
TID a/c meals
Repaglinide (Prandin)

32. Alpha-glucosidase Inhibitors
Action: inhibit an enzyme called alpha- glucosidase (enzyme responsible for the hydrolysis of saccharides to be converted to glucose)
Must be taken with meals
May be given with sulfonylureas

33. Thiazolidinediones (Glitazones)
Action
Decrease insulin resistance by decreasing gluconeogenesis, glucose output, and triglyceride synthesis in the liver
Monitor for hepatic toxicity.
May be given with sulfonylureas

34. Side Effects Biguanides
Abdomen bloating, nausea, cramping, and diarrhea
Alpha-glucosidase inhibitors
Flatulence, diarrhea, and abdominal pain
Thiazolidinediones
Hepatic toxicity, weight gain, edema, and mild anemia

35. Nursing Considerations
Alcohol use by patients on sulfonylureas can cause flushing, nausea, and/or palpitations
Diabetes education is an ongoing process of assessment, evaluation, and teaching
A-1-C serum levels should be monitored
Normal adult values 3.5%-6.0%
Assess for presence of depression

36. Nursing considerations
Weight assessments
Skin assessment (especially to lower legs and feet)
Teaching of self-care skills
Teaching injection skills
When drawing up two compatible types of insulin in the same syringe, withdraw the clear one first and then the cloudy one

37. Treating for Hypo or Hyperglycemia
If unsure whether patient is having low or high blood sugar symptoms, treat for low blood sugar
If patient able to swallow, give juice followed by complex carbohydrate food
Glucagon can be administered parenterally
Do not give insulin when patient fasting
Beta-blockers can mask symptoms of hypoglycemia