1. Antidiabetic Medications & The Nursing Process
Karen Ruffin RN, MSN Ed.

2. Is there a difference and if so what is it??
Is it Diabetes or is it Hyperglycemia???????????????
Is there a difference and if so what is it??

3. What is ??????? Hyperglycemia Insulin
The primary source of energy for our bodies
Any glucose level that is above 110, normal blood glucose is
Is a hormone that helps the body use or store glucose form the food we eat. It is secreted by the pancreas
Glucose

4. What is the difference between
Basel Insulin
Prandial Insulin

6. Optimal Levels of Blood Sugars
Preprandial-110 mg/dl
Postprandial-180 mg/dl

9. What happens to our bodies when we are hyperglycemic?
Blood Glucose
>110
Insulin
Resistance
Decreased
Insulin
Increased
Free Fatty
Acid
Cardiovascular system
Fatty acids can be bound or attached to other molecules, such as in triglycerides or phospholipids. When they are not attached to other molecules, they are known as "free" fatty acids.
The uncombined fatty acids or free fatty acids may come from the breakdown of a triglyceride into its components (fatty acids and glycerol). However as fats are insoluble in water they must be bound to appropriate regions in the plasma protein albumin for transport around the body. The levels of "free fatty acid" in the blood are limited by the number of albumin binding sites available.
Free fatty acids are an important source of fuel for many tissues since they can yield relatively large quantities of ATP. Many cell types can use either glucose or fatty acids for this purpose. In particular, heart and skeletal muscle prefer fatty acids. The brain cannot use fatty acids as a source of fuel; it relies on glucose, or on ketone bodies. Ketone bodies are produced in the liver by fatty acid metabolism during starvation, or during periods of low carbohydrate intake.
Oxidative stress is caused by an imbalance between the production of reactive oxygen and a biological system's ability to readily detoxify the reactive intermediates or easily repair the resulting damage. All forms of life maintain a reducing environment within their cells. This reducing environment is preserved by enzymes that maintain the reduced state through a constant input of metabolic energy. Disturbances in this normal redox state can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell, including proteins, lipids, and DNA.
Oxidative
Stress

10. Oxidative Stress Nitric Oxide Nitric oxide Tissue factor Plasminogen
Activator
Prostaccyclin
Nitric Oxide
Angiotensin ll
Endothelin-1
Activation of
activator protein -l
Angiotensin ll
Vasoconstriction
Inflammation
Thrombosis
hypertension
Release of chemokines
Release of cytokines
Expression of cellular
adhesion molecules
Vascular smooth
muscle cell growth
Hyper coagulation
Platelet Activation
Decreased Fibrinolysis

11. So what disease states are you at risk for???MI
DVT PE
Stroke
AAA
Retinopathy

12. What happens to our bodies when we are hyperglycemic?
Metabolic
Stress Response
Stress hormones
and peptides
Increased Glucose
Decreased Insulin

13. Increased Glucose Decreased Insulin
Increase in:
Ketones
Free Fatty Acids
Lactate
Immune
Dysfunction
Reactive 02
Species
Cellular Injury
Acidosis
Inflammation
Thrombosis
Tissue Damage
Global Infarction
Altered Tissue Healing
Ischemia
Infection
Dissemination
Increase
Transcription
Factors
Leads to
Secondary
Meadiators

14. DID YOU KNOW ANY BLOOD SUGAR >200
Stuns your ???????? for 2week

15. Criteria for Diagnosis of DM DM Screening
Symptoms of diabetes + casual plasma glucose level less than or equal to 200 mg/dL OR
Fasting plasma glucose higher than or equal to 126 mg/dL
2-hour postload glucose level higher than or equal to 200 mg/dL during an oral glucose tolerance test
Impaired glucose tolerance (IGT)
FPG <110 mg/dL: normal fasting glucose
FPG ≥110 mg/dL but <126 mg/dL: impaired fasting glucose (IFG)
FPG ≥126 mg/dL: provisional diagnosis of diabetes mellitus

16. What is a HbA1c?
It is a test that allows healthcare providers to see how diabetics have managed their blood glucose level over the last 2-3 months….
Why do you think this is important????

18. So, what do you think we are doing to our patients???
At what blood glucose level do we start treating with sliding scale?
???????
So, what do you think we are doing to our patients???

19. What is the Difference??
Type 1 diabetes
Type 2 diabetes

20. Type 1 Diabetes Lack of insulin production OR
Production of defective insulin
Affected patients need exogenous insulin
Complications
Diabetic ketoacidosis (DKA)
Hyperosmolar nonketotic syndrome
Oral antidiabetic drugs not effective

21. Diabetes Mellitus Symptoms Polyuria Polydipsia Polyphagia Glycosuria
Unexplained weight loss
Fatigue
Hyperglycemia

22. Type 2 Diabetes Most common type
Caused by insulin deficiency and insulin resistance
Many tissues are resistant to insulin
Reduced number insulin receptors
Insulin receptors less responsive
These people respond to oral hypoglycemics

24. Type 2 Diabetes Several comorbid conditions
metabolic syndrome OR insulin-resistance syndrome OR syndrome X
Obesity
Coronary artery disease
Dyslipidemia
Hypertension
Microalbuminemia (protein in the urine)
Enhanced conditions for embolic events (blood clots)
Insulin Resistance

25. Coronary Artery Disease

26. Treatment DIfferences
Type 1
Exogenous insulin
Dietary control
Type 2
Lifestyle changes
Weight reduction
Exercise
May require oral hypoglycemic therapy or exogenous insulin
Insulin when oral hypoglycemic medications can no longer provide glycemic control

27. Gestational Diabetes Hyperglycemia that develops during pregnancy
Insulin must be given to prevent birth defects
4% of all pregnancies
Must be reclassified if it persists 6 weeks post- delivery
Usually subsides after delivery
30% of patients may develop Type 2 DM within 10 to 15 years

28. Major Long-Term Complications of DM (Both Types)
Macrovascular (atherosclerotic plaque)
Coronary arteries
Cerebral arteries
Renal arteries
Peripheral vessels
Microvascular (capillary damage)
Retinopathy
Neuropathy
Nephropathy

29. Complications Associated with Diabetes Mellitus
Cardiovascular disease, including hypertension
Peripheral vascular disease
Delayed healing
Visual defects, including blindness
Renal disease
Infection
Neuropathies
Impotence

30. Oral Hypoglycemics Sulfonylureas (oldest) Meglitinides Biguanide
Thiazolidinediones

31. Indications for Oral Hypoglycemics
They are used to lower blood sugar levels in patients that diet and exercise have failed.
The patient must have some pancreatic function left.
They can be used as a monotherapy or in conjunction with other oral hypoglycemics.

32. Contraindications Know drug allergy Active hypoglycemia
Usually not used during pregnancy subq insulin's are used then.
Liver disease
Kidney disease
Depending on the metabolic pathways of the medication

33. Sulfonylureas First generation: Second generation:
chlorpropamide (Diabinese),
tolazamide (Tolinase)
tolbutamide (Orinase)
Second generation:
glimepiride (Amaryl)
glipizide (Glucotrol)
glyburide (DiaBeta, Micronase)

34. Sulfonylureas
Stimulate insulin secretion from the beta cells of the pancreas, thus increasing insulin levels
Beta cell function must be present
Improve sensitivity to insulin in tissues
Result: lower blood glucose levels
First-generation drugs not used as frequently now

35. Adverse Effects Sulfonylureas Hypoglycemia hematologic effects nausea
epigastric fullness
heartburn
many others

36. Interactions Sulfonylureas
Hypoglycemic effect increases when taken with alcohol, anabolic steroids, many other drugs
Adrenergics (beta blockers) may mask many of the symptoms of hypoglycemia
Hyperglycemia: corticosteroids, phenothiazines, diuretics, oral contraceptives, thyroid replacement hormones, phenytoin, diazoxide and lithium.
Allergic cross-sensitivity may occur with loop diuretics and sulfonamide antibiotics
May interact with alcohol/OTC medication containing alcohol) - causing a disulfiram (Antabuse) -type reaction (facial flushing, pounding headache, feeling of breathlessness, and nausea)

37. Meglitinides Meglitinides repaglinide (Prandin) nateglinide (Starlix)
Action similar to sulfonylureas
Increase insulin secretion from the pancreas

38. Adverse Effects Meglitinides Headache hypoglycemic effects Dizziness
weight gain
joint pain
upper respiratory infection or flu-like symptoms

39. Biguanides Biguanides metformin (Glucophage)
Decrease production of glucose
Increase uptake of glucose by tissues
Does not increase insulin secretion from the pancreas (does not cause hypoglycemia)

40. Adverse Effects Metformin
Primarily affects GI tract: abdominal bloating, nausea, cramping, diarrhea, feeling of fullness
May also cause metallic taste, reduced vitamin B12 levels
Lactic acidosis is rare but lethal if it occurs
Does not cause hypoglycemia

41. Thiazolidinediones Thiazolidinediones pioglitazone (Actos),
rosiglitazone (Avandia)
Also known as “glitazones”
Decrease insulin resistance
“Insulin sensitizing drugs”
Increase glucose uptake and use in skeletal muscle
Inhibit glucose and triglyceride production in the liver

42. Adverse Effects Thiazolidinediones Moderate weight gain Edema
Mild anemia
Hepatic toxicity—monitor liver function tests

43. Alpha-glucosidase Inhibitors
acarbose (Precose)
miglitol (Glyset)
Reversibly inhibit the enzyme alpha-glucosidase in the small intestine
Result: delayed absorption of glucose
Must be taken with meals to prevent excessive postprandial blood glucose elevations (with the “first bite” of a meal)

44. Adverse Effects α-glucosidase inhibitors Flatulence diarrhea
abdominal pain
Do not cause hypoglycemia, hyperinsulinemia, or weight gain

45. Insulins Mechanism of Action
Substitute for & same effects as endogenous insulin
Restores the diabetic patient’s ability to:
Metabolize carbohydrates, fats, and proteins
Store glucose in the liver
Convert glycogen to fat stores
Some derived from porcine sources
Most now human-derived, using recombinant DNA technologies
Goal: tight glucose control
To reduce the incidence of long-term complications

46. Indications To treat both types of diabetes
Each patient requires careful customization of the dosing regimen for optimal glycemic control

47. Contraindications
Anyone who is hypoglycemic?????

48. Adverse Effects
Are all signs and symptoms of hypoglycemia including shock and death.

49. Human-Based Insulins Rapid-Acting
Most rapid onset of action
Shorter duration
May be given SC or via continuous SC infusion pump (but not IV)
Insulin
Onset (mins)
Peak (hrs)
Duration (hrs)
aspart (Novolog)
2-33
1-3
3-5
lispro (Humalog)
30mins – 2.5
3-6.5
glulisine (Apidra)
30mins – 1.5
1.-25

51. Human-Based Insulins Short-Acting
regular insulin (Humulin R, Novolin R)
Onset 30 – 60 minutes
The only insulin product that can be given by IV bolus, IV infusion, or even IM
Insulin
Onset (mins)
Peak (hrs)
Duration (hrs)
Humulin R
30 mins to 4 hrs
2.5-5
5-10
Novolin R 30 8

52. Sliding-Scale Insulin Dosing
SC rapid or short-acting doses adjusted according to blood glucose test results
Typically used in hospitalized diabetic patients
Or in patients on TPN / enteral tube feedings or receiving steroids
Subcutaneous insulin is ordered in an amount that increases as the blood glucose increases

54. Human-Based Insulins Intermediate-Acting
isophane insulin suspension (also called NPH) (Humulin N, Novolin N)
isophane insulin suspension & insulin injection
(Humulin 50/50 , Humulin 70/30, Novolin 70-30)
Lispro protamine suspension (Humalog 75/25, Novolog Mix 70/30)
insulin zinc suspension (Lente, Novolin L)
Cloudy appearance
Slower in onset and more prolonged duration than endogenous insulin

55. Human-Based Insulins Intermediate-Acting
Onset (hrs)
Peak (hrs)
Duration (hrs)
Isophane (NPH):
Humulin N
1-4
4-12
16-28
Novolin N
1-5 24
Isophane & Insulin:
Humulin 50/50
0.5
4-8
Humulin 70/30
Novolin70/30
2-12

56. Human-Based Insulins Intermediate-Acting
Onset (hrs)
Peak (hrs)
Duration (hrs)
lispro protamine & lispro:
Humalog Mix 75/25
12-24
Novolog Mix 70/30
2.4 24
Insulin Zinc Suspension:
Lente Iletin II
1-1.5
8-12
Novolin L
1-4
7-15
20-28

57. Human-Based Insulins
Combination Insulin Products
NPH 70% and regular insulin 30% (Humulin 70/30, Novolin 70/30)
NPH 50% and regular insulin 50% (Humulin 50/50)
insulin lispro protamine suspension 75% and insulin lispro 25% (Humalog Mix 75/25)

59. Human-Based Insulins Long-Acting
Onset
Peak
Duration
glargine (Lantus 1
No peak activity
24 (when administered at hs)
detemir (Levemir)
6-8
6-28

62. DM Monitoring – Daily AC & HS
Ante Cibum: before meals
HS: Hour of Sleep: prior to taking any HS snack
Rapid or short acting insulin used to cover any blood sugar (accucheck, chemstrip)
Dose by protocol (protocols are usually hospital-based)
for any result greater than 150mg/dL
Usually 1-2U for every 50mg/dL >150 with special instructions to notify physician if >300 mg/dL

63. Injection Sites

64. Insulin Pumps External Internal

65. Hypoglycemia Adverse Effect of Insulin
Early
Confusion, irritability, tremor, sweating
Later
Hypothermia, seizures
Coma and death will occur if not treated
Abnormally low blood glucose level (<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

68. Good way to remember!!!

69. Diabetic Ketoacidosis
State of hyperglycemia with ketosis
Usually results from infection, environment, or emotional stressor
As a result of Lack of Insulin, Breakdown:
Fat – free fatty acids in liver – ketone bodies – ketones in urine
Protein – to form new glucose / increased BUN
Glycogen to glucose (decrease use of glucose because of decreased insulin)
Osmotic diuresis
Dehydration / Electrolyte Imbalance
Hyperosmolality Hemoconcentration
Acidosis
Death

70. Diabetic Ketoacidosis
Sudden onset
Factors: infection, stressors, inadequate insulin
Kussmaul respiration / fruity odor to breath, nausea, abdominal pain
Dehydration, electrolyte imbalance, polyuria, polydipsia, weight loss, dry skin, sunken eyes, soft eyeballs, lethargy, coma
Glucose >300 mg/dL
pH < / Bicarbonate < 15 mEq/L
Na – low / K+ </> / Cr >1.5 mg/dL
Blood & Urine Ketones - Positive

72. Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
State of hyperglycemia without ketosis
Little breakdown of fat (little or no ketone bodies)
Breakdown
Glycogen– formation of new glucose – hyperglycemia
Very high levels of glucose >800mg dL
Osmotic diuresis – extracellular dehydration
Renal insufficiency – hyperosmolality – intracellular dehydration
Hypokalemia – shock – tissue hypoxia - Coma

73. Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS)
Gradual onset
Factors: infection, other stressors, poor fluid intake
Altered CNS function – neurologic symptoms
Dehydration / electrolyte loss
Glucose > 800 mg/dL
pH >7.4 / Bicarbonate >20 mEq/L
Na & K+ normal or low
Bun & Cr – elevated
Blood & Urine Ketones - negative

74. Hyperglycemic-hyperosmolar nonketotic syndrome (HHNS
Treatment
Rehydrate with NS (if severe) or ½ NS
Use CVP or PCWP / UO / blood pressure monitoring
IV insulin According to Sliding Scale
Never Reduce hyperglycemia by 10% /hr
Replace Potassium (will not be as severe as DKA)

75. Antidiabetic Drugs: Nursing Implications
Before giving any drugs that alter glucose levels, obtain and document:
A thorough history
Vital signs
Blood glucose level, HbA1c level
Potential complications and drug interactions

76. Antidiabetic Drugs: Nursing Implications
Before giving any drugs that alter glucose levels:
Assess the patient’s ability to consume food
Assess blood glucose level
Assess for nausea or vomiting
Hypoglycemia may be a problem if antidiabetic drugs are given and the patient does not eat
If a patient is NPO for a test or procedure, consult physician to clarify orders for antidiabetic drug therapy

77. Antidiabetic Drugs: Nursing Implications
Keep in mind that overall concerns for any diabetic patient increase when the patient:
Is under stress
Has an infection
Has an illness or trauma
Is pregnant or lactating

78. Antidiabetic Drugs: Patient Education
Thorough patient education is essential regarding:
Disease process
Other Risk Factors:
Smoking
HTN
CAD
Self-Care:
Medication
Psychological adjustment
Nutrition
Activity and Exercise
Blood-glucose testing
Self-administration of insulin or oral drugs
Potential complications
How to recognize and treat hypoglycemia and hyperglycemia

79. FIGURE 36-3 Diabetes health care plan.
Mosby items and derived items © 2007, 2004 by Mosby, Inc., an affiliate of Elsevier Inc.

80. Nursing Implications Insulin
When insulin is ordered, ensure:
Correct route
Correct type of insulin
Timing of the dose
Correct dosage
Insulin order and prepared dosages are second-checked with another nurse
Check blood glucose level before giving insulin
Roll vials between hands them to mix suspensions – no shaking!
Ensure correct storage of insulin vials
ONLY insulin syringes, calibrated in units, to administer insulin
Ensure correct timing of insulin dose with meals

81. Nursing Implications Insulin
When drawing up two types of insulin in one syringe:
Always withdraw the regular or rapid-acting insulin first
Provide thorough patient education regarding self-administration of insulin injections, including timing of doses, monitoring blood glucoses, and injection site rotations

82. Nursing Implications Oral Antidiabetic drugs
Always check blood glucose levels before giving
Usually given 30 minutes before meals
Administer the medication at exact time – with meal or when food is in sight*
Alpha-glucosidase inhibitors are given with the first bite of each main meal
Metformin is taken with meals to reduce GI effects
Nursing Implications Oral Antidiabetic drugs

83. Nursing Implications Insulin & hypoglycemic medications
Assess for signs of hypoglycemia
If hypoglycemia occurs:
Give glucagon or
Have the patient eat glucose tablets or gel, corn syrup, honey, fruit juice, or nondiet soft drink or
Have the patient eat a small snack such as crackers or half a sandwich
Monitor blood glucose levels

85. Nursing Implications Monitor for therapeutic response
Decrease in blood glucose levels to the level prescribed by physician
Measure hemoglobin A1c to monitor long-term compliance to diet and drug therapy
Watch for hypoglycemia and hyperglycemia

87. Review
When administering insulin, the nurse must keep in mind that the most immediate and serious adverse effect of insulin therapy is which of the following?
A: Hyperglycemia
B: Hypoglycemia
C: Bradycardia
D: Orthostatic Hypotension

88. Review
A dose of long acting insulin has been ordered for bedtime for a diabetic patient. The nurse expects to give which type of insulin?
A: Regular
B: Lente
C: NPH
D: Glargine (Lantus)

89. Review
A Patient is to be placed on an insulin drip to control his high blood glucose levels. The nurse knows that which of the following is the only type of insulin that can be given IV?
A: Regular
B: Lente
C: NPH
D: Ultralente

90. Review
While monitoring a patient who is receiving insulin therapy, the nurse observes for signs of hypoglycemia, such as which of the following?
A: Decreased pulse and respiratory rate and flush skin.
B: Increased pulse rate and a fruity, acetone breath odor.
C: Weakness, sweating, and confusion.
D: Increased urine output and edema.

91. Review
When giving oral acarbose (Precose), the nurse should administer it at what time?
A: 15 minutes before meal
B: 30 minutes before meal
C: with the first bite of a meal
D: 1 hour after eating

92. Review
A patient taking rosiglitazone (Avandia) tells the nurse, “There’s my insulin pill!” The nurse describes the mechanism of action of Avandia by explaining that this drug is not insulin but it works by:
A: Stimulating the beta cells of the pancreas to produce insulin.
B: Decreasing insulin production.
C: Inhibiting hepatic glucose production.
D: Decreasing intestinal absorption of glucose.