1. Diabetes Mellitus (Part II)
Treatment
Acute Complications
Chronic Complications
Patient Teaching

2. Treatment Drug Therapy: Nutritional Therapy Exercise
Insulin
Oral Agents
Nutritional Therapy
Exercise
Pancreas Transplant

3. Treatment The goal of any treatment for Diabetes:
Reduce symptoms
Promote well-being
Prevent acute complications
Prevent or delay the onset and progression of long-term complications
Above goals can only be met by patient maintaining blood glucose levels at or near normal!

4. Insulin Therapy (Exogenous Insulin)
Patients with Type 1 Diabetes always require Exogenous insulin (insulin from a source outside the body)
Type 2 Diabetics may not need any insulin
Blood Glucose Levels can be controlled by diet & exercise alone
May need insulin eventually due to chronic and progressive nature of the disease

5. Types of Insulin No longer made from beef or pork pancreas
Only human insulin is used today
Human insulin made from bacteria or yeast cells
Insulins differ in regard to:
Onset
Peak action
Duration
Characterized according to the amount of time they need to take effect
Read the label carefully
See Insulin Comparison Chart

6. Insulin Therapy
Specific properties of each type of insulin are matched with the patient’s diet and activity
Can range from one injection per day to several injections of various types of insulin
Most closely resembles endogenous insulin production:
Basal-bolus regimen
The regimen chosen should be mutually selected by the patient and the HCP
Criteria for selection are based on the desired and feasible levels of glycemic control and the patient’s lifestyle

7. Fast/Rapid Acting Insulin
Mealtime Insulin – Bolus
Used to control post-meal blood glucose levels
Rapid Acting Insulin: Onset = 15 minutes
Should be given 15 minutes before a meal
Humalog
Novolog
Short acting Regular Insulin: Onset = minutes
“Regular”
Should be injected minutes before a meal

8. Intermediate Acting Insulin
NPH Insulin
Onset 2-4 hours
Peaks 4-12 hours
Duration hours
Generally given twice a day before meals

9. Long Acting (Basal) Background Insulin
Long-acting/basal (background) insulin to control blood glucose levels between meals and overnight
Provides 24 hour steady and continual background insulin to keep blood glucose levels at a constant or controlled level
Lantus
Levemir
No Peak
Risk for hypoglycemia greatly reduced

10. Long Acting Insulin (cont’d)
Lantus and/or Levemir:
Given once in the morning or at bedtime
Cannot be mixed (in syringe) with other insulins
Cannot be pre-filled

11. Combination Insulin
Insulins can generally be mixed in the same syringe
Some Insulins Come Pre-mixed
Novolin 70/30 mix
70% NPH – 30% Novolin Regular
Novolog 70/30 mix
70% NPH – 30% Novolog Regular
Humulin 50/50 mix
Humalog 75/25

13. Administration of Insulin
Insulin is inactivated by gastric juices – cannot be taken orally
Injection
Insulin Pen
Insulin Pump
Inhaled Insulin

14. Administration of Insulin: Subcutaneous Injection
Gently rotate insulin in hands to warm
Mixing Insulins for Injection
Lantus/Levemir cannot be mixed
Don’t mix insulins from different manufacturers
Regular/NPH Insulin mix:
Draw up Regular insulin first, then add NPH

15. Subcutaneous Insulin Injection (cont’d)
Absorption of Insulin varies according to the injection site used
Slower
Fastest

17. Insulin Administration (cont’d) The Insulin Pen
Compact & Portable
Looks less like a syringe
Handy, Calibrated
Pre-filled with Insulin
* Change needle for each use

18. Insulin Pump Can be worn on belt or clothing
Tubing inserted into subcutaneous tissue in abdomen
Site must be changed every 3 days
Can deliver basal rate, short and long acting insulin
User programs according to exercise, diet, etc. )

19. Insulin Pump
The MiniMed Paradigm insulin pump (A) delivers insulin into a cannula (B) that sits under the skin. Continuous glucose monitoring occurs through a tiny sensor (C) inserted under the skin. Sensor data are sent continuously to the insulin pump through wireless technology. Courtesy of Medtronic Diabetes.

20. Inhaled Insulin (Exubera)
Alternative to injectable insulin
Rapid Acting; replaces short-acting ‘coverage’ insulins
Inhaled before meals
Usually added to longer acting insulins for type 1 diabetics
Type 2 diabetics: Alone or with any combination of prescribed insulins
Contraindications:
Smoker
Quit smoking within last 6 months
Asthma
PFTs before prescribed

21. Problems with Insulin Therapy
Allergic Reactions
Local; itching, burning usually due to additives
True insulin allergy is rare, but can be anaphylactic
Lipodystrophy: Atrophy of subcutaneous tissue
Prevented by rotation of sites
May result in poor absorption of insulin
Somogyi Effect
Dawn Phenomenon

22. Somogyi Effect Somogyi Effect is a ‘rebound’ effect
Overdose of insulin induces hypoglycemia
Usually occurs during hours of sleep
Normal/elevated blood glucose at bedtime, a decrease at 2-3 am  hypoglycemic levels, and increase caused by the production of counterregulatory hormones released, producing rebound hyperglycemia
The danger  the morning BGL can be high in response to the counterregulatory hormones and the MD may increase the insulin dose

23. Dawn Phenomenon Similar to Somogyi
Relatively normal glucose until about 3am then the glucose level begins to rise.
Hyperglycemia is present on awakening in the morning due to the release of counterregulatory hormones in the pre-dawn hours.
Possibly caused by growth hormone
Affects all diabetics at one time or another, more severe when growth hormone is at it’s peak
Adolescence and young adulthood
Careful monitoring of insulin, snacks and BGLs

24. Oral Drug Therapy Oral Agents are NOT oral forms of insulin
Oral agents work to improve the mechanisms by which insulin and glucose are produced and used by the body – they work on the 3 defects of type 2 diabetes:
Insulin resistance
Decreased insulin production
Increased hepatic glucose production
May be taken in combination with each other or with insulin to achieve BGL targets

25. Oral Hypoglycemic Agents
Sulfonylureas: increases insulin production from the pancreas
Drug of choice in Type 2 Diabetes because of decreased chance of hypoglycemia
glipizide (Glucotrol, Glucatrol XL)
glyburide (Micronase, DiaBeta, Glynase)
glimiperide (Amaryl)
Interacts with oral anticoagulants

26. Oral Hypoglycemics (cont’d)
Biguanides: Primary action is to reduce glucose production by the liver
Metformin (Glucophage)
Can be used alone or with other oral agents or insulin to treat Type 2 Diabetes
Also used in prediabetics to prevent type 2 diabetes
Does not promote weight gain
Cannot be taken with contrast dye!

27. Oral Hypoglycemic Agents (cont’d)
a -Glucosidase Inhibitors: (starch blockers) work by slowing down absorption of carbohydrates in the small intestine
Acarbose (Precose)
Miglitol (Glyset)
Taken with first bite of each meal
Most effective in lowering post-prandial BGLs

28. Oral Hypoglycemic Agents (cont’d)
Thiazolidinediones: a/k/a Insulin Sensitizers, work by improving insulin sensitivity, transport and utilization at target tissues
Pioglitazone (Actos)
Rosiglitazone (Avandia)
Most effective for people with insulin resistance
Do not cause hypoglycemia because they don’t increase insulin production
Can cause edema – do not use in patients with heart failure

29. Diabetes Treatment
The Priority Nursing Considerations for any diabetic patient on Insulin or oral Hypoglycemic agents is
Monitor/prevent Hypoglycemia
Hypoglycemia is an emergency and needs to be treated immediately

30. Nutritional Therapy Meal planning based on patient’s usual food intake
Type 1 Diabetes Mellitus
Type 2 Diabetes Mellitus
Meal planning based on patient’s usual food intake
Balance with insulin and exercise programs
Plan is developed with the person’s eating habits and activity pattern in mind
Emphasis is based on achieving glucose, lipid and blood pressure goals
Reduce total fat, simple sugars, carbohydrates
Space Meals
Weight loss of even 5 – 7% can improve glycemic control

31. Diabetes: Nutritional Therapy
The Cornerstone of Care for the patient with Diabetes
The Goal (according to the ADA) is to assist people with diabetes to make good food choices and maintain healthy exercise habits that lead to:
Good Metabolic Control
Maintain blood glucose levels at or near normal
Achieve lipid profiles and BP levels
Modify Lifestyle changes as appropriate
Improve health through healthy food choices and physical activity
Must address individual nutritional needs, personal and cultural preferences and respect the individual’s willingness to change

32. Patient Teaching (Nutritional Tx)
Nurses often assume responsibilities of teaching
Ideally: Diabetic teacher or interdisciplinary diabetes care team
Include
Patient’s family and significant others
Culture
Teach the person who does the cooking
Caloric intake

33. Patient Teaching: Exercise Therapy
Regular, consistent exercise is an essential part of diabetes and prediabetes management
Exercise increases insulin receptor sites in the tissue and has a direct effect on lowering blood glucose levels
Can also decrease triglycerides, LDL cholesterol
Can increase HDL
Can reduce blood pressure
Can improve circulation

34. Exercise Therapy (cont’d)
Exercise can lower BGLs to dangerously low levels
Small carbohydrate snacks can be taken 1 hour before, 1 hour after exercise
Patient should exercise and carry a fast acting carbohydrate
Exercise can also raise BGLs
The body sometimes perceives the exercise as a stress
Counterregulatory hormones released, raising BGLs
BGLs should be monitored before, during & after when beginning an exercise regimen, especially if the patient formerly led a sedentary lifestyle

35. Monitoring Blood Glucose Levels
Self-Monitoring of Blood Glucose (SMBG) = a cornerstone of diabetes management
SMBG enables the patient to make self- management decisions regarding
Diet
Exercise
Medications
Important for detecting episodes of hyperglycemia and hypoglycemia
Teaching SMBG is an important nursing responsibility

36. Pancreatic Transplant
Treatment option for Type 1 Diabetics with poorly controlled BGLs
Rare, usually not done alone
Can be done following kidney transplant to protect the new kidney from further damage from high BGLs
Pancreas transplant only partially successful in reversing long-term damage
Patient must take life-long immunosuppressants

37. Acute Complications of Diabetes Mellitus
Hypoglycemia
Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycemic Syndrome (HHS)

38. Hypoglycemia
Hypoglycemia occurs when there is too much insulin in proportion to available glucose in the blood . BGL drops to <70
Common Manifestations of hypoglycemia:
Confusion
Irritabililty
Diaphoresis
Tremors
Hunger
Weakness
Visual Disturbances

39. Hypoglycemia
The brain requires a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental function
Manifestations of hypoglycemia can mimic alcohol intoxication
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, death

40. Low Blood Glucose Levels
Hypoglycemia may also result if high glucose levels are treated too aggressively and brought down too quickly
It is important to ascertain why the BGL dropped

41. Treatment of Hypoglycemia
Conscious Patient
Unconscious Patient
Hypoglycemia is an emergency and needs to be treated immediately
Give the patient grams of quick acting carbohydrate
4-6 oz Regular soda
8-10 Candies
4-6 oz Orange Juice
Repeat in 15 minutes if no improvement
Longer acting carbohydrate
Crackers with peanut butter or cheese
Immediate notification of health care provider especially if symptoms do not subside
Subcutaneous or IM injection of 1 mg Glucagon
IV administration of 50 mls of 50% Glucose

42. Diabetic Ketoacidosis (DKA)
Also known as Diabetic Coma
Caused by: A profound deficiency of insulin and characterized by:
hyperglycemia
ketosis
acidosis
dehydration
Most likely to occur in Type 1 Diabetics, but sometimes occurs in Type 2 Diabetics during conditions of severe illness and/or stress

43. Diabetic Ketoacidosis (cont’d)
Ketones are the acidic by-products of fat metabolism
Ketosis (presence of ketones in the blood) alters the Ph balance causing metabolic acidosis
Ketonuria begins – ketone bodies are excreted in the urine
The kidneys use more water to eliminate the ketones – causes dehydration
The existing insulin deficiency causes proteins to break down and stimulates production of glucose (in the liver) leading to worsening hyperglycemia

44. Diabetic Ketoacidosis (cont’d)
The rise in glucose levels and lack of insulin make the blood glucose levels rise even further
With cell death, potassium is released from cell into the bloodstream -> hyperkalemia
Kidneys continue to excrete ketones – leading to a severe depletion of Potassium & other electrolytes

45. Diabetic Ketoacidosis
Acidosis causes nausea & vomiting which results in severe hypovolemia, possibly shock
Renal failure results from hypovolemic shock (which causes retention of ketones & glucose and the acidosis progresses)

46. Diabetes Ketoacidosis (cont’d)
Result: Patient becomes comatose as the result of dehydration, electrolyte imbalance and acidosis
Coma
Cardiac irregularities (due to hyperkalemia)
Renal insufficiency
Eventual death

47. DKA: Clinical Manifestations
Dehydration- Early signs include:
Poor Skin Turgor
Dry mucous membranes
Tachycardia
Orthostatic Hypotension
Lethargy, weakness
Severe Dehydration:
Skin dry & loose
Eyeballs soft, sunken

48. DKA: Clinical Manifestations (cont’d)
Abdominal Pain accompanied by anorexia & vomiting
Kussmaul respirations (rapid, deep breathing associated with dyspnea)
The body is attempting to reverse the metabolic acidosis through exhalation of excess Co2.
Acetone noted on the breath
Sweet, fruity breath odor
Ketonuria

49. Management
Correct dehydration
Correct electrolyte loss
Acidosis

50. Hyperosmolar Hyperglycemic Syndrome
Formerly known as Hyperosmolar Hyperglycemic Non-Ketoacidosis (HHNK)
HHS is a life-threatening syndrome that can occur when the person is able to produce enough insulin to prevent DKA (and ketoacidosis) but not enough to prevent severe hyperglycemia, osmotic diuresis and extracellular fluid depletion.

51. DKA vs. HHS (HHNK) DKA usually Type 1 Diabetics
HHNK usually Type 2 Diabetics
Seen more often in elderly with pre-existing cardiac or renal problems
Usually patient can produce enough insulin to avoid ketoacidosis but not enough to prevent profound hyperglycemia, dehydration and hyperosmolality
Risk factors
Clinical picture

52. Treatment DKA/HHS IV Fluids IV Insulin Electrolyte Replacement
Rapid Acting Insulin
Continual drip
Electrolyte Replacement
Assessment of Mental Status
Safety
I & O’s
Central Venous Pressure Monitoring (if indicated)
Blood Glucose Levels
ECG Monitoring
Cardiovascular and Respiratory Status

53. Chronic Complications of Diabetes Mellitus
Macrovascular/Microvascular Complications
Diabetic Retinopathy
Nephropathy
Neuropathy
Complications of Feet & Lower Extremities
Integumentary Complications

54. Complications: Diabetes Mellitus
Macrovascular
Microvascular
Diseases of the large & medium size blood vessels
Exact cause unknown – related to the altered lipid metabolism -> atherosclerotic plaque formation
Cerebrovascular
Coronary Artery
Peripheral Vascular
Diseases resulting from the thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia (Microangiopathy)
Diabetic Retinopathy
Diabetic Nephropathy
Dermopathy
Diabetic Foot Ulcers

55. Macrovascular Complications
Adults with Diabetes have 2-4 x increased risk of cerebrovascular and cardiovascular disease
Genetic risk not modifiable
Other risk factors can be modified (obesity, smoking, HTN, high fat intake, sedentary lifestyle)
Blood Pressure Control significantly reduces the risk of microvascular complications
Eye
Kidney
Nerves

56. Diabetic Retinopathy
The process of microvascular damage to the retina as the result of chronic hyperglycemia in patients with diabetes
Subject to many visual complications
Assessment /Dx
Treatment:
Photocoagulation (Laser) destroys the ischemic area producing the growth factors
Vitrectomy: aspiration of fluid & fibers from the inside of the eye

58. Diabetic Nephropathy
Definition: A microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney.
Leading cause of End Stage Renal Disease (ESRD) in the U.S.
Same risk, type 1 or type 2 Diabetics

59. Diabetic Nephropathy (cont’d)
The risk for kidney disease in diabetics can be significantly reduced when blood glucose levels are closely controlled to near-normal levels
Tight blood glucose control critical
ACE inhibitor (Angiotensin Converting Enzyme) medications sometimes prescribed for diabetics because of the protective effect they have on the kidneys

61. Diabetic Neuropathy 60-70% of diabetics have some form of neuropathy
Occurs with equal frequency in Type 1 & Type 2
Can lead to loss of (protective) sensation in lower extremities
Increases risk of complications that result in amputation of lower limbs
More than 60% of non-traumatic amputations are diabetics

62. Diabetic Neuropathy (cont’d)
Sensory Neuropathy
Autonomic Neuropathy
Distal symmetric neuropathy
Affects hands and/or feet bilaterally
Loss of Sensation: Can be complete or partial loss of sensation
Pain: burning, crushing
Abnormal sensations
Paresthesias Tingling, burning or itching
Autonomic Neuropathy: Can affect all body systems and lead to hypoglycemic unawareness, constipation or diarrhea or urinary retention
Gastroparesis
Cardiovascular abnormalities
Sexual dysfunction often the first manifestation
Decreased libido
Erectile dysfunction
Vaginal infection
Neurogenic Bladder
Urinary retention

63. Diabetic Neuropathy Management diet high in sodium
avoid agents that stimulate ANS
wear elastic garments
frequent monitoring blood glucose
low-fat diet
increase gastric motility
anti-diarrhea medications
high fiber diet/hydration

64. Diabetic Neuropathy

65. Complications of the Feet & Lower Extremities
Foot complications = the most common cause of hospitalization of the person with diabetes
“Diabetic Foot” is the result of both microvascular and macrovascular disease processes which frequently leads to:
Injury
Serious Infection (Cellulitis)
Amputation

66. Feet & Lower Extremities (cont’d)
Multifactoral Process: The Two Major Causes of Diabetic Foot Ulcers are:
Sensory neuropathy causes Loss of Protective Sensation (LOPS)
Patient is unaware of injury
Repetitive injury
Stepping on foreign objects when barefoot
Ill-fitting footwear
Peripheral Arterial Disease
Causes a reduction in blood flow to lower extremities
Wounds take longer to heal
Increases the risk for infection

67. Diabetic Foot Ulcers

68. Integumentary Diabetic Dermatopathy Necrobiosis lipoidica diabeticorum
Red-brown, flat-topped papules
Necrobiosis lipoidica diabeticorum
May appear before other clinical signs & symptoms

69. Foot /Leg Problems Risk factors Diabetes for more than 10 years
Older than 40 years
History of smoking
Decreased peripheral pulses
Decreased sensation
History of previous foot ulcers

70. Foot /Leg Problems Daily assessment of the feet
Examine feet at least once a year
Assess for neuropathy
Proper bathing/drying/lubricating
Closed - toed shoes/socks
Protect feet from hot/cold