Answer questions

Edith Johnson

Diabetesmellitus.ppt

Home >Nursing homework help >Answer questions

Diabetes Mellitus

OBJECTIVES

Describe the pathophysiology and clinical manifestations of diabetes mellitus.
Differentiate between type 1 and type 2 diabetes mellitus.
Describe the collaborative care of the patient with diabetes mellitus.
Describe the role of nutrition and exercise in the management of diabetes mellitus.
Discuss the nursing management of a patient with newly diagnosed diabetes mellitus.
Describe the nursing management of the patient with diabetes mellitus in the ambulatory and home care settings.
Relate the pathophysiology of acute and chronic complications of diabetes mellitus to the clinical manifestations.
Explain the collaborative care and nursing management of the patient with acute and chronic complications of diabetes mellitus.

DIABETES MELLITUS

A chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both Disorder of glucose metabolism related to the absent or insufficient insulin supply and/or poor utilization of insulin that is available.

Affects 25.8 million people have been dx; 54 million with “pre-diabetes”
Estimated that the number will double in the next 25 years and the cost to care for them will triple.
Seventh leading cause of death

Diabetes mellitus (DM) is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both.
Diabetes mellitus is a serious health problem throughout the world, and its prevalence is rapidly increasing.
Currently in the United States, an estimated 25.8 million people, or 8.3% of the population, have diabetes mellitus, and 79 million more people have prediabetes.
In approximately 7.0 million people with diabetes mellitus, the disease has not been diagnosed, and they are unaware that they have the disease.
Diabetes mellitus is the seventh leading cause of death in the United States, but it is likely to be underreported.
The annual cost of diabetes exceeds $174 billion, with $116 billion in direct medical costs.

HISTORICALLY…THE NAME HAD SOMETHING TO DO WITH THE KIDNEY…

Diabetes (Greek)— “to siphon”
Mellitus— “sweet” or “honeyed”
(1674)“Taste thy patient’s urine, for if it be sweet…”

---Dr. Thomas Willis

NURSE!...

Most diabetics lived 3-6 years after diagnosis “back in the day…”

DIABETES MELLITUS

Leading cause of
Adult blindness
End-stage kidney disease
Nontraumatic lower limb amputations
Major contributing factor
Heart disease
Stroke
Hypertension

Inc.

Elevated blood glucose damages the intima.

Inc.

The long-term complications of diabetes make it a devastating disease.
Diabetes is the leading cause of adult blindness, end-stage kidney disease, and nontraumatic lower limb amputations.
It is also a major factor contributing to heart disease and stroke.
Adults with diabetes have heart disease death rates two to four times higher than adults without diabetes.
The risk for stroke is also two to four times higher among people with diabetes.
In addition, it is estimated that 67% of adults with diabetes have hypertension.

ETIOLOGY AND PATHOPHYSIOLOGY

Combination of causative factors
Genetic
Autoimmune
Environmental
Absent/insufficient insulin and/or poor utilization of insulin

Normal insulin metabolism

Produced by -cells in islets of Langerhans

Released continuously into bloodstream in small increments with larger amounts released after food

Stabilizes glucose level in range of 70 to
120 mg/dL

Current theories link the causes of diabetes, singly or in combination, to genetic, autoimmune, and environmental factors (e.g., viruses, obesity).
Regardless of its cause, diabetes is primarily a disorder of glucose metabolism related to absent or insufficient insulin supply and/or poor utilization of the insulin that is available.

INSULIN RELEASE

ETIOLOGY AND PATHOPHYSIOLOGY

Insulin
Promotes glucose transport in skeletal muscle and adipose tissue
Storage of glucose as glycogen in the liver
Inhibits gluconeogenesis

Insulin promotes glucose transport from the bloodstream across the cell membrane to the cytoplasm of the cell.
Skeletal muscle and adipose tissue have specific receptors for insulin and are considered insulin-dependent tissues.
Insulin is required to “unlock” these receptor sites, allowing the transport of glucose into the cells to be used for energy.
The rise in plasma insulin after a meal stimulates storage of glucose as glycogen in liver and muscle, inhibits gluconeogenesis, enhances fat deposition of adipose tissue, and increases protein synthesis.
For this reason, insulin is an anabolic or storage hormone.
The fall in insulin level during normal overnight fasting facilitates the release of stored glucose from the liver, protein from muscle, and fat from adipose tissue.

Other tissues (e.g., brain, liver, blood cells) do not directly depend on insulin for glucose transport but require an adequate glucose supply for normal function.
Although liver cells are not considered insulin-dependent tissue, insulin receptor sites on the liver facilitate the hepatic uptake of glucose and its conversion to glycogen.

NORMAL INSULIN SECRETION

Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood; they peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.

THE ROLE OF INSULIN

https://www.youtube.com/watch?v=CuQMpN7rM-4

CLASSES OF DIABETES

Type 1
Type 2
Gestational

The American Diabetes Association (ADA) recognizes four different classes of diabetes.
The two most common are type 1 and type 2 diabetes mellitus.
The two other classes are gestational diabetes and other specific types of diabetes due to various causes.

TYPE 1 DIABETES MELLITUS
ETIOLOGY AND PATHOPHYSIOLOGY

Autoimmune destruction of β-cells
Total absence of insulin
Genetic predisposition and viral exposure

Type 1 diabetes is an immune-mediated disease, caused by autoimmune destruction of the pancreatic β-cells, the site of insulin production.
This eventually results in a total absence of insulin production.
Autoantibodies to the islet cells cause a reduction of 80% to 90% of normal function before hyperglycemia and other manifestations occur.
A genetic predisposition and exposure to a virus are factors that may contribute to the pathogenesis of immune-related type 1 diabetes.
Predisposition to type 1 diabetes is related to human leukocyte antigens (HLAs).
Theoretically, when an individual with certain HLA types is exposed to a viral infection, the β-cells of the pancreas are destroyed, either directly or through an autoimmune process.
The HLA types associated with an increased risk for type 1 diabetes include HLA-DR3 and HLA-DR4.
Idiopathic diabetes is a form of type 1 diabetes that is strongly inherited and not related to autoimmunity. This occurs only in a small number of people with type 1 diabetes, most often of African or Asian ancestry.
Latent autoimmune diabetes in adults (LADA), a slowly progressing autoimmune form of type 1 diabetes, usually occurs in people who are older than 35 and are not obese. This type of diabetes is thought to account for 2% to 12% of all cases of diabetes.

TYPE 1 DIABETES MELLITUS

Formerly known as juvenile-onset or insulin-dependent diabetes
Accounts for 5% of all cases of diabetes
Generally onset in people younger than 40 years;40% develop diabetes before 20years of age.
Incidence increasing
More frequently in younger children
Type 1 A 95%
Type 1 B 5%

Type 1 diabetes mellitus, formerly known as juvenile-onset diabetes or insulin-dependent diabetes, accounts for approximately 5% of all cases of diabetes.
Type 1 diabetes generally affects people younger than 40 years, and 40% develop it before 20 years of age.
The incidence of type 1 diabetes has increased 3% to 5% over recent decades and, for unknown reasons, is occurring more frequently in younger children.

TYPE 1 DIABETES MELLITUS
ONSET OF DISEASE

Autoantibodies are present for months to years before symptoms occur
Manifestations develop when pancreas can no longer produce insulin—then rapid onset with ketoacidosis
Necessitates insulin

In type 1 diabetes, the islet cell autoantibodies responsible for β-cell destruction are present for months to years before the onset of symptoms.
Manifestations of type 1 diabetes develop when the person’s pancreas can no longer produce sufficient amounts of insulin to maintain normal glucose levels.
Once this occurs, the onset of symptoms is usually rapid, and patients often present with impending or actual ketoacidosis.
The patient usually has a history of recent and sudden weight loss, as well as the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger).
The individual with type 1 diabetes requires insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient will develop diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis.
Patients with newly diagnosed type 1 diabetes may experience a remission, or “honeymoon period,” for 3 to 12 months after treatment is initiated. During this time, the patient requires very little injected insulin because β-cell insulin production remains sufficient for glucose control. Eventually, as more β-cells are destroyed and blood glucose levels increase, the honeymoon period ends, and the patient will require insulin on a permanent basis.

CLINICAL MANIFESTATIONS
TYPE 1 DIABETES MELLITUS

Classic symptoms
Polyuria (frequent urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue

Because the onset of type 1 diabetes is rapid, the initial manifestations are usually acute.
The classic symptoms are polyuria, polydipsia, and polyphagia.
The osmotic effect of glucose produces the manifestations of polydipsia and polyuria.
Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents utilization of glucose for energy.
Weight loss may occur because the body cannot get glucose and turns to other energy sources, such as fat and protein.
Weakness and fatigue may result because body cells lack needed energy from glucose.

TYPE 2 DIABETES MELLITUS

Formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (IDDM)
Most prevalent type (90% to 95%)
Risk factors: overweight, obesity, advancing age, family history
Increasing prevalence in children
Greater prevalence in ethnic groups- African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans

Type 2 diabetes mellitus was formerly known as adult-onset diabetes (AODM) or non–insulin-dependent diabetes (NIDDM).
Type 2 diabetes mellitus is, by far, the most prevalent type of diabetes, accounting for over approximately 90% to 95% of cases of diabetes.
Overweight, obesity, advancing age, and a family history of type 2 diabetes are risk factors for developing the disease.
Although the disease is seen less frequently in children, the incidence in children is increasing as a result of the increase in prevalence of childhood obesity.
Prevalence of type 2 diabetes is greater in some ethnic populations. African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans have a higher rate of type 2 diabetes than do white people.

TYPE 2 DIABETES MELLITUS
ETIOLOGY AND PATHOPHYSIOLOGY

Pancreas continues to produce some endogenous insulin
Insulin insufficient or poorly utilized
Multiple etiologic factors
Obesity is greatest risk factor
Genetic component increases insulin resistance and obesity

In type 2 diabetes, the pancreas usually continues to produce some endogenous (self-made) insulin.
However, the insulin that is produced is insufficient for the needs of the body, is poorly used by the tissues, or both.
The presence of endogenous insulin is a major distinction between type 1 and type 2 diabetes. (In type 1 diabetes, there is an absence of endogenous insulin.)
A multitude of factors contributes to the development of type 2 diabetes.
The most powerful risk factor is obesity, especially abdominal and visceral adiposity.
Although the genetics of type 2 diabetes is not yet fully understood, it is likely that multiple genes are involved. Genetic mutations that lead to insulin resistance and a higher risk for obesity have been found in many people with type 2 diabetes. Individuals with a first-degree relative with the disease are 10 times more likely to develop type 2 diabetes.

TYPE 2 DIABETES MELLITUS
ETIOLOGY AND PATHOPHYSIOLOGY

Major metabolic abnormalities

Insulin resistance- body tissues do not respond to the action of insulin

Decreased insulin production by pancreas

Gradual onset

Hyperglycemia may go many years without being detected

Many times discovered with routine laboratory testing

Four major metabolic abnormalities have a role in the development of type 2 diabetes.

The first factor is insulin resistance, a condition in which body tissues do not respond to the action of insulin.
This is because insulin receptors are unresponsive to the action of insulin and/or insufficient in number.
Most insulin receptors are located on skeletal muscle, fat, and liver cells.
When insulin is not properly used, the entry of glucose into the cell is impeded, resulting in hyperglycemia.
In the early stages of insulin resistance, the pancreas responds to high blood glucose by producing greater amounts of insulin (if β-cell function is normal). This creates a temporary state of hyperinsulinemia that coexists with hyperglycemia.
A second factor in the development of type 2 diabetes is a marked decrease in the ability of the pancreas to produce insulin, as the β-cells become fatigued from the compensatory overproduction of insulin or when β-cell mass is lost.
The underlying reason why the β-cells fail to adapt is unknown.
It may be linked to the adverse effects of chronic hyperglycemia or high levels of circulating free fatty acids.
A third factor is inappropriate glucose production by the liver.
Instead of properly regulating the release of glucose in response to blood levels, the liver does so in a haphazard way that does not correspond to the body’s needs at the time.
However, this is not considered a primary factor in the development of type 2 diabetes.
A fourth factor is altered production of hormones and cytokines by adipose tissue (adipokines).
Adipokines secreted by adipose tissue appear to play a role in glucose and fat metabolism and are likely to contribute to the pathophysiology of type 2 diabetes.
Adipokines are thought to cause chronic inflammation, a factor involved in insulin resistance, type 2 diabetes, and cardiovascular disease.
The two main adipokines believed to affect insulin sensitivity are adiponectin and leptin.

CLINICAL MANIFESTATIONS
TYPE 2 DIABETES MELLITUS

Nonspecific symptoms
Classic symptoms of type 1 may manifest
Fatigue
Recurrent infection
Recurrent vaginal yeast or candidal infection
Prolonged wound healing
Visual changes

The clinical manifestations of type 2 diabetes are often nonspecific, although it is possible that an individual with type 2 diabetes will experience some of the classic symptoms associated with type 1 diabetes, including polyuria, polydipsia, and polyphagia.
Some of the more common manifestations associated with type 2 diabetes are fatigue, recurrent infections, recurrent vaginal yeast or candidal infections, prolonged wound healing, and visual changes.

A GROWING PROBLEM…OBESE KIDS

The type 2 diabetes epidemic has paralleled the weight gain issue in the U.S. and around the world
Nearly 1 in 3 kids in the U.S. is overweight or obese
Approximately 35% of adults in the U.S. are overweight or obese
Type 2 diabetes in KIDS—as many as 50% of newly diagnosed diabetes in kids is Type 2
Adolescents with T2DM account for 45% of the new cases in the U.S.

AGE AND TYPE 2 DIABETES

50% of all type 2 diabetics are over 60;
18% are 65-75;
40% of people over 80 have diabetes
As we age the beta cells of the pancreas do not function as well.

TYPE 2 DIABETES RISK FACTORS

Weight gain
85% are overweight or obese

PREDIABETES

Individuals at risk for type 2 diabetes
Impaired glucose intolerance (IGT)
Two-hour oral glucose tolerance test (OGTT): 140 to 199 mg/dL
Impaired fasting glucose (IFG)
Fasting glucose level: 100 to 125 mg/dL

Individuals with diagnosed prediabetes are at increased risk for the development of type 2 diabetes.
Prediabetes is defined as impaired glucose intolerance (IGT), impaired fasting glucose (IFG), or both.
It is an intermediate stage between normal glucose homeostasis and diabetes in which the blood glucose levels are elevated but not high enough to meet the diagnostic criteria for diabetes.
A diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 mg/dL [7.8 mmol/L] to 199 mg/dL [11.0 mmol/L]).
IFG is diagnosed when fasting blood glucose levels are 100 mg/dL [5.56 mmol/L] to 125 mg/dL [6.9 mmol/L]).

PREDIABETES

Source ADA

PREDIABETES

Asymptomatic but long-term damage already occurring
Patient teaching important
Undergo screening
Manage risk factors
Monitor for symptoms of diabetes
Maintain healthy weight, exercise, healthy diet

Persons with prediabetes usually do not have symptoms. However, long-term damage to the body, especially the heart and blood vessels, may already be occurring.
It is important to encourage patients to undergo screening and for you to provide education about managing risk factors for diabetes.
Patients with prediabetes can take action to prevent or delay the development of type 2 diabetes.
Those with prediabetes should have their blood glucose and hemoglobin A1C levels tested regularly and should monitor for symptoms of diabetes, such as polyuria, polyphagia, and polydipsia.
Maintaining a healthy weight, exercising regularly, and eating a healthy diet have all been found to reduce the risk of developing overt diabetes in people with prediabetes.

GESTATIONAL DIABETES

Develops during pregnancy
Increases risk of need for cesarean delivery and of perinatal complications
Screen high-risk patients first visit; others at 24 to 28 weeks of gestation
Usually glucose levels normal
6 weeks post partum

Gestational diabetes develops during pregnancy and occurs in about 2% to 10% of pregnancies in the United States.
Women with gestational diabetes are at higher risk of needing cesarean delivery, and their babies have increased risk for perinatal death, birth injury, and neonatal complications. Women who are at high risk for gestational diabetes should be screened at the first prenatal visit.
Those at high risk include women who are obese, are of advanced maternal age, and have a family history of diabetes.
Women with an average risk for gestational diabetes are screened with an OGTT at 24 to 28 weeks of gestation.
Most women with gestational diabetes have normal glucose levels within 6 weeks post partum.
Be aware that women with a history of gestational diabetes have a 35% to 60% chance of developing type 2 diabetes within 10 years.

DIAGNOSTIC STUDIES FOR DM

Hemoglobin A1C level: 6.5% or higher

Fasting plasma glucose level: higher than 126 mg/dL

Two-hour plasma glucose level during OGTT: 200 mg/dL (with glucose load of 75 g)

Classic symptoms of hyperglycemia with random plasma glucose level of 200 mg/dL or higher

The diagnosis of diabetes mellitus is made through one of four methods. These methods and their criteria for diagnosis are as follows:

1. Hemoglobin A1C level of 6.5% or higher.

2. Fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or higher. Fasting is defined as no caloric intake for at least 8 hours.

3. Two-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during an OGTT, with a glucose load of 75 g.

4. In a patient with classic symptoms of hyperglycemia (polyuria, polydipsia, unexplained weight loss) or hyperglycemic crisis, a random plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher.

If a patient presents with a hyperglycemic crisis or clear symptoms of hyperglycemia (polyuria, polydipsia, polyphagia) with a random plasma glucose level of 200 or higher, repeat testing is not warranted.
Otherwise, criteria 1 through 3 should be confirmed by repeat testing to rule out laboratory error. It is preferable for the repeat test to be the same test used initially. For example, if a random blood glucose test showed elevated blood glucose levels, the same test should be used again when the person is retested.
The accuracy of test results depends on adequate patient preparation and attention to the many factors that may influence the test results. For example, factors that can cause falsely elevated values include recent severe restrictions of dietary carbohydrate, acute illness, medications (e.g., contraceptives, corticosteroids), and restricted activity such as bed rest. A patient with impaired GI absorption or who has recently taken acetaminophen may have false-negative test results.

DIAGNOSTIC STUDIES

Hemoglobin A1C test
Glycosylated hemoglobin: reflects glucose levels over past 2 to 3 months
Used to diagnose, monitor response to therapy, and screen patients with prediabetes
Goal: less than 6.5% to 7%
Elderly under 8%

Hemoglobin A1C reflects the amount of glycosylated hemoglobin as a percentage of total hemoglobin (e.g., hemoglobin A1C of 6.5% means that 6.5% of the total hemoglobin has glucose attached to it). The amount of hemoglobin that is glycosated depends on the blood glucose level. When blood glucose levels are elevated over time, the amount of glucose attached to hemoglobin molecules increases. This glucose remains attached to the red blood cell (RBC) for the life of the cell (approximately 120 days).
Therefore, the hemoglobin A1C test provides a measurement of glycemic control over the previous 2 to 3 months, with increases in the A1C reflecting elevated blood glucose levels. The hemoglobin A1C test has several advantages over the FPG test, including greater convenience because fasting is not required.
Diseases affecting RBCs (e.g., iron deficiency anemia or sickle cell anemia) can influence the hemoglobin A1C level and should be considered in interpreting test results.
All patients with diabetes and prediabetes should have their hemoglobin A1C monitored regularly to determine the success of the current treatment plan and make changes in the plan if glycemic goals are not achieved.
The ADA identifies a hemoglobin A1C goal for patients with diabetes of less than 7.0%.
The American College of Endocrinology recommends a hemoglobin A1C level of less than 6.5%.
When the hemoglobin A1C level is maintained at near-normal levels, there is a greatly reduced risk for the development of microvascular and macrovascular complications.
For individuals with prediabetes, hemoglobin A1C level can help detect overt diabetes and provide patients with feedback regarding efforts to prevent diabetes.

A1C AND THE DIAGNOSIS OF DIABETES

A1C—gold standard for measuring long-term glycemic control—how does it work? RBC life span
Glucose binds irreversibly with hemoglobin over the lifespan of the RBC (glycated/glycosylated hemoglobin) – over 2 to 3 months.
Normal range is 4-5.6%; Diagnosis of diabetes with level greater than 6.5% (ADA, WHO)
“Pre-diabetes”—A1C range of 5.7 -- 6.4%

GOALS—A1C

A management plan to achieve normal or near-normal glycemia with specific A1C goals
American College of Clinical Endocrinologists—≤ 6.5%
American Diabetic Association--≤ 7%
Why can’t we all just get along? 
Goals should be individualized, of course; less stringent treatment goals may be appropriate for patients with a history of severe hypoglycemia, patients with limited life expectancies, elderly adults, and individuals with co-morbid conditions

COLLABORATIVE CARE

Goals of diabetes management
Decrease symptoms
Promote well-being
Prevent acute complications
Delay onset and progression of
long-term complications
Need to maintain blood glucose levels as near to normal as possible

The goals of diabetes management are to reduce symptoms, promote well-being, prevent acute complications of hyperglycemia, and prevent or delay the onset and progression of long-term complications.
These goals are most likely to be met when the patient is able to maintain blood glucose levels as near to normal as possible.

COLLABORATIVE CARE

Patient teaching
Nutritional therapy
Drug therapy
Exercise
Self-monitoring of blood glucose
Diet, exercise, and weight loss may be sufficient for patients with type 2 diabetes
All patients with type 1 require insulin

Diabetes is a chronic disease that requires daily decisions about food intake, blood glucose testing, medication, and exercise.
Patient teaching, which enables the patient to become the most active participant in his or her own care, is essential for a successful treatment plan. Nutritional therapy, drug therapy, exercise, and self-monitoring of blood glucose are the tools used in the management of diabetes.
For some people with type 2 diabetes, a regimen of proper nutrition, regular physical activity, and maintenance of desirable body weight is sufficient to attain an optimal level of blood glucose control. However, for the majority, drug therapy is necessary.
The major types of glucose-lowering agents (GLAs) used in the treatment of diabetes are insulin, oral agents (OAs), and nonisulin injectable agents.
All individuals with type 1 diabetes require insulin.

DIABETES
NUTRITIONAL THERAPY

Counseling
Education
Ongoing monitoring
Interdisciplinary team with registered dietitian as lead
DCCT study 1983-1993(Diabetic Control and Complication Trial): intensive control of blood glucose resulting in decrease retinopathy, neuropathy and nephropathy.

Individualized medical nutrition therapy (MNT), consisting of counseling, education, and ongoing monitoring, is a cornerstone of care for person with diabetes and prediabetes.
Although MNT has many positive outcomes, adherence to a dietary regimen is often challenging for many people.
Achieving nutritional goals requires a coordinated team effort that takes into account the behavioral, cognitive, socioeconomic, cultural, and religious aspects of the patient.
Because of these complexities, it is recommended that a registered dietitian with expertise in diabetes management takes the lead in MNT. The dietitian should conduct a dietary assessment and develop an individualized food plan.
Additional team members involved in MNT may include nurses, certified diabetes educators, clinical nurse specialists, health care providers, and social workers.

DIABETES
NUTRITIONAL THERAPY GOALS

ADA healthy food choices for improved metabolic control
Maintain blood glucose levels to as near normal as safely possible
Normal lipid profiles and blood pressure
Prevent or slow complications
Individual needs; personal, cultural preferences
Maintain pleasure of eating

Guidelines from the ADA indicate that within the context of an overall healthy eating plan, a person with diabetes can eat the same foods as a person who does not have diabetes. This means that the same principles of good nutrition that apply to the general population also apply to the person with diabetes.
According to the ADA, the overall goal of MNT is to assist people with diabetes in making healthy nutritional choices that will lead to improved metabolic control. Additional specific goals include the following:

1. Maintain blood glucose levels to as near normal as safely possible to prevent or reduce the risk for complications of diabetes.

2. Achieve lipid profiles and blood pressure levels that reduce the risk for cardiovascular disease.

3. Prevent or slow the rate of development of chronic complications of diabetes by modifying nutrient intake and lifestyle.

4. Address individual nutritional needs while taking into account personal and cultural preferences and respecting the individual’s willingness to

change.

5. Maintain the pleasure of eating by allowing as many food choices as appropriate.

DIABETES
NUTRITIONAL THERAPY: TYPE 1 DM

Meal plan is based on individual’s usual food intake and is balanced with insulin and exercise patterns
Day-to-day consistency important for patients using conventional, fixed insulin regimens
More flexibility with rapid-acting insulin, multiple daily injections, and insulin pump

Meal planning should be based on the individual’s usual food intake and preferences and balanced with insulin and exercise patterns.
The insulin regimen should be developed with the patient’s eating habits and activity pattern in mind.
Day-to-day consistency in timing and amount of food eaten is important for individuals using conventional, fixed insulin regimens.
Patients using rapid-acting insulin can make adjustments in dosage before the meal on the basis of the current blood glucose level and the carbohydrate content of the meal. Intensified insulin therapy, such as multiple daily injections or the use of an insulin pump, allows considerable flexibility in food selection and can be adjusted for alterations from usual eating and exercise habits.

DIABETES
NUTRITIONAL THERAPY: TYPE 2 DM

Emphasis on achieving glucose, lipid, and blood pressure goals
Weight loss
Nutritionally adequate meal plan with ↓ fat and CHO
Spacing meals
Regular exercise

The emphasis for nutritional therapy in type 2 diabetes should be placed on achieving glucose, lipid, and blood pressure goals.
Modest weight loss has been associated with improved insulin resistance. Therefore, weight loss is recommended for all individuals with diabetes who are overweight or obese.
There is no one proven strategy or method that can be uniformly recommended.
A nutritionally adequate meal plan with appropriate serving sizes, a reduction of saturated and trans fats, and low carbohydrates can bring about decreased calorie consumption.
Spacing meals is another strategy that spreads nutrient intake throughout the day.
A weight loss of 5% to 7% of body weight often improves glycemic control, even if desirable body weight is not achieved.
Weight loss is best attempted by a moderate decrease in calories and an increase in caloric expenditure. Regular exercise and learning new behaviors and attitudes can help facilitate long-term lifestyle changes.
Monitoring of blood glucose levels, hemoglobin A1C, lipids, and blood pressure provide feedback on how well the goals of nutritional therapy are being met.

DIABETES
NUTRITIONAL THERAPY

Food composition
Nutrient balance of diabetic diet is essential
Nutritional energy intake should be balanced with energy output
Individualized

The nutrient balance of a diabetic diet is essential to maintain blood glucose levels.
Nutritional energy intake should be balanced with the energy output of the patient, taking into account exercise and metabolic bodywork.
Each patient’s individual meal plan should be constructed with her or his lifestyle and health goals in mind.
The following slides discuss general recommendations for nutrient balance.

DIABETES
NUTRITIONAL THERAPY

Carbohydrates
Minimum of 130 g/day
Fruits, vegetables, whole grains, legumes, low-fat milk
Monitor with CHO counting, exchanges, or experienced-based estimation
Protein should make up 15% to 20% of total calories
Use glycemic index

Carbohydrates include sugars, starches, and fiber. Carbohydrates provide important sources of energy, fiber, vitamins, and minerals and are therefore important to all people, as well as those with diabetes.
The recommended daily allowance for carbohydrates is a minimum of 130 g/day
Foods containing carbohydrates from fruits, vegetables, whole grains, and low-fat milk should be included as part of a healthy meal plan.
Monitor by carbohydrate counting, exchanges, or experienced-based estimation.
Glycemic index may provide additional benefit.
Sucrose-containing food can be substituted for other carbohydrates in the meal plan.
Fiber intake should be 25 to 30 g/day.
Nonnutritive sweeteners are safe when consumed within FDA daily intake levels.

DIABETES
NUTRITIONAL THERAPY

Glycemic index
Term used to describe rise in blood glucose levels after carbohydrate-containing food is consumed
High glycemic index foods increase glucose levels faster
Goal is to avoid a sharp rise in blood glucose
http://www.glycemicindex.com

Glycemic index is the term used to describe the rise in blood glucose levels after a person has consumed a carbohydrate-containing food. The glycemic index of foods was developed to compare the postprandial responses of carbohydrate-containing foods.
Foods with a high glycemic index raise glucose levels faster and higher than foods with a low glycemic index.
The use of glycemic index may provide a modest additional benefit over that found when total carbohydrates are considered alone.
An online calculator for glycemic index is available at http://www.glycemicindex.com.

DIABETES
NUTRITIONAL THERAPY

Fats
Limit saturated fats to less than 7% of total calories
Limit cholesterol to less than 200 mg/day
Minimize trans fat
Two or more servings of fish per week to provide polyunsaturated fatty acids
Accelerated lipolysis in the fat cells—high serum TG = small, dense LDLs (even though the total LDL can be normal).

Dietary fat provides energy, carries fat-soluble vitamins, and provides essential fatty acids.
The ADA recommends limiting saturated fat to less than 7% of total calories.
Less than 200 mg/day of cholesterol and limited trans fats are also recommended as part of a healthy meal plan.
Decreasing fat and cholesterol intake assists in reducing the risk for cardiovascular disease.
Two or more servings of fish per week provide polyunsaturated fatty acids.

DECREASE LIPOPROTEIN LIPASE

Lipoprotein Lipase: an enzyme that breaks down triglycerides (very low density lipoprotein)

DIABETES
NUTRITIONAL THERAPY

Alcohol
Limit to moderate amount alcohol is absorbed before other nutrients (alcohol high in calories)
Consume with CHO to reduce hypoglycemia, but then watch for hyperglycemia from CHOs
Alcohol inhibits gluconeogenesis (may cause hypoglycemia)
Impair ability to treat hypoglycemia

Alcohol inhibits gluconeogenesis (breakdown of glycogen to glucose) by the liver. This can cause severe hypoglycemia in patients taking insulin or oral hypoglycemic medications that increase insulin secretion. Encourage patients to discuss their use of alcohol honestly with their health care providers because its use can make blood glucose more difficult to control.
Moderate alcohol consumption can sometimes be safely incorporated into the meal plan if blood glucose levels are well controlled and if the patient is not taking medications that will cause adverse effects. Moderate consumption is defined as one drink per day for women and two drinks per day for men.
A patient can reduce the risk for alcohol-induced hypoglycemia by eating carbohydrates when drinking alcohol. To decrease the carbohydrate content, recommend the use of sugar-free mixes and drinking dry, light wines.

DIABETES
NUTRITIONAL THERAPY

Diet teaching
Dietitian initially provides instruction
Carbohydrate counting (100% CHO coverts to glucose; 50% protein converts to glucose)
Serving size is 15 g of CHO
Typically 45 to 60 g per meal
Insulin dose based on number of CHOs consumed
Patient teaching essential ; pace food do not skip meals keep BMI<25. Consistency with meals helps prevent hypoglycemia.

Most often the dietitian initially teaches the principles of the nutrition therapy prescription.
Whenever possible, be prepared to work with dietitians as part of an interdisciplinary diabetes care team.
In some instances, access to a dietitian is not possible for patients with limited insurance coverage or who live in remote areas.
In these cases, you may need to assume responsibility for teaching basic dietary management to patients with diabetes.
Carbohydrate counting is a meal planning technique that people with diabetes use to keep track of the amount of carbohydrates they eat with each meal and per day.
Often they are advised to limit carbohydrates to a predetermined number.
The amount of total carbohydrates per day depends on previous glycemic control, age, weight, activity level, patient preference, and prescribed medications.
A serving size of carbohydrates is 15 g. Patients usually start with 45 to 60 g of carbohydrate per meal.
For some patients, insulin regimens are tailored to the number of carbohydrates a patient will consume at the meal, with a set number of units insulin given per every 15 g of carbohydrate (or sometimes another number).
Teach the patient about the foods that contain carbohydrates, how to read food labels, and appropriate serving sizes.

DIABETES EXERCISE

Type/amount
Minimum 150 minutes/week aerobic
Resistance training three times/week
Benefits
↓ Insulin resistance and blood glucose
Weight loss
↓ Triglycerides and LDL , ↑ HDL
Improve BP and circulation

Regular, consistent exercise is an essential part of diabetes and prediabetes management.
The ADA recommends that people with diabetes perform at least 150 minutes per week (30 minutes, 5 days per week) of a moderate-intensity aerobic physical activity.
The ADA also encourages people with type 2 diabetes to perform resistance training three times a week, in the absence of contraindications.
Exercise decreases insulin resistance and can have a direct effect on lowering blood glucose levels. It also contributes to weight loss, which decreases insulin resistance.
The therapeutic benefits of regular physical activity may result in a decreased need for diabetes medications in order to reach target blood glucose goals.
Regular exercise may also help reduce triglyceride and LDL cholesterol levels, increase HDL levels, reduce blood pressure, and improve circulation.

WHAT DOES EXERCISE DO?

Improvements in tissue insulin sensitivity independent of weight loss
Boost beta cell receptor sensitivity
Increase glucose uptake; decreases hepatic glucose production
Both aerobic & resistance training
Effect lasts 24 – 72 hours; no more than 2 consecutive days w/out

EXERCISE PRECAUTIONS

Pts taking insulin: Monitor blood glucose before, during and after exercise.
Glucose-lowering effect up to 48 hours after exercise
Exercise 1 hour after a meal
Snack to prevent hypoglycemia

Any new exercise program for diabetic patients should be started only after medical clearance.
Patients should start slowly with gradual progression toward the desired goal.
Patients who use insulin, sulfonylureas, or meglitinides are at increased risk for hypoglycemia when there is an increase in physical activity, especially if the patient exercises at the time of peak drug action or if food intake has not been sufficient to maintain adequate blood glucose levels. This can also occur if a normally sedentary patient with diabetes has an unusually active day.
The glucose-lowering effects of exercise can last up to 48 hours after the activity, so it is possible for hypoglycemia to occur for that long after the activity.
It is recommended that patients who use medications that can cause hypoglycemia schedule exercise about 1 hour after a meal or that they have a 10- to 15-g carbohydrate snack and check their blood glucose level before exercising. Small carbohydrate snacks can be taken every 30 minutes during exercise to prevent hypoglycemia. Patients using medications that place them at risk for hypoglycemia should always carry a fast-acting source of carbohydrate, such as glucose tablets or hard candies, when exercising.
Although exercise is generally beneficial to blood glucose levels, strenuous activity can be perceived by the body as a stress, causing a release of counterregulatory hormones that result in a temporary elevation of blood glucose. In a person with type 1 diabetes who is hyperglycemic and ketotic, exercise can worsen hyperglycemia and ketosis. Therefore, vigorous activity should be avoided if the blood glucose level exceeds 300 mg/dL and if ketones are present in the urine. If hyperglycemia is present without ketosis, it is not necessary to postpone exercise.

ACUTE COMPLICATIONS

DKA (Diabetic Ketoacidosis)
HHNK (hyperglycemic hyperosmolar syndrome)
Hypoglycemia

TOO MUCH INSULIN OR NOT ENOUGH

High morning blood glucose levels before breakfast can be a puzzle. If patient has not eaten why is glucose level high?
Two causes
Dawn Phenomenon (naturally occurring with non diabetics and also occur with DM)
Symogyi effect (DM and insulin)

Dawn Phenomena
Naturally occurring
Cause:
Hormonal effect
(cortisol, epinephrine, growth hormone)
How to check – Set alarm for 2-3 AM and check sugars
What to do ?
Nothing body will release insulin (if not DM)
If DM under physician care may
Add snack, avoid CHO snacks before bed
Change med
Change med dose
Change med time (from dinner to before bed)
Use insulin pump

Somogyi effect
Disease treatment effect
Usually occurs with Type I DM
Cause
Rebound effect due to night time hypoglycemia
How to check -
Set alarm for 2-3 AM -Check sugars and discuss with physician
What to do?
possible options
Decrease insulin dose
Increase activity
Bedtime snack

HYPOGLYCEMIA

BG Less than 70 mg/dL (3.88 mmol/L)
Hypoglycemia—may not be able to self manage due to impaired cognitive and motor function;
NEVER LEAVE THE HYPOGLYCEMIC PATIENT ALONE
IMPORTANT CAVEAT: the signs and symptoms consistent with hypoglycemia can often be confused with intoxication or withdrawal from drugs or alcohol.
If the patient has S & S consistent w/ hypoglycemia, particularly altered mental status, agitation, combativeness, and diaphoresis, measure their finger-stick blood glucose levels immediately.

HYPOGLYCEMIA—LOTS OF CAUSES

too much insulin or oral hypoglycemic meds (except metformin—metformin alone does not cause hypoglycemia)

administered insulin without eating

Didn’t eat enough food for the amount of insulin given; snack or meal was delayed after giving insulin

Took insulin and then purged (teenage girls)

Medic Alert bracelet or a tattoos on the wrist

HYPOGLYCEMIA

Common manifestations
Shakiness
Palpitations**
Nervousness
Irritability
Diaphoresis
Anxiety
Hunger
Pallor

The usual signs of hypoglycemia are the result of a surge in the sympathetic nervous system “sensing” the low blood sugar—include tachycardia, tremor, light-headedness, sweating

Epinephrine release causes manifestations that include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor.

HYPOGLYCEMIA

Altered mental functioning
Difficulty speaking
Visual disturbances
Stupor
Confusion
Coma
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death

Because the brain requires a constant supply of glucose in sufficient quantities to function properly, hypoglycemia can affect mental functioning.
The manifestations are speaking difficulties, visual disturbances, stupor, confusion, and coma.
Manifestations of hypoglycemia can mimic those of alcohol intoxication.
Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.

HYPOGLYCEMIA

Check blood glucose level
If less than 70 mg/dL, begin treatment
If more than 70 mg/dL, investigate further for cause of signs/symptoms
If monitoring equipment not available, treatment should be initiated

Treatment: rule of 15

Consume 15 g of a simple carbohydrate

Fruit juice or regular soft drink, 4 to 6 oz

Recheck glucose level in 15 minutes

Repeat if still less than 70 gm/dL

Avoid foods with fat

Decrease absorption of sugar

Avoid overtreatment

Give complex CHO after recovery

Hypoglycemia can usually be quickly reversed with effective treatment.
At the first sign of hypoglycemia, check the blood glucose level if possible.
If it is less than 70 mg/dL (3.9 mmol/L), immediately begin treatment for hypoglycemia.
If the blood glucose is greater than 70 mg/dL (3.9 mmol/L), investigate other possible causes of the signs and symptoms.
If the patient has manifestations of hypoglycemia and monitoring equipment is not available or the patient has a history of chronic poor glycemic control, hypoglycemia should be assumed and treatment should be initiated.

SUGAR SOURCES TO HAVE HANDY FOR HYPOGLYCEMIA

3 glucose tablets or 4 dextrose tablets
glucose gel
4 ounces of fruit juice
½ can of Coca- cola or Pepsi (not DIET)
7-8 Life Savers
2 Tbs. raisins
1 Tbs. sugar or jelly
YOU DON’T NEED 6 packs of sugar in an 8 ounce glass of orange juice!!
NO CANDY BARS (fat inhibits the rapid absorption of sugar)
Teach patient to always have something on hand

HYPOGLYCEMIA

Treatment
In acute care settings
Fifty percent dextrose, 20 to 50 mL, IV push
Patient not alert enough to swallow
Glucagon, 1 mg, IM or subcutaneously
Explore reason why occurred

In an acute care setting, patients with hypoglycemia may be treated with 20 to 50 mL of 50% dextrose, IV push.
Another option if the patient is not alert enough to swallow and no IV access is available is to administer 1 mg of glucagon by intramuscular (IM) or subcutaneous injection.
An IM injection in a site such as the deltoid muscle will result in a quicker response.
Glucagon stimulates a strong hepatic response to convert glycogen to glucose and therefore makes glucose rapidly available.
Nausea is a common reaction after glucagon injection.
Therefore, to prevent aspiration if vomiting occurs, turn the patient on the side until he or she becomes alert.
Once the acute hypoglycemia has been reversed, explore with the patient the reasons why the situation developed. This assessment may indicate the need for additional teaching of the patient and the family to avoid future episodes of hypoglycemia.

CHRONIC COMPLICATIONS

Identify chronic complications to be discussed.

Chronic Complications

Damage to blood vessels secondary to chronic hyperglycemia
Leading cause of diabetes-related death
Macrovascular and microvascular
Tight glucose control can prevent or minimize complications

Chronic complications of diabetes are primarily those of end-organ disease from damage to blood vessels (angiopathy) secondary to chronic hyperglycemia
Angiopathy is one of the leading causes of diabetes-related deaths; approximately 68% of deaths are due to cardiovascular disease and 16% to strokes in patients aged 65 and older.
These chronic blood vessel dysfunctions are divided into two categories: macrovascular complications and microvascular complications.
The Diabetes Control and Complications Trial (DCCT), a landmark study in diabetes management, demonstrated that in patients with type 1 diabetes, the risk for microvascular complications could be significantly reduced by keeping blood glucose levels as near to normal as possible for as much of the time as possible (tight glucose control).
Subjects who maintained tight glucose control reduced their risk for the development of retinopathy and nephropathy, some of the most common microvascular complications. On the basis of these findings, the ADA issued recommendations for the management of diabetes that included treatment goals to maintain blood glucose levels as near to normal as possible. Specific targets for individual patients must take into account the risk for severe or undetected hypoglycemia as a side effect of tight glucose control.
The United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that intensive treatment of type 2 diabetes significantly lowered the risk for developing diabetes-related eye, kidney, and neurologic problems. The findings from this study included a 25% reduction of microvascular disease and a 16% reduction in the risk for myocardial infarction in subjects who maintained long-term glycemic control.

CHRONIC COMPLICATIONS
MACROVASCULAR VESSELS

Diseases of large and medium-sized blood vessels
Greater frequency and earlier onset in patients with diabetes
Cerebrovascular disease
Cardiovascular disease
Peripheral vascular disease

Macrovascular complications are diseases of the large and medium-size blood vessels that occur with greater frequency and with an earlier onset in people with diabetes.
Macrovascular diseases include cerebrovascular, cardiovascular, and peripheral vascular disease.

CHRONIC COMPLICATIONS
MACROVASCULAR VESSELS

Decrease risk factors (yearly screening)
Obesity
Smoking
Hypertension
High fat intake
Sedentary lifestyle
Screen for and treat hyperlipidemia

Patients with diabetes can decrease several risk factors associated with macrovascular complications, such as obesity, smoking, hypertension, high fat intake, and sedentary lifestyle. Smoking, which is detrimental to health in general, is especially injurious to people with diabetes and significantly increases their risk for blood vessel and cardiovascular disease (CVD), stroke, and lower extremity amputation. The ADA recommends yearly screening of diabetic patients for CVD risk factors.
Optimizing blood pressure (BP) control in patients with diabetes is significant for the prevention of cardiovascular and renal disease.
Treating hypertension in diabetic patients results in a decrease in macrovascular and microvascular complications. Hypertension causes an increase in mortality rate among people with diabetes in comparison with those with hypertension without diabetes. A target BP of less than 130/80 mm Hg is recommended for all patients with diabetes.
Patients with diabetes have an increase in lipid abnormalities.
This contributes to the increase in cardiovascular disease seen in this population. The American Diabetes Association recommends the LDL cholesterol goal of less than 100 mg/dL (2.6 mmol/L), triglyceride levels of less than 150 mg/dL (1.7 mmol/L), and HDL cholesterol levels greater than 40 mg/dL (1.0 mmol/L) in men and greater than 50 mg/dL (1.3 mmol/L) in women as target values.
The ADA advocates lifestyle interventions including MNT, exercise, and weight loss and smoking cessation to treat hyperlipidemia.
Medications (primarily statins) are recommended for patients who do not reach lipid goals with lifestyle modifications and for people older than 40 years with other CVD risk factors, regardless of their baseline lipid levels.

CHRONIC COMPLICATIONS
MICROVASCULAR VESSELS

Thickening of vessel membranes in capillaries and arterioles
Specific to diabetes and includes
Retinopathy
Nephropathy
Neuropathy
Usually appear 10 to 20 years after diagnosis

Microvascular complications result from thickening of the vessel membranes in the capillaries and arterioles in response to conditions of chronic hyperglycemia.
They differ from the macrovascular complications in that they are specific to diabetes.
Although microangiopathy can be found throughout the body, the areas most noticeably affected are the eyes (retinopathy), the kidneys (nephropathy), and the skin (dermopathy).
Microvascular changes are present in some patients with type 2 diabetes at the time of diagnosis. However, clinical manifestations usually do not appear until 10 to 20 years later.

CHRONIC COMPLICATIONS
DIABETIC RETINOPATHY

Microvascular damage to retina
Most common cause of new cases of adult blindness
Initially no changes in vision
Annual eye examinations with dilation to monitor
Maintain glycemic control and manage hypertension

Diabetic retinopathy refers to the process of microvascular damage to the retina as a result of chronic hyperglycemia, presence of nephropathy, and hypertension in patients with diabetes.
Diabetic retinopathy is estimated to be the most common cause of new cases of adult blindness.
Retinopathy can be classified as nonproliferative or proliferative.

DIABETIC RETINOPATHY

CHRONIC COMPLICATIONS
DIABETIC NEPHROPATHY

Damage to small blood vessels that supply the glomeruli of the kidney
Leading cause of end-stage kidney disease
Risk factors
Hypertension
Genetics
Smoking
Chronic hyperglycemia

Diabetic nephropathy is a microvascular complication associated with damage to the small blood vessels that supply the glomeruli of the kidney. It is the leading cause of end-stage kidney disease in the United States and is seen in 20% to 40% of people with diabetes.
Risk factors for the development of diabetic nephropathy include hypertension, genetic predisposition, smoking, and chronic hyperglycemia.
Results of the DCCT and UKPDS research have demonstrated that kidney disease can be significantly reduced when near-normal blood glucose control is achieved and maintained.

THE HEALTHY KIDNEY…

Afferent arteriole

(vasodilated via

(prostaglandins)

Blood entering

glomerulus

Glomerulus→filter

Efferent arteriole

(vasoconstricted via

(angiotensin 2)

Blood exiting

glomerulus

AT2

Toilet

filter

THE DIABETIC KIDNEY

Afferent arteriole

( ⁭ vasodilation by

( ⁭ prostaglandins)

Blood entering

glomerulus

Glomerulus→filter
Efferent arteriole

( ⁭ vasoconstriction via

( ⁭ angiotensin 2)

Blood exiting

glomerulus

**CVD and microalbuminuria

Microalbuminuria**

CHRONIC COMPLICATIONS
DIABETIC NEPHROPATHY

Annual screening
If albuminuria present, drugs to delay progression:
ACE inhibitors
Angiotensin II receptor antagonists
Control of hypertension and tight blood glucose control: imperative

Patients with diabetes are screened for nephropathy annually for albuminuria and a measurement of the albumin-to-creatinine ratio in a random spot urine collection. Serum creatinine is also measured. Serum creatinine measurements provide an estimation of the glomerular filtration rate and thus the degree of kidney function.
Patients with diabetes who have microalbuminuria or macroalbuminuria should receive either angiotensin-converting enzyme (ACE) inhibitor drugs (e.g., lisinopril [Prinivil, Zestril]) or angiotensin II receptor antagonists (e.g., losartan [Cozaar]).
Both classifications of these drugs are used to treat hypertension and have been found to delay the progression of nephropathy in patients with diabetes.
Hypertension will significantly accelerate the progression of nephropathy. Therefore, aggressive blood pressure management is indicated for all patients with diabetes. Tight blood glucose control is also critical for the prevention and delay of diabetic nephropathy.

CHRONIC COMPLICATIONS
DIABETIC NEUROPATHY

Nerve damage due to metabolic derangements of diabetes
Of patients with diabetes, 60% to 70% have some degree of neuropathy
Reduced nerve conduction and demyelinization
Sensory or autonomic

Sensory neuropathy

Loss of protective sensation in lower extremities

Major risk for amputation**

*Especially detrimental to the elderly

Diabetic neuropathy is nerve damage that occurs because of the metabolic derangements associated with diabetes mellitus.
Approximately 60% to 70% of patients with diabetes have some degree of neuropathy.
Screening for neuropathy should begin in patients with type 2 diabetes at the time of diagnosis and 5 years after diagnosis in patients with type 1 diabetes.
The pathophysiologic processes of diabetic neuropathy are not well understood.
Several theories exist, including metabolic, vascular, and autoimmune factors.
The prevailing theory is that persistent hyperglycemia leads to an accumulation of sorbitol and fructose in the nerves that causes damage by an unknown mechanism.
The result is reduced nerve conduction and demyelinization.
Ischemia in blood vessels damaged by chronic hyperglycemia that supply the peripheral nerves is also implicated in the development of diabetic neuropathy.
Neuropathy can precede, accompany, or follow the diagnosis of diabetes.
The two major categories of diabetic neuropathy are sensory neuropathy, which affects the peripheral nervous system, and autonomic neuropathy. Each of these types can take several forms.

CHRONIC COMPLICATIONS
DIABETIC NEUROPATHY

Distal symmetric polyneuropathy
Most common form
Affects hands and/or feet bilaterally
Loss of sensation, abnormal tingling sensations, pain, and paresthesias. Although approximately half of patients with diabetic neuropathy do not have symptoms, initial symptoms may include paresthesias (prickling, tingling, or heightened sensation) and burning sensations.

The most common form of sensory neuropathy is distal symmetric polyneuropathy, which affects the hands and/or feet bilaterally.
This is sometimes referred to as stocking-glove neuropathy.
Characteristics of distal symmetric polyneuropathy include loss of sensation, abnormal sensations, pain, and paresthesias.
The pain, which is often described as burning, cramping, crushing, or tearing, is usually worse at night and may occur only at that time.
The paresthesias may be associated with tingling, burning, and itching sensations.
The patient may report a feeling of walking on pillows or numb feet.
At times the skin becomes so sensitive (hyperesthesia) that even light pressure from bed sheets cannot be tolerated.
Complete or partial loss of sensitivity to touch and temperature is common.

NEUROPATHY: NEUROTROPHIC ULCERATION

Defect in mobilization of inflammatory cells and impaired phagocytosis

Recurring or persistent infections

Treat promptly and vigorously

Patient teaching for prevention

Hand hygiene

Flu and pneumonia vaccine

Foot injury and ulcerations can occur without the patient’s ever having pain. Neuropathy can also cause atrophy of the small muscles of the hands and feet, causing deformity and limiting fine movement.

CHRONIC COMPLICATIONS
FOOT COMPLICATIONS

Patient teaching to prevent foot ulcers
Proper footwear
Avoidance of foot injury
Skin and nail care
Daily inspection of feet
Prompt treatment of small problems
Avoid heating pads or hot water bottles
Diligent wound care for foot ulcers

If the patient has LOPS or PAD, aggressive measures must be taken to teach the patient how to prevent foot ulcers. These measures include the selection of proper footwear, including prescription shoes. Other measures are to carefully avoid injury to the foot, practice diligent skin and nail care, inspect the foot thoroughly each day, and treat small problems promptly.
Proper care of a diabetic foot ulcer is critical for wound healing.
Several forms of treatment can be used for management of the foot ulcers.
Casting can be done to redistribute the weight on the plantar surface of the foot.
Wound control for the ulcer can include debridement, dressings, advanced wound healing products (becaplermin [Regranex]), vacuum-assisted closure, ultrasonography, hyperbaric oxygen, and skin grafting.
Neuropathic arthropathy, or Charcot’s foot, results in ankle and foot changes that ultimately lead to joint dysfunction and footdrop. These changes occur gradually and promote an abnormal distribution of weight over the foot, further increasing the chances of developing a foot ulcer as new pressure points emerge. Foot deformity should be recognized early and proper footwear fitted before ulceration occurs.

NECROTIC TOE BEFORE AND AFTER AMPUTATION

Necrosis in the toe developed as a complication of diabetes. A, Before amputation. B, After amputation.

CHRONIC COMPLICATIONS
SKIN PROBLEMS

Diabetic dermopathy
Most common
Red-brown, round or oval patches
Acanthosis nigricans
Velvety light brown to black skin

Up to two thirds of persons with diabetes develop skin problems.
Diabetic dermopathy, the most common diabetic skin lesion, is characterized by reddish-brown and round or oval patches. They initially are scaly and then flatten out and become indented. The lesions appear most frequently on the shins but can also be found on the front of the thighs, forearm, side of the foot, scalp, and trunk.
Acanthosis nigricans is a velvety light brown to black skin thickening seen predominantly on flexures, axillae, and the neck.
Necrobiosis lipoidica diabeticorum usually appears as red-yellow lesions, with atrophic skin that becomes shiny and transparent, revealing tiny blood vessels under the surface. This condition is uncommon and occurs more frequently in young women. It may appear before other clinical signs or symptoms of diabetes. Because the thin skin is prone to injury, special care must be taken to protect affected areas from injury and ulceration.

NURSING ASSESSMENT

Subjective data
Past health history
Viral infections, trauma, infection, stress, pregnancy, chronic pancreatitis, Cushing syndrome, acromegaly, family history of diabetes
Medications
Insulin, OAs, corticosteroids, diuretics, phenytoin
Obesity, weight loss or gain
Thirst, hunger Poor healing

Objective data

Dry mouth, Vomiting, Fruity breath

Confusion, stupor, coma

Muscle wasting

Fasting blood glucose level of 126 mg/dL or higher

Oral glucose tolerance test and/or random glucose level exceeding 200 mg/dL

↑ Blood urea nitrogen, creatinine, Albuminuria

Hemoglobin A1C value higher than 6.0%

Obtain the following important health information from the patient:

Past health history: mumps, rubella, coxsackievirus or other viral infections; recent trauma, infection, or stress; pregnancy, delivering infant weighing more than 9 lb; chronic pancreatitis; Cushing syndrome; acromegaly; family history of type 1 or type 2 diabetes mellitus
Medications: use of and compliance with insulin or OA regimen; use of corticosteroids, diuretics, phenytoin (Dilantin)
Surgery or other treatments: any recent surgery

NURSING DIAGNOSES/PLANNING

Ineffective self-health management
Risk for unstable blood glucose levels
Risk for infection
Risk for peripheral neurovascular dysfunction

Overall goals

Active patient participation

Few or no episodes of acute hyperglycemic emergencies or hypoglycemia

Maintain normal blood glucose levels

Prevent or minimize chronic complications

Adjust lifestyle to accommodate diabetes regimen

Nursing diagnoses related to diabetes mellitus may include, but are not limited to

Ineffective self-health management related to deficient knowledge of diabetes management and lack of adherence to diabetes management plan as evidenced by inaccurate statements regarding diabetes and its management and stated confusion regarding the pathophysiology of diabetes
Risk for unstable blood glucose levels related to inadequate blood glucose monitoring and lack of adherence to diabetes management plan
Risk for injury related to decreased tactile sensation, episodes of hypoglycemia
Risk for peripheral neurovascular dysfunction related to vascular effects of diabetes

MEDICAL ALERT

Instruct the patient to carry medical identification at all times that indicates that he or she has diabetes.
Police, paramedics, and many private citizens are aware of the need to look for this identification when working with sick or unconscious persons. Every person with diabetes should wear a MedicAlert bracelet or necklace.
An identification card can supply valuable information, such as the name of the health care provider, the type of diabetes, and the type and dose of insulin or OA.

NURSING MANAGEMENT
EVALUATION

Expected outcomes
Knowledge
Self-care measures
Balanced diet and activity
Stable, normal blood glucose levels
No injuries

The patient should be evaluated with regard to the following outcomes:

Verbalizes key elements of the therapeutic regimen, including knowledge of disease and treatment plan
Describes self-care measures that may prevent or decrease progression of chronic complications
Maintains a balance of nutrition, activity, and insulin availability that results in stable, normal blood glucose levels
Experiences no injury resulting from decreased sensation in feet
Experiences no injury resulting from hypoglycemia
Verbalizes effects of diabetes on peripheral artery circulation
Implements measures to increase peripheral circulation

SOMETHING TO THINK ABOUT…..

When you’re just about ready to take a bite.. Think about this…

It takes 2 hours and one minute for a 130-pound person to walk off the calories in a McDonald’s BIG MAC;
3 hours and 26 minutes to walk off a Burger King Double Whopper, with cheese

QUESTIONS???