Chapter 41

Assessment and Management

of Patients With Diabetes
Mellitus

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Diabetes Mellitus
• Diabetes mellitus is a group of metabolic diseases characterized by elevated levels of
glucose in the blood (hyperglycemia) resulting from defects in insulin secretion,
insulin action, or both.
• Insulin, a hormone produced by the pancreas, controls the level of glucose in the
blood by regulating the production and storage of glucose. In the diabetic state, the
cells may stop responding to insulin or the pancreas may stop producing insulin
entirely. This leads to hyperglycemia, which may result in acute metabolic
complications such as diabetic ketoacidosis (DKA) and hyperglycemic
hyperosmolar nonketotic syndrome (HHNS).
• Long-term effects of hyperglycemia contribute to macrovascular complications
(coronary artery disease, cerebrovascular disease, and peripheral vascular disease),
chronic microvascular complications (kidney and eye disease), and neuropathic
complications.
• The primary goals of treatment for patients with diabetes include controlling blood
glucose levels and preventing acute and long-term complications. Thus, the nurse who
cares for diabetic patients must assist them to develop self-care management skills.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Diabetes Mellitus
• There are several different types of diabetes mellitus; they may differ in cause, clinical
course, and treatment. The major classifications of diabetes are:
• Type 1 diabetes (previously referred to as insulin-dependent diabetes mellitus)
• Type 2 diabetes (previously referred to as non-insulindependent diabetes mellitus)
• Gestational diabetes mellitus
• Diabetes mellitus associated with other conditions or syndromes
• Approximately 5% to 10% of people with diabetes have type 1 diabetes, in which the
insulin-producing pancreatic beta cells are destroyed by an autoimmune process. As a
result, they produce little or no insulin and require insulin injections to control their
blood glucose levels. Type 1 diabetes is characterized by an acute onset, usually before
age 30.
• Approximately 90% to 95% of people with diabetes have type 2 diabetes (CDC, Data
Factsheet, 2002), which results from decreased sensitivity to insulin (called insulin
resistance) and impaired beta cell functioning resulting in decreased insulin
production.
• Type 2 diabetes is first treated with diet and exercise. If elevated glucose levels persist,
diet and exercise are supplemented with oral hypoglycemic agents. In some
individuals with type 2Copyright
diabetes,
© 2010 oral
Woltersagents do| Lippincott
Kluwer Health not controlWilliams &hyperglycemia,
Wilkins and insulin
 Diabetes Mellitus
• In addition, some individuals whose type 2 diabetes can usually be controlled with diet,
exercise, and oral agents may require insulin injections during periods of acute
physiologic stress (eg, illness or surgery). Type 2 diabetes occurs more among people
who are older than 30 years and obese.
• PHYSIOLOGY OF DIABETES
• Insulin is secreted by beta cells, which are one of four types of cells in the islets of
Langerhans in the pancreas. Insulin is an anabolic, or storage, hormone. When a
person eats a meal, insulin secretion increases and moves glucose from the blood into
muscle, liver, and fat cells. In those cells, insulin:
1. Transports and metabolizes glucose for energy
2. Stimulates storage of glucose in the liver and muscle (in the form of glycogen)
3. Signals the liver to stop the release of glucose
4. Enhances storage of dietary fat in adipose tissue
5. Accelerates transport of f amino acids (derived from dietary protein) into cells
• Inhibits the breakdown of stored glucose, protein, and fat.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• PHYSIOLOGY OF DIABETES
• During fasting periods (between meals and overnight), the pancreas
continuously releases a small amount of insulin (basal insulin); another
pancreatic hormone called glucagon (secreted by the alpha cells of the islets
of Langerhans) is released when blood glucose levels decrease and stimulate
the liver to release stored glucose. The insulin and the glucagon together
maintain a constant level of glucose in the blood by stimulating the release of
glucose from the liver.
• Initially, the liver produces glucose through the breakdown of glycogen
(glycogenolysis). After 8 to 12 hours without food, the liver forms glucose
from the breakdown of noncarbohydrate substances, including amino acids
(gluconeogenesis).

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

• PATHOPHYSIOLOGY OF DIABETES

• TYPE 1 DIABETES
• Type 1 diabetes is characterized by destruction of the pancreatic beta cells. It is
thought that combined genetic, immunologic, and possibly environmental (eg, viral)
factors contribute to beta cell destruction.
• There is also evidence of an autoimmune response in type 1 diabetes. This is an
abnormal response in which antibodies are directed against normal tissues of the body,
responding to these tissues as if they are foreign.
• Regardless of the specific etiology, the destruction of the beta cells results in decreased
insulin production, unchecked glucose production by the liver, and fasting
hyperglycemia. In addition, glucose derived from food cannot be stored in the liver but
instead remains in the bloodstream and contributes to postprandial (after meals)
hyperglycemia. If the concentration of glucose in the blood exceeds the renal threshold
for glucose, usually 180 to 200 mg/dL (9.9 to 11.1 mmol/L), the kidneys may not
reabsorb all of the filtered glucose; the glucose then appears in the urine (glucosuria).
When excess glucose is excreted in the urine, it is accompanied by excessive loss of
fluids and electrolytes. This is called osmotic diuresis.
• Because insulin normally inhibits glycogenolysis (breakdown of stored glucose) and
gluconeogenesis (production of new glucose from amino acids and other substrates), in
people with insulin deficiency, these processes occur in an unrestrained fashion and
contribute further to hyperglycemia. In addition, fat breakdown occurs, resulting in an
increased production of ketone
Copyright © 2010bodies, which
Wolters Kluwer Health |are theWilliams
Lippincott byproducts
& Wilkins of fat breakdown.
• PATHOPHYSIOLOGY OF DIABETES

• TYPE 2 DIABETES
• The two main problems related to insulin in type 2 diabetes are insulin resistance and
impaired insulin secretion. Insulin resistance refers to a decreased tissue sensitivity to
insulin. Normally, insulin binds to special receptors on cell surfaces and initiates a
series of reactions involved in glucose metabolism. In type 2 diabetes, these
intracellular reactions are diminished, thus rendering insulin less effective at
stimulating glucose uptake by the tissues and at regulating glucose release by the liver.
• To overcome insulin resistance and to prevent the buildup of glucose in the blood,
increased amounts of insulin must be secreted to maintain the glucose level at a
normal or slightly elevated level. However, if the beta cells cannot keep up with the
increased demand for insulin, the glucose level rises, and type 2 diabetes develops.
• Despite the impaired insulin secretion that is characteristic of type 2 diabetes, there is
enough insulin present to prevent the breakdown of fat and the accompanying
production of ketone bodies. Therefore, DKA does not typically occur in type 2 diabetes.
Uncontrolled type 2 diabetes may, however, lead to another acute problem, HHNS.
• Because insulin resistance is associated with obesity, the primary treatment of type 2
diabetes is weight loss. Exercise is also important in enhancing the effectiveness of
insulin. Oral antidiabetic agents may be added if diet and exercise are not successful in
controlling blood glucose levels. If maximum doses of a single category of oral agents
fail to reduce glucose levels to satisfactory levels, additional oral agents may be used.
Insulin may be added to oral ©agent
Copyright therapy,
2010 Wolters or patients
Kluwer Health may& Wilkins
| Lippincott Williams move to insulin
 Pre-diabetes:
(1) Impaired Glucose Tolerance (IGT)
(2) Impaired Fasting Glucose (IFG)
 β cell destruction Progressive glucose
resulted from genetic, intolerance, insulin resistance
immunologic or impaired insulin secretion
environmental factors.

Symptoms include:
Onset associated with
• Fatigue & irritability; numbness
sudden wt loss or
• Polyuria, polyphagia & Polydipsia
nausea, vomiting, or
• Skin wounds that heal poorly
stomach pain.
• Blurred vision
• Recurrent infections, particularly vaginal
Symptoms include: infections
• Postprandial hypoglycemia
• Glucosuria
• Excessive loss of fluids & electrolytes linked with glucoseuria (osmotic diuresis).
• Increased production of ketone bodies.
At risk for diabetes
Anyone age 45 and older.
Obesity people
Ethnic group ( African-American , Hispanic –American , some native American
group).
Having a baby weighting more than 9 pounds .
History of gestational diabetes mellitus .
Hypertension .
High density lipoprotein level of 35 mg/dl or less or triglyceride level of 250 mg/
dl or more .

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Gestational DM

Occur in up to 14% of
pregnant women
Many who had this type
will develop type II later in
life.
Risk increases with age ˃
25y, obesity, family history,
& certain ethnic/racial
groups.

Rx: dietary modification,

Bld glucose monitoring (≤
105 mg/dl before meals &
≤ 120 mg/dl 2h after
meals), and insulin if
hyperglycemia persists
(oral agents should not be
used).
Question
Is the following statement True or False?

Type 1 diabetes mellitus is treated initially with diet and

exercise.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Answer
False

Type 2 diabetes mellitus, NOT type 1 diabetes mellitus, is

treated initially with diet and exercise.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Clinical Manifestations
• “Three Ps”
– Polyuria
– Polydypsia
– Polyphagia
• Fatigue, weakness, vision changes, tingling or numbness in hands or feet, dry
skin, skin lesions or wounds that are slow to heal, recurrent infections
• Type 1 may have sudden weight loss, nausea, vomiting, and abdominal pain if
DKA has developed

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Diagnostic Findings
Fasting blood glucose 126 mg/dL or more
Random glucose exceeding 200 mg/dL
Gerontologic considerations: age-related elevation of blood glucose

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Question
Is the following statement True or False?

The renal threshold for glucose is 180 to 200 mg/dL.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Answer
True

The renal threshold for glucose is 180 to 200 mg/dL.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Treatment goal is to normalize blood
glucose levels
Promote
Drug
Wellbeing Therapy
Nutritional
Therapy

Delay onset
&
Reduce
Collaborativ progression
Symptoms of long-term
e care
complications
:
1. Neuropathy
Exercise
2. Nephropathy
Self monitoring Prevent 3. Retenopathy
Of Bld glucose
& ketone.
acute
complications
These goals are met when pt is able to
:maintain blood glucose levels near to
1. NORMAL as possible
Hypoglycemia
Dietary Management—Goals
• Provide optimal nutrition; all essential food constituents
• Meet energy needs
• Achieve and maintain a reasonable weight
• Prevent wide fluctuations of blood glucose levels
• Decrease serum lipids, if elevated

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Meal Planning
• Consider food preferences, lifestyle, usual eating times,
and cultural/ethnic background
• Review diet history and need for weight loss, gain, or
maintenance
• Caloric requirements and calorie distribution throughout
the day
• Carbohydrates: 50–60% carbohydrates, emphasize
whole grains
• Fat: 20–30%, with >10% from saturated fat and < 300
mg cholesterol
• Fiber
• Exchange lists

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Glycemic Index
• Describes how much a food increases blood glucose
• Combine starchy food with protein and fat containing
food slows absorption, and glycemic response
• Raw or whole foods tend to have lower response than
cooked, chopped, or pureed foods
• Eat whole fruits rather than juices; decreases glycemic
response due to fiber-slowing absorption
• Adding food with sugars may produce lower response if
eaten with foods that are more slowly absorbed

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Other Dietary Concerns
• Alcohol
• Nutritive and nonnutritive sweeteners
• Reading labels

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Exercise
• Physical activity promote weight reduction and improve insulin sensitivity , thus
lowering blood glucose level .
• Together with dietary treatment , a program of regular physical activity and
exercise be considered for each person . Such a programmed must be tailored
to the individuals health status and fitness .
• People should , however be educated about the potential risk of hypoglycemia
and how to avoid it.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Exercise Precautions
• Exercise with elevated blood sugar levels (above 250 mg/dL) and ketones in
urine should be avoided
• Insulin normally decreases with exercise; patients on exogenous insulin should
eat a 15g carbohydrate snack before moderate exercise to prevent
hypoglycemia
• If exercising to control or reduce weight, insulin must be adjusted
• Potential post-exercise hypoglycemia
• Need to monitor blood glucose levels

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Exercise Recommendations
Encourage regular daily exercise
Gradual, slow increase in exercise period is encouraged
Modify exercise regimen to patient needs and presence of diabetic
complications or potential cardiovascular problems
Exercise stress test for patients older than age 30 who have 2 or more risk
factors is recommended
Gerontologic considerations.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Insulin Therapy
Blood glucose monitoring
Categories of insulin

Rapid-acting
Short-acting
Intermediate-acting
Very long-acting
Inhaled insulin

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Normal Pancreatic Insulin Release

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

One Injection Per Day

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Two Injections Per Day-Mixed

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Three or Four Injections Per Day

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Insulin Pump

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins
Teaching Patients Insulin Self-
Management
• Use and action of insulin
• Symptoms of hypoglycemia and hyperglycemia
– Required actions
• Blood glucose monitoring
• Self-injection of insulin
• Insulin pump use

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

 Question
What category of insulin is rapid acting?
A. Humalog
B. Humalog R
C. Humulin N
D. Glargine (Lantus)

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Answer
A

Humalog is a rapid-acting insulin. Humalog R is a short-

acting insulin. Humulin N is an intermediate-acting
insulin. Glargine (Lantus) is a very long-acting insulin.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Oral Antidiabetic Agents
Used for patients with type 2 diabetes who cannot be treated with diet and
exercise alone.
Combinations of oral drugs may be used
Major side effect: hypoglycemia
Nursing interventions: monitor blood glucose, and for hypoglycemia and other
potential side effects
Patient teaching

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Teaching Patients Self-Care
Assess knowledge and adherence to plan of care.
Provide basic information about diabetes, its cause and symptoms, and acute
and chronic complications and their treatment.
Teach self-care activities to prevent long-term complications including foot care,
eye care, and risk-factor management.
Include family in plan of care.
Provide information, encourage health promotion activities, and recommended
health screenings.

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Acute Complications of Diabetes
Hypoglycemia
Diabetic ketoacidosis (DKA)
Hyperglycemic hyperosmolar nonketotic syndrome (HHNS), aka hyperosmolar
nonketotic coma or hyperglycemia hyperosmolar syndrome (HHS)

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins

Long-Term Complications of Diabetes
Macrovascular complications
Accelerated atherosclerotic changes
Coronary artery disease, cerebrovascular disease, and peripheral
vascular disease
Microvascular complications
Diabetic retinopathy, nephropathy
Neuropathic changes
Peripheral neuropathy, autonomic neuropathies, hypoglycemic
unawareness, neuropathy, sexual dysfunction

Copyright © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins