INSULIN SECRETION AND FUNCTION

Insulin is a hormone secreted by the beta cells of the islet of Langerhans in the pancreas.
Small amounts of insulin are released into the bloodstream in response to changes in blood glucose levels
throughout the day.
Increased secretion or a bolus of insulin, released after a meal, helps maintain euglycemia.
Through an internal feedback mechanism that involves the pancreas and the liver, circulating blood glucose
levels are maintained at a normal range of 60 to 110 mg/dL.
Insulin is essential for the utilization of glucose for cellular metabolism as well as for the proper metabolism of
protein and fat.
Carbohydrate metabolisminsulin affects the conversion of glucose into glycogen for storage in the liver and
skeletal muscles, and allows for the immediate release and utilization of glucose by the cells.
Protein metabolismamino acid conversion occurs in the presence of insulin to replace muscle tissue or to
provide needed glucose (gluconeogenesis).
Fat metabolismstorage of fat in adipose tissue and conversion of fatty acids from excess glucose occurs
only in the presence of insulin.
Glucose can be used in the endothelial and nerve cells without the aid of insulin.
Without insulin, plasma glucose concentration rises and glycosuria results.
Absolute deficits in insulin result from decreased production of endogenous insulin by the beta cell of the
pancreas.
Relative deficits in insulin are caused by inadequate utilization of insulin by the cell.
CLASSIFICATION OF DIABETES
Type 1 Diabetes Mellitus
Type 1 diabetes mellitus was formerly known as insulin dependent diabetes mellitus and juvenile diabetes
mellitus.
Little or no endogenous insulin, requiring injections of insulin to control diabetes and prevent ketoacidosis.
Five to 10% of all diabetic patients have type 1.
Etiology: autoimmunity, viral, and certain histocompatibility antigens as well as a genetic component.
Usual presentation is rapid with classic symptoms of polydipsia, polyphagia, polyuria, and weight loss.
Most commonly seen in patients under age 30 but can be seen in older adults.
Type 2 Diabetes Mellitus
Type 2 diabetes mellitus was formerly known as noninsulin dependent diabetes mellitus or adult onset
diabetes mellitus.
Caused by a combination of insulin resistance and relative insulin deficiencysome individuals have
predominantly insulin resistance, whereas others have predominantly deficient insulin secretion, with
little insulin resistance.
Approximately 90% of diabetic patients have type 2.
Etiology: strong hereditary component, commonly associated with obesity.
Usual presentation is slow and typically insidious with symptoms of fatigue, weight gain, poor wound
healing, and recurrent infection.
Found primarily in adults over age 30; however, may be seen in younger adults and adolescents who
are overweight.
Patients with this type of diabetes, but who eventually may be treated with insulin, are still referred to
as having type 2 diabetes.

Prediabetes
Prediabetes is an abnormality in glucose values intermediate between normal and overt diabetes.
Impaired Fasting Glucose A new category adopted by the American Diabetes Association in 1997 and
redefined in 2004. Occurs when fasting blood glucose is greater than or equal to 100 but less than 126 mg/dL.
Impaired Glucose Tolerance Defined as blood glucose measurement on a glucose tolerance test greater than or
equal to 140 mg/dl but less than 200 in the 2-hour sample. Asymptomatic; it can progress to type 2 diabetes or
remain unchanged. May be a risk factor for the development of hypertension, coronary heart disease, and
hyperlipidemias.

Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance occurring during pregnancy.
Occurs in approximately 4% of pregnancies and usually disappears after delivery. Women with GDM are at
higher risk for diabetes at a later date. GDM is associated with increased risk of fetal morbidity. Screening for
GDM for all pregnant women other than those at lowest risk (under age 25, of normal body weight, have no
family history of diabetes, are not a member of an ethnic group with high prevalence of diabetes) should occur
between the 24th and 28th weeks of gestation.
Diabetes Associated with Other Conditions

Certain drugs can decrease insulin activity resulting in hyperglycemiacorticosteroids, thiazide diuretics,
estrogen, phenytoin. Disease states affecting the pancreas or insulin receptorspancreatitis, cancer of the
pancreas, Cushing's disease or syndrome, acromegaly, pheochromocytoma, muscular dystrophy, Huntington's
chorea.

DIAGNOSTIC TESTS
LABORATORY TESTS
Laboratory tests include those tests used to make the diagnosis as well as measures to monitor short- and long-
term glucose control.
Blood Glucose
Description
Fasting blood sugar (FBS), drawn after at least an 8-hour fast, to evaluate circulating amounts of glucose;
postprandial test, drawn usually 2 hours after a well-balanced meal, to evaluate glucose metabolism; and
random glucose, drawn at any time, nonfasting.

Nursing and Patient Care Considerations

For fasting glucose, make sure that patient has maintained 8-hour fast overnight; sips of water are allowed.
Advise patient to refrain from smoking before the glucose sampling because this affects the test results
For postprandial test, advise patient that no food should be eaten during the 2-hour interval.
For random blood glucose, note the time and content of the last meal.

Interpret blood values as diagnostic for diabetes mellitus as follows:

FBS greater than or equal to 126 mg/dL on two occasions

Random blood sugar greater than or equal to 200 mg/dL and presence of classic symptoms of diabetes
(polyuria, polydipsia, polyphagia, and weight loss)
Fasting blood glucose result of greater than or equal to 100 mg/dL demands close follow-up and repeat
monitoring.
NURSING ALERT
Capillary blood glucose values obtained by finger stick samples tend to be higher than values in venous
samples.
Oral Glucose Tolerance Test
Description
The oral glucose tolerance test (OGTT) evaluates insulin response to glucose loading. FBS is obtained before
the ingestion of a 50- to 200-g glucose load (usual amount is 75 g), and blood samples are drawn at , 1, 2,
and 3 hours (may be 4- or 5-hour sampling).

Nursing and Patient Care Considerations

Advise patient that for accuracy in results, certain instructions must be followed:
Usual diet and exercise pattern must be followed for 3 days before OGTT.
During OGTT, the patient must refrain from smoking and remain seated.
Oral contraceptives, salicylates, diuretics, phenytoin, and nicotinic acid can impair results and may be
withheld before testing based on the advice of the health care provider.
Diagnostic for diabetes mellitus if 2-hour value is 200 mg/dL or greater.

Glycated Hemoglobin (Glycohemoglobin, HbA1c)

Description
Measures glycemic control over a 60- to 120-day period by measuring the irreversible reaction of glucose to
hemoglobin through freely permeable erythrocytes during their 120-day lifecycle.

Nursing and Patient Care Considerations

No prior preparation, such as fasting or withholding insulin, is necessary.
Test results can be affected by red blood cell disorders (eg, thalassemia, sickle cell anemia), room
temperature, ionic charges, and ambient blood glucose values.
Many methods exist for performing the test, making it necessary to consult the laboratory for normal
values.
C-Peptide Assay (Connecting Peptide Assay)
Description
Cleaved from the proinsulin molecule during its conversion to insulin, C-peptide acts as a marker for
endogenous insulin production.

Nursing and Patient Care Considerations

Test can be performed after an overnight fast or after stimulation with Sustacal, I.V. glucose, or 1 mg of
glucagon subcutaneously.
Absence of C-peptide indicates no beta cell function, reflecting possible type 1 diabetes.
Fructosamine Assay
Description
Glycated protein with a much shorter half-life than glycated hemoglobin, reflecting control over a shorter
period, approximately 14 to 21 days. May be advantageous in patients with hemoglobin variants that interfere
with the accuracy of glycated hemoglobin tests.

Nursing and Patient Care Considerations

Note if patient has hypoalbuminemia or elevated globulins because test may not be reliable.
Should not be used as a diagnostic test for diabetes mellitus.
No special preparation or fasting is necessary.
GENERAL PROCEDURES AND TREATMENT MODALITIES
BLOOD GLUCOSE MONITORING
Accurate determination of capillary blood glucose assists patients in the control and daily management of
diabetes mellitus. Blood glucose monitoring helps evaluate effectiveness of medication; reflects glucose
excursion after meals; assesses glucose response to exercise regimen; and assists in the evaluation of episodes
of hypoglycemia and hyperglycemia to determine appropriate treatment.
Procedure

Guidelines for glucose monitoring are included in Procedure Guidelines 25-1.

The most appropriate schedule for glucose monitoring is determined by the patient and health care
provider.
Medication regimens and meal timing are considered to set the most effective monitoring schedule.
Scheduling of glucose tests should reflect cost effectiveness for the patient. Glucose meter test strips
may cost up to $1 each.
Glucose monitoring is intensified during times of stress or illness or when changes in therapy are
prescribed.
Patients with type 2 diabetes controlled with oral hypoglycemic agents or a single injection of
intermediate-acting insulin may test glucose levels before breakfast and before supper or at bedtime
(twice-per-day monitoring).
Patients with type 1 diabetes using a multiple-dose insulin regimen may test before meals and at
bedtime, occasionally adding a 2 to 3 a.m. test (four to six times daily monitoring).
Alternate site testing has been recommended by some clinicians for patients who complain of painful
fingers and for individuals such as musicians, who use their fingertips for occupational activities.
However, testing in such sites as the forearm, palm, thigh, and calf have not proved as accurate as
fingertip testing in most studies.
If alternate site is used, the area should be rubbed until it is warm before testing.
Do not use an alternate site when accuracy is critical; for example, if hypoglycemia is suspected, before
or after exercise, or before driving.
Check with the glucometer manufacturer to see if it is approved for alternate site testing.
INSULIN THERAPY
Insulin therapy involves the subcutaneous injection of immediate-, short-, intermediate-, or long-acting insulin
at various times to achieve the desired effect. Short-acting regular insulin can also be given I.V. About 20 types
of insulin are available in the United States; most of these are human insulin manufactured synthetically. Only
about 6% of diabetics are still using beef or pork insulin due to problems with immunogenicity.
Self-Injection of Insulin
Teaching of self-injection of insulin should begin as soon as the need for insulin has been established.
Teach the patient and another family member or significant other.
Use written and verbal instructions and demonstration techniques.
Teach injection first because this is the patient's primary concern; then teach loading the syringe.

DIABETES AND RELATED DISORDERS

DIABETES MELLITUS
Diabetes mellitus is a metabolic disorder characterized by hyperglycemia and results from defective insulin
production, secretion, or utilization.
Pathophysiology and Etiology
There is an absolute or relative lack of insulin produced by the beta cell, resulting in hyperglycemia.
Defects at the cell level, impaired secretory response of insulin to rises in glucose, and increased nocturnal
hepatic glucose production (gluconeogenesis) are seen in type 2 diabetes.
Etiology of type 1 diabetes is not well understood; viral, autoimmune, and environmental theories are under
review.
Etiology of type 2 diabetes involves heredity, genetics, and obesity.
Clinical Manifestations
Onset is abrupt with type 1 and insidious with type 2.
Hyperglycemia
Weight loss, fatigue
Polyuria, polydipsia, polyphagia
Blurred vision
Altered Tissue Response
Poor wound healing
Recurrent infections, particularly of the skin
Diagnostic Evaluation
Diabetes can be diagnosed in any of the following ways (and should be confirmed on a different day by any of
these tests):
FBS of greater than or equal to 126 mg/dL
Random blood glucose of greater than or equal to 200 mg/dL with classic symptoms (polyuria, polydipsia,
polyphagia, weight loss)
OGTT greater than or equal to 200 mg/dL on the 2-hour sample
Tests for glucose control over time are glycated hemoglobin and fructosamine assay
Management
Diet
Dietary control with caloric restriction of carbohydrates and saturated fats to maintain ideal body weight.
The goal of meal planning is to control blood glucose and lipid levels
Exercise
Regularly scheduled, moderate exercise performed for at least 30 minutes most days of the week promotes the
utilization of carbohydrates, assists with weight control, enhances the action of insulin, and improves
cardiovascular fitness.
Medication
Oral antidiabetic agents for patients with type 2 diabetes who do not achieve glucose control with diet and
exercise only
Act by a variety of mechanisms, including stimulation of insulin secretion from functioning beta cells,
reduction of hepatic glucose production, enhancement of peripheral sensitivity to insulin, and reduced
absorption of carbohydrates from the intestine.
Sulfonylureas and meglitinide analogues may cause hypoglycemic reactions.
Biguanides, alpha-glucosidase inhibitors, and meglitinide analogues may cause significant flatus and GI
adverse effects.
Insulin therapy for patients with type 1 diabetes who require replacement
Complications
Acute
Hypoglycemia occurs as a result of an imbalance in food, activity, and insulin/oral antidiabetic agent.
Diabetic ketoacidosis (DKA) occurs primarily in type 1 diabetes during times of severe insulin deficiency or
illness, producing severe hyperglycemia, ketonuria, dehydration, and acidosis.
Hyperosmolar hyperglycemic nonketotic syndrome (HHNKS) affects patients with type 2 diabetes, causing
severe dehydration, hyperglycemia, hyperosmolarity, and stupor.
Chronic Macroangiopathy
Cerebrovascular Disease
Incidence: Twice as frequent in diabetes
Hypertension, increased lipids, smoking, and uncontrolled blood glucose increase risk of stroke and transient
ischemic attack.
Coronary Artery Disease (CAD)
Incidence: Increased vessel disease with more vessels affected in diabetes. Higher incidence of silent
myocardial infarctions (MIs).
Hyperglycemia contributes to atherosclerosis and vessel deterioration
Peripheral Vascular Disease
Incidence: 50% of nontraumatic amputations are related to diabetes.
Intermittent claudication, absent pedal pulses, and ischemic gangrene are increased in diabetes.
Microangiopathy
Retinopathy
Incidence: Type 110 years postdiagnosis 60% have some degree of retinopathy. Type 2approximately
20% present with retinopathy at diagnosis, which increases to 60% -85% after 15 years.
Appearance of hard exudates, blot hemorrhages, and microaneurysms on the retina in background
retinopathy. Progresses to neurovascularization in proliferative diabetic retinopathy.
Nephropathy
Thickening of the glomerular basement membrane, mesangial expansion, and renal vessel sclerosis are caused
by diabetes.
Subsequently, diffuse and nodular intercapillary glomerulosclerosis diminishes renal function.
Peripheral Neuropathy
Distal symmetrical polyneuropathy involving the lower extremities is most commonly seen.
In conjunction with peripheral vascular disease, neuropathy to the feet increases susceptibility to
trauma and infection.
Three clinical syndromes of distal symmetrical polyneuropathy are seen: acute painful, small fiber, and
large fiber neuropathy.
Autonomic Neuropathy
Gastroparesis
Characteristics: Delayed gastric emptying, prolonged pylorospasms and loss of the powerful contractions
of the distal stomach to grind and mix foods.
Diarrhea
Frequent, watery movements
Mild steatorrhea
Can be intermittent, persistent, or alternate with constipation.
Impotence/Sexual Dysfunction
Incidence is not well documented due to inhibitions about reporting this problem to health care providers.
Sexual dysfunction can involve changes in erectile ability, ejaculation, or libido.
Orthostatic Hypotension
One of three syndromes associated with cardiovascular autonomic neuropathy, orthostatic hypotension occurs
when the postural reflex, which increases heart rate and peripheral vascular resistance is dysfunctional.
Nursing Assessment
Obtain a history of current problems, family history, and general health history.
Has the patient experienced polyuria, polydipsia, polyphagia, and any other symptoms?
Number of years since diagnosis of diabetes
Family members diagnosed with diabetes, their subsequent treatment, and complications

Perform a review of systems and physical examination to assess for signs and symptoms of diabetes, general
health of patient, and presence of complications.

General: recent weight loss or gain, increased fatigue, tiredness, anxiety

 Skin: skin lesions, infections, dehydration, evidence of poor wound healing
Eyes: changes in visionfloaters, halos, blurred vision, dry or burning eyes, cataracts, glaucoma
Mouth: gingivitis, periodontal disease
Cardiovascular: orthostatic hypotension, cold extremities, weak pedal pulses, leg claudication
Nursing Diagnoses
Imbalanced Nutrition: More than Body Requirements related to intake in excess of activity expenditures
Fear related to insulin injection
Risk for Injury (hypoglycemia) related to effects of insulin, inability to eat
Activity Intolerance related to poor glucose control
Deficient Knowledge related to use of oral hypoglycemic agents
Risk for Impaired Skin Integrity related to decreased sensation and circulation to lower extremities
Ineffective Coping related to chronic disease and complex self-care regimen
Improving Nutrition
Assess current timing and content of meals.
Advise patient on the importance of an individualized meal plan in meeting weight-loss goals. Reducing intake
of carbohydrates may benefit some patients; however, fad diets or diet plans that stress one food group and
eliminate another are generally not recommended.
Discuss the goals of dietary therapy for the patient. Setting a goal of a 10% (of patient's actual body weight)
weight loss over several months is usually achievable and effective in reducing blood sugar and other
metabolic parameters.
Assist patient to identify problems that may have an impact on dietary adherence and possible solutions to
these problems. Emphasize that lifestyle changes should be maintainable for life.
Explain the importance of exercise in maintaining/reducing body weight.
DIABETIC KETOACIDOSIS
DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia,
ketonuria, acidosis, and dehydration.

Pathophysiology and Etiology

Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for
fuel.
Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver.
Ketone bodies are organic acids that cause metabolic acidosis.
Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to the
hyperglycemia caused by insulin deficiency, accelerates the development of DKA.
Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium,
sodium, phosphate, and water.
Caused by inadequate amounts of endogenous or exogenous insulin.
Clinical Manifestations
Early
Polydipsia, polyuria
Fatigue, malaise, drowsiness
Anorexia, nausea, vomiting
Abdominal pains, muscle cramps

Later

Kussmaul respiration (deep respirations)

Fruity, sweet breath
Hypotension, weak pulse
Diagnostic Evaluation
Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL.
Serum and urine ketone bodies are present.
Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon
dioxide is decreased as a respiratory compensation mechanism.
Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and dehydration,
despite total body depletion.
 BUN, creatinine, hemoglobin, and hematocrit are elevated due to dehydration.
Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic
diuresis and dehydration.
Management
I.V. fluids to replace losses from osmotic diuresis, vomiting.
I.V. insulin dripregular insulin infused only to increase glucose utilization and decrease lipolysis.
Electrolyte replacementsodium chloride and phosphate as required, potassium chloride and
bicarbonate based on laboratory results.
Complications
Premature discontinuation of I.V. insulin can result in prolongation of DKA.
Too-rapid infusion of I.V. fluids in cases of severe dehydration can cause cerebral edema and death.
Failure to institute subcutaneous insulin injections before discontinuation of I.V. insulin can result in
extended hyperglycemia.
Nursing Diagnoses
Deficient Fluid Volume related to hyperglycemia
Ineffective Therapeutic Regimen Management related to failure to increase insulin during illness
Nursing Interventions
Restoring Fluid and Electrolyte Balance
Assess BP and heart rate frequently, depending on patient's condition; assess skin turgor and
temperature.
Monitor intake and output every hour.
Replace fluids as ordered through peripheral I.V. line.
Monitor urine specific gravity to assess fluid changes.
Monitor blood glucose frequently.
Assess for symptoms of hypokalemiafatigue, anorexia, nausea, vomiting, muscle weakness,
decreased bowel sounds, paresthesia, arrhythmias, flat T waves, ST-segment depression.

HYPEROSMOLAR HYPERGLYCEMIC NONKETOTIC SYNDROME

HHNS is an acute
hyperglycemia, complication
dehydration, andofhyperosmolarity,
diabetes mellitusbut
(particularly
little or no type 2 diabetes) characterized by
ketosis.
Pathophysiology and Etiology
Prolonged hyperglycemia with glucosuria produces osmotic diuresis.
Loss of water, sodium, and potassium results in severe dehydration, causing hypovolemia and
hemoconcentration.
Hyperosmolarity
dehydration. is a result of excessive blood sugar and increasing sodium concentration in
Insulin continues to be produced at a level that prevents ketosis.
Increased blood viscosity decreases blood flow to the organs, creating tissue hypoxia.
Intracellular fluid and electrolyte shifts produce neurologic signs and symptoms.
Caused by inadequate amounts of endogenous/exogenous insulin to control hyperglycemia.
o Precipitating event may occur, such as cardiac failure, burn, or chronic illness that increases
need for insulin.
o Use of therapeutic agents
immunosuppressive that increase blood glucose levels (eg, glucocorticoids,
agents).
o Use of therapeutic
hyperosmolar procedures thatperitoneal
hyperalimentation, cause stress or increase blood glucose levels (eg,
dialysis).
Clinical Manifestations
Early
Polyuria, dehydration
Fatigue, malaise
Nausea, vomiting
Later
Hypothermia
Seizures, stupor, coma
Muscle weakness
Diagnostic Evaluation
Serum glucose and osmolality are greatly elevated.
Serum and urine ketone bodies are minimal to absent.
Serum sodium and potassium levels may be elevated, depending on degree of dehydration, despite total
body losses.
BUN and creatinine may be elevated due to dehydration.
Urine specific gravity is elevated due to dehydration.
Management
 Correct fluid and electrolyte imbalances with I.V. fluids.
Provide insulin via I.V. drip to lower plasma glucose.
Evaluate complications, such as stupor, seizures, or shock, and treat appropriately.
Identify and treat underlying illnesses or events that precipitated HHNS.
Complications
Too rapid infusion of I.V. fluids can cause cerebral edema and death.
HHNS is a medical emergency that, if not treated properly, can cause death.
Patients who become comatose will need nasogastric (NG) tubes to prevent aspiration.
Nursing Assessment
Assess level of consciousness (LOC).
Assess for dehydrationpoor turgor, flushing, dry mucous membranes.
Assess cardiovascular status for shockrapid, thready pulse, cool extremities, hypotension,
electrocardiogram changes.
Interview family or significant other regarding precipitating events to episode of HHNS.
Evaluate patient's self-care regimen before hospitalization.
Determine events, treatments, or drugs that may have caused the event.
Nursing Diagnoses
Deficient Fluid Volume related to severe dehydration
Risk for Aspiration related to reduced LOC and vomiting
Nursing Interventions
Restoring Fluid Balance
Assess patient for increasing signs and symptoms of dehydration, hyperglycemia, or electrolyte
imbalance.
Institute fluid replacement therapy as ordered (usually normal or half-strength saline initially),
maintaining patent I.V. line.
Assess patient for signs and symptoms of fluid overload and cerebral edema as I.V. therapy progresses.
Administer regular insulin I.V. as ordered, and add dextrose to I.V. infusion as blood glucose falls
below 300 mg/dL, to prevent hypoglycemia.