D

Dementia

Description

Dementia is a syndrome characterized by dysfunction or loss of memory, orientation, attention, language, judgment, and reasoning. Personality changes and behavioral problems such as agitation, delusions, and hallucinations may occur. Ultimately these problems result in alterations in the individual’s ability to work, fulfill social and family responsibilities, and perform activities of daily living.

■ Fifteen percent of older Americans have dementia. In the United States, about half of all patients in long-term care facilities have Alzheimer’s disease (AD) or a related dementia.

■ About 60% to 80% of patients with dementia have a diagnosis of AD.

Pathophysiology

The two most common causes of dementia are neurodegenerative conditions (e.g., AD) and vascular disorders. Dementia is sometimes caused by treatable conditions that initially may be reversible, such as vitamin B₁ and B₁₂ deficiencies, thyroid disorders, subarachnoid hemorrhage, prescribed drugs (e.g., anticholinergics, hypnotics, cocaine), alcoholism, and head injury. However, with prolonged exposure or disease, irreversible changes may occur.

Vascular dementia is loss of cognitive function resulting from ischemic or hemorrhagic brain lesions caused by cardiovascular disease. Vascular dementia may be caused by a single stroke (infarct) or by multiple strokes.

■ The greatest risk factor for dementia is aging, although it is not a normal part of aging. Family history is also an important risk factor, as those with a first-degree relative with dementia are more likely to develop the disease. Other risk factors include diabetes mellitus, obesity, smoking, cardiac dysrhythmias (e.g., atrial fibrillation), hypertension, hypercholesterolemia, and coronary artery disease.

Clinical manifestations

■ Dementia associated with neurologic degeneration is often gradual and progressive over time. Causes of vascular dementia often result in more abrupt symptoms or symptoms that progress in a more stepwise pattern.

■ An acute (days to weeks) or subacute (weeks to months) pattern of change may be indicative of an infectious or metabolic cause, including encephalitis, meningitis, hypothyroidism, or drug-related dementia.

■ Depression is often mistaken for dementia in older adults, and, conversely, dementia for depression. Manifestations of depression (especially in the older adult) include sadness, difficulty thinking and concentrating, fatigue, apathy, feelings of despair, and inactivity.

Other clinical manifestations of dementia are discussed with Alzheimer’s disease (p. 23).

Diagnostic studies

■ Comprehensive medical, neurologic, and psychologic histories are important in determining the presence and cause of dementia.

■ Physical examination is performed to rule out other medical conditions.

■ Dementia is often diagnosed when two or more brain functions are significantly impaired (e.g., memory loss, impaired language skills).

Diagnosis of dementia related to vascular causes is based on the presence of cognitive loss, the presence of vascular brain lesions demonstrated by neuroimaging techniques (CT or MRI), and the exclusion of other causes of dementia (e.g., AD).

Nursing and collaborative management

Management of dementia is similar to management of the patient with AD (see Alzheimer’s Disease, p. 27). One form of dementia, vascular dementia, can often be prevented. Preventive measures include treatment of risk factors such as hypertension, diabetes, smoking, hypercholesterolemia, and cardiac dysrhythmias. Drugs that are used for patients with AD are also useful in patients with vascular dementia.

Diabetes insipidus

Description

Diabetes insipidus (DI) is caused by a deficiency of production or secretion of antidiuretic hormone (ADH) or a decreased renal response to ADH. The decrease in ADH results in fluid and electrolyte imbalances caused by increased urine output and increased plasma osmolality. Depending on the cause, DI may be transient or a lifelong condition.

There are several types of DI. Central DI (also known as neurogenic DI) results from an interference with ADH synthesis, transport, or release. Causes include brain tumor or surgery, central nervous infections, and head injury. It is the most common form of DI.

Nephrogenic DI occurs when there is adequate ADH, but there is a decreased response to ADH in the kidney. Causes include drug therapy (especially lithium), renal damage, and hereditary renal disease.

Psychogenic DI, a less common condition, is associated with excessive water intake. This can be caused by a structural lesion in the thirst center or a psychologic disorder.

Clinical manifestations

The primary characteristic of DI is excretion of large quantities of urine (2 to 20 L/day) with a very low specific gravity (<1.005) and urine osmolality (<100 mOsm/kg). Serum osmolality is elevated as a result of hypernatremia, which is caused by pure water loss in the kidney.

■ Most patients compensate for fluid loss by drinking great amounts of water (polydipsia) so that serum osmolality is normal or only moderately elevated. The patient may be fatigued from nocturia and may experience generalized weakness.

■ Central DI is usually acute and accompanied by excessive fluid loss. Central DI that results from head trauma is usually self-limiting and improves with treatment of the underlying problem. DI following cranial surgery is more likely to be permanent.

■ Although the clinical manifestations of nephrogenic DI are similar, the onset and amount of fluid losses are less dramatic than with central DI.

■ If oral fluid intake cannot keep up with urinary losses, severe dehydration results. This is manifested by poor tissue turgor, hypotension, tachycardia, and hypovolemic shock.

■ The patient may also show central nervous system (CNS) manifestations ranging from irritability and mental dullness to coma, which are related to rising serum osmolality and hypernatremia.

Diagnostic studies

■ Water deprivation test differentiates central DI from nephrogenic DI. Patients with central DI exhibit a dramatic increase in urine osmolality with this test, from 100 to 600 mOsm/kg, and a significant decrease in urine volume. The patient with nephrogenic DI will not be able to increase urine osmolality to >300 mOsm/kg.

■ Measuring ADH levels after an analog of ADH (e.g., desmopressin) is given also differentiates central DI from nephrogenic DI. If the cause is central DI, the kidneys will respond to the hormone by concentrating urine. If the kidneys do not respond in this way, then the cause is nephrogenic.

Nursing and collaborative management

Management of the patient with DI includes early detection, maintenance of adequate hydration, and patient teaching for long-term management. A therapeutic goal is the maintenance of fluid and electrolyte balance.

For central DI, fluid and hormone therapy is necessary. Fluids are replaced orally or IV, depending on the patient’s condition and ability to drink copious amounts of fluids. If IV glucose solutions are used, monitor serum glucose levels because hyperglycemia and glucosuria can lead to osmotic diuresis, which increases the fluid volume deficit.

■ Monitor BP, heart rate, and urine output and specific gravity hourly in the patient who is acutely ill.

■ Monitor level of consciousness and assess for signs of acute dehydration by assessing alertness, mucous membranes, tachycardia, and skin turgor.

■ Maintain an accurate record of intake and output and daily weights to determine fluid volume status.

■ DDAVP, an analog of ADH, is the hormone replacement of choice for central DI. Other ADH replacement drugs include aqueous vasopressin (Pitressin) or lysine vasopressin (Diapid). Assess response to DDAVP (e.g., weight gain, headache, depression, restlessness, hyponatremia).

Treatment for nephrogenic DI revolves around dietary measures (low-sodium diet) and thiazide diuretics. Limiting sodium intake to no more than 3 g/day often helps decrease urine output. When a low-sodium diet and thiazide drugs are not effective, indomethacin (Indocin) may be prescribed. Indomethacin, a nonsteroidal antiinflammatory drug (NSAID), helps increase renal responsiveness to ADH.

Diabetes mellitus

Description

Diabetes mellitus (DM) is a chronic multisystem disease related to abnormal insulin production, impaired insulin utilization, or both. Currently in the United States an estimated 25.8 million people, or 8.3% of the population, have diabetes mellitus. Approximately 7 million people with diabetes mellitus have not been diagnosed and are unaware that they have the disease.

■ Diabetes is the leading cause of adult blindness, end-stage kidney disease, and nontraumatic lower limb amputations. It is also a major contributing factor to heart disease and stroke.

■ The two most common types of diabetes are classified as type 1 or type 2 diabetes mellitus (Table 30).

Table 30

Comparison of Type 1 and Type 2 Diabetes Mellitus

Factor	Type 1 Diabetes Mellitus	Type 2 Diabetes Mellitus
Age at onset	More common in young people but can occur at any age.	Usually age 35 yr or older but can occur at any age.Incidence is increasing in children.
Type of onset	Signs and symptoms abrupt, but disease process may be present for several years.	Insidious, may go undiagnosed for years.
Prevalence	Accounts for 5%-10% of all types of diabetes.	Accounts for 90%-95% of all types of diabetes.
Environmental factors	Virus, toxins.	Obesity, lack of exercise.
Primary defect	Absent or minimal insulin production.	Insulin resistance, decreased insulin production over time, and alterations in production of adipokines.
Islet cell antibodies	Often present at onset.	Absent.
Endogenous insulin	Absent.	Initially increased in response to insulin resistance. Secretion diminishes over time.
Nutritional status	Thin, normal, or obese.	Frequently overweight or obese. May be normal.
Symptoms	Polydipsia, polyuria, polyphagia, fatigue, weight loss.	Frequently none, fatigue, recurrent infections. May also experience polyuria, polydipsia, and polyphagia.
Ketosis	Prone at onset or during insulin deficiency.	Resistant except during infection or stress.
Nutritional therapy	Essential.	Essential.
Insulin	Required for all.	Required for some. Disease is progressive and insulin treatment may need to be added to treatment regimen.
Vascular and neurologic complications	Frequent.	Frequent.

Type 1 diabetes mellitus

Type 1 diabetes, formerly known as “juvenile onset” or “insulin-dependent” diabetes, accounts for approximately 5% of all people with diabetes. This type generally affects people younger than 40 years of age, and 40% develop it before 20 years of age.

Pathophysiology.

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.

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 develop when the person’s pancreas can no longer produce sufficient amounts of glucose to maintain normal glucose. Once this occurs, the onset of symptoms is usually rapid.

■ The patient usually has a history of recent and sudden weight loss and the classic symptoms of polydipsia (excessive thirst), polyuria (frequent urination), and polyphagia (excessive hunger).

■ The individual with type 1 diabetes requires a supply of insulin from an outside source (exogenous insulin) to sustain life. Without insulin, the patient develops diabetic ketoacidosis (DKA), a life-threatening condition resulting in metabolic acidosis.

Type 2 diabetes mellitus

Type 2 diabetes mellitus was formerly known as “adult-onset diabetes (AODM)” or “non–insulin-dependent diabetes (NIDDM).” This type is the most prevalent type of diabetes, accounting for greater than 90% of patients with diabetes.

Pathophysiology.

In type 2 diabetes, the pancreas usually continues to produce some endogenous (self-made) insulin. However, the insulin that is produced either is insufficient for the body’s needs or is poorly used by the tissues. The presence of endogenous insulin is the major pathophysiologic distinction between type 1 and type 2 diabetes.

■ Risk factors for developing type 2 diabetes include being overweight or obese, being older, and having a family history of type 2 diabetes. The incidence is increasing in children because of the increasing prevalence of obesity in these individuals.

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

■ The first factor is insulin resistance, which describes a condition in which body tissues do not respond to the action of insulin because insulin receptors are unresponsive, insufficient in number, or both. Entry of glucose into the cell is impeded, resulting in hyperglycemia.

■ A second factor 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.

■ 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.

■ A fourth factor is alteration in the production of hormones and cytokines by adipose tissue (adipokines). Adipokines appear to play a role in glucose and fat metabolism and likely contribute to pathophysiology of type 2 diabetes.

Individuals with metabolic syndrome are at an increased risk for the development of type 2 diabetes (see Metabolic Syndrome, p. 415).

Disease onset in type 2 diabetes is usually gradual. The person may go for many years with undetected hyperglycemia that might produce few, if any, symptoms. Many people are diagnosed on routine laboratory testing or when they undergo treatment for other conditions and elevated glucose or glycosylated hemoglobin (A1C) levels are found.

Prediabetes

Individuals diagnosed with prediabetes are at increased risk for the development of type 2 diabetes. It is an intermediate stage between normal glucose homeostasis and diabetes where the blood glucose levels are elevated, but not high enough to meet the diagnostic criteria for diabetes. Prediabetes is defined as impaired glucose tolerance (IGT), impaired fasting glucose (IFG), or both.

■ A diagnosis of IGT is made if the 2-hour oral glucose tolerance test (OGTT) values are 140 to 199 mg/dL (7.8 to 11.0 mmol/L). IFG is diagnosed when fasting blood glucose levels are 100 to 125 mg/dL (5.56 to 6.9 mmol/L).

People 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 for you to encourage patients to undergo screening and to provide teaching about managing risk factors for diabetes.

■ Those with prediabetes should have their blood glucose and A1C tested regularly and 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.

Clinical manifestations

Type 1 diabetes

Because the onset of type 1 DM is rapid, the initial manifestations are usually acute. The osmotic effect of glucose produces polydipsia and polyuria. Polyphagia is a consequence of cellular malnourishment when insulin deficiency prevents use of glucose for energy. Weight loss, weakness, and fatigue may also occur.

Type 2 diabetes

Manifestations of type 2 diabetes are often nonspecific, including fatigue, recurrent infections, prolonged wound healing, and visual changes. Polydipsia, polyuria, and polyphagia may also occur.

Acute complications

Acute complications arise from events associated with hyperglycemia and hypoglycemia (also referred to as insulin reaction). It is important for the health care provider to distinguish between hyperglycemia and hypoglycemia because hypoglycemia worsens rapidly and constitutes a serious threat if action is not immediately taken. Table 31 compares hyperglycemia and hypoglycemia.

Table 31

Comparison of Hyperglycemia and Hypoglycemia

Hyperglycemia	Hypoglycemia
Manifestations*
■ Elevated blood glucose † ■ Increase in urination ■ Increase in appetite followed by lack of appetite ■ Weakness, fatigue ■ Blurred vision ■ Headache ■ Glycosuria ■ Nausea and vomiting ■ Abdominal cramps ■ Progression to DKA or HHS	■ Blood glucose <70 mg/dL (3.9 mmol/L) ■ Cold, clammy skin ■ Numbness of fingers, toes, mouth ■ Rapid heart rate ■ Emotional changes ■ Headache ■ Nervousness, tremors ■ Faintness, dizziness ■ Unsteady gait, slurred speech ■ Hunger ■ Changes in vision ■ Seizures, coma
Causes
■ Illness, infection ■ Corticosteroids ■ Too much food ■ Too little or no diabetes medication ■ Inactivity ■ Emotional, physical stress ■ Poor absorption of insulin	■ Alcohol intake without food ■ Too little food—delayed, omitted, inadequate intake ■ Too much diabetic medication ■ Too much exercise without adequate food intake ■ Diabetes medication or food taken at wrong time ■ Loss of weight without change in medication ■ Use of β-adrenergic blockers interfering with recognition of symptoms
Treatment
■ Get medical care ■ Continue diabetes medication as ordered ■ Check blood glucose frequently and check urine for ketones; record results ■ Drink fluids at least on an hourly basis ■ Contact health care provider regarding ketonuria	■ Immediately ingest 15 g of simple carbohydrates ■ Wait 15 min. Then check blood glucose again. ■ If blood glucose is < 70 mg/dL, repeat 15 g of carbohydrate ■ Contact emergency medical service (EMS) if no relief obtained ■ Discuss medication dosage with health care provider
Preventive Measures
■ Take prescribed dose of medication at proper time ■ Accurately administer insulin, noninsulin injectables, OA ■ Maintain diet ■ Adhere to sick-day rules when ill ■ Check blood for glucose as ordered ■ Wear diabetic identification	■ Take prescribed dose of medication at proper time ■ Accurately administer insulin, noninsulin injectables, OA ■ Ingest all recommended foods at proper time ■ Provide adequate food intake needed for calories for exercise ■ Be able to recognize and know symptoms and treat them immediately ■ Carry simple carbohydrates ■ Teach family and caregiver about symptoms and treatment ■ Check blood glucose as ordered ■ Wear Medic Alert (diabetic) identification

DKA, Diabetic ketoacidosis; HHS, hyperosmolar hyperglycemic syndrome.OA, Oral agent.

*There is usually a gradual onset of symptoms in hyperglycemia and a rapid onset in hypoglycemia.

^†Specific clinical manifestations related to elevated levels of blood glucose vary according to the patient.

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is caused by a profound deficiency of insulin and is characterized by hyperglycemia, ketosis, acidosis, and dehydration. Precipitating factors include illness and infection, inadequate insulin dosage, undiagnosed type 1 diabetes, poor self-management, and neglect.

■ DKA is most likely to occur in type 1 diabetes, but may be seen in type 2 in conditions of severe illness or stress when the pancreas cannot meet the extra demand for insulin. If left untreated, death is inevitable.

■ Manifestations of DKA include dehydration signs (e.g., poor skin turgor, dry mucous membranes), tachycardia, orthostatic hypotension with a weak and rapid pulse, vomiting, Kussmaul respirations, and a sweet fruity odor of acetone on the breath.

■ Laboratory findings include a blood glucose level greater than or equal to 250 mg/dL (13.9 mmol/L), arterial blood pH less than 7.30, serum bicarbonate level less than 16 mEq/L (16 mmol/L), and moderate to large amount of ketones in the urine or serum.

Hyperosmolar hyperglycemic syndrome

Hyperosmolar hyperglycemic syndrome (HHS) is a life-threatening syndrome that can occur in the patient with DM who is able to produce enough insulin to prevent DKA but not enough to prevent severe hyperglycemia, osmotic diuresis, and extracellular fluid depletion.

■ The main difference between HHS and DKA is that the patient with HHS usually has enough circulating insulin so that ketoacidosis does not occur. Because HHS produces fewer symptoms in the earlier stages, blood glucose levels can climb quite high before the problem is recognized. The higher blood glucose levels increase serum osmolality and produce more severe neurologic manifestations, such as somnolence, coma, seizures, hemiparesis, and aphasia.

■ HHS is less common than DKA. It often occurs in patients greater than 60 years of age with type 2 diabetes. Common causes of HHS are urinary tract infections, pneumonia, sepsis, any acute illness, and newly diagnosed type 2 diabetes.

■ Laboratory values include a blood glucose level above 600 mg/dL (33.33 mmol/L) and a marked increase in serum osmolality. Ketone bodies are absent or minimal in both blood and urine.

Hypoglycemia

Hypoglycemia, or low blood glucose, occurs when there is too much insulin in proportion to available glucose in the blood. This causes the blood glucose level to drop below 70 mg/dL. Manifestations include shakiness, palpitations, nervousness, diaphoresis, anxiety, hunger, and pallor. Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death.

Chronic complications

Chronic complications are primarily those of end-organ disease from damage to the blood vessels from chronic hyperglycemia. Angiopathy, or blood vessel disease, is one of the leading causes of diabetes-related deaths. These chronic blood vessel problems are divided into two categories: macrovascular complications and microvascular complications.

Macrovascular complications

These complications are diseases of the large and medium-sized blood vessels that occur with greater frequency and an earlier onset in people with diabetes. Risk factors associated with macrovascular complications, such as obesity, smoking, hypertension, high fat intake, and sedentary lifestyle, can be reduced. Insulin resistance appears to play a role in the development of cardiovascular disease and is implicated in the pathogenesis of essential hypertension and dyslipidemia.

Microvascular complications

These complications result from thickening of the vessel membranes in the capillaries and arterioles in response to chronic hyperglycemia. Although microangiopathy can be found throughout the body, the areas most noticeably affected are the eyes (retinopathy), kidneys (nephropathy), and skin (dermopathy).

Diabetic retinopathy is estimated to be the most common cause of new cases of adult blindness.

■ In nonproliferative retinopathy, the most common form, partial occlusion of the small blood vessels in the retina, causes microaneurysms to develop in the capillary walls. The walls of these microaneurysms are so weak that capillary fluid leaks out, causing retinal edema and eventually hard exudates or intraretinal hemorrhages. Vision may be affected if the macula is involved.

■ Proliferative retinopathy is more severe and involves the retina and vitreous. When retinal capillaries become occluded, new, fragile blood vessels are formed. Eventually light does not reach the retina as vessels tear and bleed. A tear or retinal detachment may then occur. If the macula is involved, vision is lost. Treatment involves laser photocoagulation.

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. Tight blood glucose control is critical in the prevention and delay of diabetic nephropathy. Hypertension significantly accelerates the progression of nephropathy. Therefore aggressive BP management is indicated for all patients with diabetes.

■ Patients with diabetes are screened for nephropathy annually with a random spot urine collection to assess for albuminuria and measure the albumin-to-creatinine ratio. Serum creatinine is also measured to provide an estimation of the glomerular filtration rate and thus the degree of kidney function.

Neuropathy

Neuropathy is nerve damage that occurs because of the metabolic alterations associated with diabetes. About 60% to 70% of patients with diabetes have some degree of neuropathy. More than 60% of nontraumatic amputations in the United States occur in people with diabetes. Screening for neuropathy should begin at the time of diagnosis in patients with type 2 diabetes and 5 years after diagnosis in patients with type 1 diabetes.

Two major categories of diabetic neuropathy are sensory neuropathy, which affects the peripheral nervous system and is the more common type of neuropathy, and autonomic neuropathy, which can affect nearly all body systems.

■ The most common form of sensory neuropathy is distal symmetric neuropathy, which affects the hands or feet bilaterally. Characteristics 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. The paresthesias may be associated with tingling, burning, and itching sensations.

■ Autonomic neuropathy can lead to hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention. Delayed gastric emptying (gastroparesis), a complication of autonomic neuropathy, can produce nausea, vomiting, gastroesophageal reflux, and persistent feelings of fullness. Cardiovascular abnormalities, such as postural hypotension, painless myocardial infarction, and resting tachycardia, can occur.

Control of blood glucose is the only treatment for diabetic neuropathy. It is effective in many but not all cases. Drug therapy may be used to treat neuropathic symptoms, particularly pain.

Diagnostic studies

The diagnosis of diabetes can be made through one of the following four methods. In the absence of unequivocal hyperglycemia, criteria 1 to 3 should be confirmed by repeat testing.

1. Glycosylated hemoglobin (A1C) of 6.5% or greater.

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

3. Two-hour plasma glucose level at or above 200 mg/dL (11.1 mmol/L) during an oral glucose tolerance test (OGTT), using 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 of at least 200 mg/dL (11.1 mmol/L).

Collaborative care

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. Nutritional therapy, drug therapy, exercise, and self-monitoring of blood glucose are the tools used in the management of diabetes. The major types of glucose-lowering agents (GLAs) used in the treatment of diabetes are insulin and oral and noninsulin injectable agents. For the majority of people, drug therapy is necessary.

Drug therapy: Insulin

Exogenous (injected) insulin is needed when a patient has inadequate insulin to meet specific metabolic needs. People with type 1 diabetes require exogenous insulin to survive. People with type 2 diabetes, who are usually controlled with diet, exercise, and/or OAs, may require exogenous insulin during periods of severe stress, such as illness or surgery. When patients with type 2 diabetes cannot maintain satisfactory blood glucose levels, exogenous insulin is added to the management plan.

Human insulin is prepared using genetic engineering. The insulin is derived from common bacteria (e.g., Escherichia coli) or yeast cells using recombinant DNA technology. Insulins differ by their onset, peak action, and duration and are categorized as rapid-acting, short-acting, intermediate-acting, and long-acting insulin (Table 32).

Table 32

Drug Therapy
Types of Insulin

Classification	Examples	Clarity of Solution
Rapid-acting insulin	lispro (Humalog)	Clear
	aspart (NovoLog)
	glulisine (Apidra)
Short-acting insulin	regular (Humulin R, Novolin R)	Clear
Intermediate-acting insulin	NPH (Humulin N, Novolin N)	Cloudy
Long-acting insulin	glargine (Lantus) detemir (Levemir)	Clear
Combination therapy (premixed)	NPH/regular 70/30* (Humulin 70/30, Novolin 70/30) NPH/regular 50/50* (Humulin 50/50) lispro protamine/lispro 75/25* (Humalog Mix 75/25) lispro protamine/lispro 50/50* (Humalog Mix 50/50) aspart protamine/aspart 70/30* (NovoLog Mix 70/30)	Cloudy

*These numbers refer to percentages of each type of insulin.

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Tags: Clinical Companion to Medical-Surgical Nursing

Oct 26, 2016 | Posted by admin in NURSING | Comments Off

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D

D

Dementia

Description

Pathophysiology

Clinical manifestations

Diagnostic studies

Nursing and collaborative management

Diabetes insipidus

Description

Clinical manifestations

Diagnostic studies

Nursing and collaborative management

Diabetes mellitus

Description

Type 1 diabetes mellitus

Pathophysiology.

Type 2 diabetes mellitus

Pathophysiology.

Prediabetes

Clinical manifestations

Type 1 diabetes

Type 2 diabetes

Acute complications

Diabetic ketoacidosis

Hyperosmolar hyperglycemic syndrome

Hypoglycemia

Chronic complications

Macrovascular complications

Microvascular complications

Neuropathy

Diagnostic studies

Collaborative care

Drug therapy: Insulin

Related

Stay updated, free articles. Join our Telegram channel

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Nurse Key

Fastest Nurse Insight Engine

D

D

Dementia

Description

Pathophysiology

Clinical manifestations

Diagnostic studies

Nursing and collaborative management

Diabetes insipidus

Description

Clinical manifestations

Diagnostic studies

Nursing and collaborative management

Diabetes mellitus

Description

Type 1 diabetes mellitus

Pathophysiology.

Type 2 diabetes mellitus

Pathophysiology.

Prediabetes

Clinical manifestations

Type 1 diabetes

Type 2 diabetes

Acute complications

Diabetic ketoacidosis

Hyperosmolar hyperglycemic syndrome

Hypoglycemia

Chronic complications

Macrovascular complications

Microvascular complications

Neuropathy

Diagnostic studies

Collaborative care

Drug therapy: Insulin

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