1elsevier items and derived items © 2007 by saunders, an imprint of elsevier, inc. chapter 46...
TRANSCRIPT
1Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Chapter 46
Diabetes Mellitus and Hypoglycemia
2Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Learning Objectives
• Describe the role of insulin in the body.• Explain the pathophysiology of diabetes mellitus and
hypoglycemia.• Describe the signs and symptoms of diabetes mellitus
and hypoglycemia.• Explain tests and procedures used to diagnose diabetes
mellitus and hypoglycemia.• Discuss treatment of diabetes mellitus and
hypoglycemia.• Explain the difference between type 1 and type 2 diabetes mellitus.
3Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Learning Objectives
• Differentiate between acute hypoglycemia and diabeticketoacidosis.
• Describe the treatment of a patient experiencing acutehypoglycemia or diabetic ketoacidosis.
• Describe the complications of diabetes mellitus.• Identify nursing interventions for a patient diagnosed
with diabetes mellitus or hypoglycemia.• Identify nursing interventions for a patient diagnosed
with ketoacidosis.
4Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Diabetes Mellitus
5Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Pathophysiology
• Chronic disorder of impaired metabolism with vascular and neurologic complications
• Key feature is elevated blood glucose, called hyperglycemia • Blood glucose level normally regulated by insulin, a
hormone produced by beta cells in the islets of Langerhans located in the pancreas
6Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Type 1
• Absence of endogenous insulin • Formerly called juvenile-onset diabetes because it most
commonly occurs in juveniles and young adults
• An autoimmune process, possibly triggered by a viral infection, destroys beta cells, the development of insulin antibodies, and the production of islet cell antibodies (ICAs)
• Affected people require exogenous insulin for the rest of their lives
7Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Type 2
• Inadequate endogenous insulin and body’s inability to properly use insulin
• Beta cells respond inadequately to hyperglycemia; results in chronically elevated blood glucose
• Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to the elevated glucose
• More common in adults; increasing in children • Controlled by diet and exercise; may require oral
hypoglycemic agents or exogenous insulin
8Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Role of Insulin
• Glucose • Insulin stimulates active transport of glucose into cells • If insulin absent, glucose remains in the bloodstream • Blood becomes thick, which increases its osmolality • Increased osmolality stimulates the thirst center• Increased fluid does not pass into body tissues; high serum
osmolality retains fluid in the bloodstream • As blood passes through the kidneys, some glucose
eliminated • Osmotic force created by glucose draws extra fluid and
electrolytes with it, causing abnormally increased urine volume
9Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Role of Insulin
• Fatty acids• Promotes fatty acid synthesis and conversion of fatty acids
into fat, which is stored as adipose tissue • Also spares fat by inhibiting breakdown of adipose tissue and
mobilization of fat and by inhibiting the conversion of fats to glucose
• Without adequate insulin, fat stores break down and increased triglycerides are stored in the liver
• Increased fatty acids in the liver can triple the production of lipoproteins; promotes atherosclerosis
10Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Role of Insulin
• Protein• Enhances protein synthesis in tissues and inhibits the
conversion of protein into glucose • Amino acids are admitted into cells; enhances rate of protein
formation while preventing protein degradation • Without adequate insulin, protein storage halts; large amounts
of amino acids dumped into the bloodstream • High levels of plasma amino acids place people with diabetes
at risk for development of gout • Changes in protein metabolism lead to extreme weakness and
poor organ functioning
11Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Etiology
• An autoimmune malfunction may cause complete destruction of the islets of Langerhans in the pancreas, creating type 1 diabetes
• Islet cell antibodies are identified in more than 80% of all people with type 1 diabetes at the time of diagnosis
12Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Figure 46-1
13Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Risk Factors
• Obesity • Sedentary lifestyle • Family history of diabetes • Age 40 years and older • History of gestational DM • History of delivering infant weighing more than 10 lb • African American (33% higher risk for type 2 DM) • Latin American/Hispanic (>300% higher risk for type 2 DM)• American Indians (33%-50% higher risk for type 2 DM)
14Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Risk Factors
• Metabolic syndrome • Thought to be a precursor to diabetes • Impaired glucose tolerance, high serum insulin, hypertension,
elevated triglycerides, low HDL cholesterol, altered size and density of LDL cholesterol
• Believed that metabolic syndrome is a chronic low-grade inflammatory process affecting endothelial tissue
• Long-term effects: atherosclerosis, ischemic heart disease, left ventricular hypertrophy, type 2 DM
• Research directed at learning how to detect this syndrome early and what interventions might slow or arrest the progress
15Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Long-Term Complications
16Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Microvascular Complications
• Retinopathy • Pathological changes in the retina that are
associated with DM
• Nephropathy • Kidney damage
17Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Macrovascular Complications
• Accelerated atherosclerotic changes in the person with diabetes
• Associated with coronary artery disease (CAD), cerebral vascular accidents (CVA or stroke), and peripheral vascular disease (PVD)
18Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Long-Term Complications
19Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Neuropathic Complications
• Neuropathy: pathologic changes in nerve tissue• Mononeuropathy affects a single nerve or group of
nerves • Polyneuropathy involves both sensory and
autonomic nerves • Autonomic neuropathy affects the sympathetic and
parasympathetic nervous systems
20Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Hypoglycemic Unawareness
• The usual symptoms of tachycardia, palpitations, tremor, sweating, and nervousness may be absent
• Patient may suddenly have changes in mental status as the first sign of hypoglycemia
21Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Long-Term Complications
• Foot complications of diabetes• May have foot problems associated with
neuropathy, inadequate blood supply, or a combination
• Mechanical irritation • Thermal injury • Chemical irritation
22Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Long-Term Complications: Prevention
• Diabetes Control and Complications Trial (DCCT): intensive treatment of type 1 DM delayed the onset or slowed the progress of diabetic retinopathy, nephropathy, and neuropathy
• Outcome of United Kingdom Prospective Diabetes Study (UKPDS): similar benefits of tight control with type 2 DM
23Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Long-Term Complications: Prevention
• ADA recommends • Blood pressure: <130 systolic, <80 diastolic • Total cholesterol: <200 mg/dL • LDL: <100 mg/dL • HDL: >45 mg/dL for men (>55 mg/dL for women) • Triglyceride: <150 mg/dL
24Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Acute Emergency Complications
25Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Acute Hypoglycemia
• Dangerous drop in blood glucose• Causes
• Taking too much insulin, not eating enough food or not eating at the right time, an inconsistent pattern of exercise
• Gastroparesis, renal insufficiency, and certain drugs including aspirin and beta-adrenergic blockers
26Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Acute Hypoglycemia
• Signs and symptoms• Adrenergic: shakiness, nervousness, irritability, tachycardia,
anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, and diaphoresis
• Neuroglucopenia: drowsiness, irritability, impaired judgment, blurred vision, slurred speech, headaches, and mood swings progressing to disorientation, seizures, and unconsciousness
27Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Acute Hypoglycemia
• Treatment• Give patient 10 to 15 g of quick-acting
carbohydrates• Repeat every 15-30 minutes until blood glucose is
>70 mg/dL for adults, 80 to 100 mg/dL for older adults and children
• If patient is unable to swallow, an IM or subcutaneous injection of 1 mg of glucagon or an IV dose of 50 mL of 50% dextrose should be given as ordered or per protocol
28Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Diabetic Ketoacidosis (DKA)
• Life-threatening emergency caused by a relative or absolute deficiency of insulin
• Early signs and symptoms• Anorexia, headache, and fatigue• As condition progresses, classic symptoms of polydipsia,
polyuria, and polyphagia develop
• If untreated, patient becomes dehydrated, weak, and lethargic with abdominal pain, nausea, vomiting, fruity breath, increased respiratory rate, tachycardia, blurred vision, and hypothermia
29Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Diabetic Ketoacidosis (DKA)
• Late signs • Air hunger (Kussmaul’s respirations), coma, and
shock • Death can result without prompt medical care
30Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Diabetic Ketoacidosis (DKA)
• Treatment aimed at correction of three main problems• Dehydration• Electrolyte imbalance• Acidosis
31Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Hyperglycemic Hyperosmolar Nonketotic Syndrome
• Patient goes into a coma from extremely high glucose levels (>600 mg/dL)• There is no evidence of elevated ketones • Pancreas produces enough insulin to prevent breakdown of
fatty acids and formation of ketones, but not enough to prevent hyperglycemia
• Persistent hyperglycemia causes osmotic diuresis, resulting in loss of fluid and electrolytes
• Dehydration and hypernatremia develop • May be caused by the same factors that trigger
ketoacidosis
32Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Diagnosis
• One or more of the following criteria on two separate occasions is considered DM• Polyuria, polydipsia, polyphagia, unexplained weight loss plus
random glucose level >200 mg/dL • Fasting serum glucose level >126 mg/dL (after at least an 8-
hour fast)• Two-hour postprandial glucose level >200 mg/dL during oral
glucose tolerance test (OGTT) under specific guidelines. Test must use a glucose load of 75 g of anhydrous glucose dissolved in water
33Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Diagnosis
• Prediabetes• Individuals with impaired fasting glucose (IFG)
and/or impaired glucose tolerance (IGT)• Individuals should receive education on weight
reduction and increasing physical activity
34Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Diagnosis
• Oral glucose tolerance test• Diet of 150 to 300 g carbohydrate for 3 days before test • Night before test, patient fasts after midnight • Morning of test, blood drawn for fasting serum glucose • Patient then given a drink (Glucola) containing 75 g of
carbohydrates and instructed to remain quiet • Blood drawn at 30 minutes and 1 hour after the ingestion of
glucose. After these two samples, blood is drawn at hourly intervals until the test is completed
35Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Treatment
• Nutritional management• Medical nutrition therapy (MNT) is an important part
of diabetes management; should be included in diabetes self-management education
• Because of complexity of nutritional management, a registered dietitian should be part of the diabetes management team, and the individual with diabetes should be included in decision making
36Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Treatment
• Exercise• Effective adjunct for people with diabetes • Aids in weight loss, improves cardiovascular
conditioning, improves insulin sensitivity, and promotes a sense of well-being
• Exercising muscle uses glucose at 20 times the rate of a muscle at rest and does not require insulin
37Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• All patients with type 1 disease need insulin injections; some patients with type 2 disease may eventually need insulin
• Insulins classified by source and course of action • Source: human, pork, or beef (beef is being phased
out)• Course of action: rapid acting, short acting,
intermediate acting, and long acting • All rapid-acting and short-acting insulins are clear• The other insulins are cloudy
38Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Figure 46-2
39Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Route• Oral: insulin cannot be given orally because it is rendered
useless in the gastrointestinal tract • Subcutaneously: all insulins can be given subcutaneously • Intravenously: ONLY regular insulin can be given
intravenously • Inhalation: a form of insulin that can be taken by inhalation has
recently been approved, but it is not yet widely used
40Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Concentrations• U-100 insulin has 100 units/mL
• Most commonly used
• U-500 insulin has 500 units/mL• Used only in emergencies and for patients who are
extremely insulin resistant
• U-40 insulin has 40 units/mL• Not available in the United States
41Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Premixed insulin products• Contain both Regular and NPH insulin• 70% NPH and 30% Regular insulin• 50% NPH and 50% Regular insulin• 75% NPH and 25% Lispro
42Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Dosing schedules• Conventional therapy
• Typically uses a combination of a short-acting and an intermediate- or long-acting insulin
• Intensive therapy • To achieve tight control; may require 3 or 4 injections daily
• Continuous subcutaneous insulin infusion • Patient has indwelling subcutaneous catheter connected to
an external portable infusion pump; pump delivers Regular insulin continuously
43Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Insulin mixing• Two types can be mixed in one syringe to avoid two injections
• Insulin injection• Site rotation helps prevent lipohypertrophy or lipoatrophy • Absorption rate varies with different body sites • American Diabetes Association recommends rotating sites
within one anatomic area rather than moving among all areas • See Figure 46-3
44Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Figure 46-3
45Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Insulin pump• Needle is inserted subcutaneously in an appropriate
part of the anatomy• Pump is programmed to deliver a steady trickle of
insulin throughout the day and can provide a bolus of insulin at mealtimes
46Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Figure 46-4
47Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Insulin Therapy
• Intranasal route • Only 10% of the drug is absorbed through the nasal mucosa,
making it relatively expensive to use • Nasal irritation is a frequent side effect • Only Regular insulin is given intranasally
• Insulin catheter• Indwelling subcutaneous catheters may be placed in the
abdomen to permit repeated insulin injections without repeated needlesticks
48Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Oral Hypoglycemic Agents
• If patients with type 2 DM unable to control blood glucose with nutrition and exercise, physician may prescribe oral hypoglycemics
• Sulfonylureas (three generations), alpha-glucosidase inhibitors, biguanides, thiazolidinediones, D-phenylalanines, meglitinides
• Combination oral medications• ACTOplus met (pioglitazone and metformin), Avandamet
(rosiglitazone and metformin), Avandaryl (rosiglitazone and glimepiride), Glucovance (glyburide and metformin), Metaglip (glipizide and metformin)
49Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Self-Monitoring of Blood Glucose
• Allows patients to monitor blood glucose levels to regulate their diet, exercise, and medication regimens to remain euglycemic
• Portable electronic glucose meters have largely replaced other methods of self-monitoring
50Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Glycosylated Glucose Levels
• Glycosylated hemoglobin (HbA1c) reflects glucose levels over the past few months
• Fructosamine levels reflect those over several weeks
51Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Complications of Therapy
• Hypoglycemia• A person injects too much insulin, does not eat enough, eats at
the wrong time, or exercises inconsistently: glucose levels may suddenly drop
• Somogyi phenomenon• Rebound hyperglycemia in response to hypoglycemia
• Dawn phenomenon• An increase in fasting blood glucose levels between 5 and 9 AM
that is not related to hypoglycemia
52Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Assessment
• Ketoacidosis: ketonuria, Kussmaul’s respirations, orthostatic hypotension, hypertension, nausea, vomiting, lethargy, or change in level of consciousness
• Hypoglycemic patient: expect to find tachycardia, anxiety, trembling, and decreasing level of consciousness
• Be alert for indications of hyperosmolar nonketotic coma
53Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Assessment
• Attempt to determine the following• Type of diabetes• Hypoglycemic agents: name, dosage, when last
dose was taken• Food and fluid intake for the past 3 days• Relevant laboratory values: blood glucose, blood
pH, bicarbonate levels, electrolytes, and osmolality and urine osmolality
54Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Health History
• Chief complaint and history of present illness• Signs/symptoms that prompted patient to seek medical care
• Past medical history • Type and duration of DM • Name and dosage of prescribed medications and when they
were last taken• If patient monitors blood glucose, record type of equipment
used, testing schedule, recent test results • Family history
• Diabetes, heart disease, stroke, hypertension, hyperlipidemia
55Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Health History
• Review of systems • Description of the patient’s general health • Changes in skin moisture or turgor• Inquire whether the patient has had floaters, diplopia (double
vision), or blurred vision, or has seen white halos around objects
• Abdominal symptoms: diarrhea, abdominal bloating, and gas • Problems passing or holding urine • If any pain in the legs, note when it occurs • Numbness, tingling, or burning in the extremities • Changes in mental alertness or seizures
56Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Health History
• Functional assessment • Explore factors that can affect patient’s ability to perform
self-care, including literacy, financial resources such as health insurance, and family support
57Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Health History
• Physical examination• Level of consciousness, posture and gait, and apparent well-
being • Vital signs, height, and weight • Skin color, warmth, turgor, and lesions noted • Inspect eye grounds for evidence of diabetic retinopathy or
cataracts• Be alert for a sweet, fruity odor to the patient’s breath that is
common with ketoacidosis • Carefully assess the feet• Test gait, balance, and motor coordination
58Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Interventions
• Ineffective Health Maintenance• Ineffective Therapeutic Regimen Management• Risk for Deficient Fluid Volume• Risk for Injury• Activity Intolerance • Chronic Pain• Disturbed Sensory Perception or Impaired Skin
Integrity• Disturbed Thought Processes• Ineffective Coping
59Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Hypoglycemia
60Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Pathophysiology
• Develops when the blood glucose level falls to less than 45 to 50 mg/dL
• Symptoms occur at different blood levels according to individual tolerances and how rapidly the level falls
61Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Causes
• Exogenous hypoglycemia • Results from outside factors acting on the body to
produce a low blood glucose • Include insulin, oral hypoglycemic agents, alcohol,
or exercise
62Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Causes
• Endogenous hypoglycemia • Occurs when internal factors cause an excessive
secretion of insulin or an increase in glucose metabolism
• These conditions may be related to tumors or genetics
63Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Causes
• Functional hypoglycemia • From a variety of causes, including gastric surgery,
fasting, or malnutrition
64Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Signs and Symptoms
• Glucose level falls rapidly, causes epinephrine, cortisol, glucagon, and growth hormone to be secreted in an attempt to increase glucose levels • Symptoms: weakness, hunger, diaphoresis, tremors, anxiety,
irritability, headache, pallor, and tachycardia
• A blood glucose level that falls over several hours: symptoms attributed to lack of essential glucose to brain tissue • Symptoms: confusion, weakness, dizziness, blurred or double
vision, seizure, and in severe cases, coma
65Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Diagnosis
• The diagnosis of hypoglycemia not associated with diabetes can be based on fasting blood glucose, OGTT, intravenous glucose tolerance test, and 72-hour inpatient fasting
• Whipple’s triad • The presence of symptoms • Documentation of low blood glucose when symptoms occur• Improvement of symptoms when blood glucose rises
66Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Treatment
• In an unconscious patient who has diabetes, hypoglycemia should be suspected until it is ruled out • 50 mL of 50% glucose solution should be administered
immediately
• The patient with a milder form of hypoglycemia• Treated with 15 g carbohydrate• If the patient’s condition does not improve, another
15 g of carbohydrate should be given after 10 minutes
67Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Medical Treatment
• Prevention of hypoglycemia by proper food intake • The diet is directed by the underlying cause • If overproduction of insulin after carbohydrate ingestion, a low-
carbohydrate, high-protein diet• Restriction of carbohydrates to no more than 100 g/day is
recommended • Simple sugars avoided; complex carbohydrates encouraged • Patients may tolerate smaller, more frequent meals. Alcohol
should be avoided
68Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Assessment
• Present illness: shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, nightmares, and crying out during sleep
• Note when episodes occur in relation to meals and particular food intake
• The past medical history documents diabetes, previous gastric surgery, abdominal cancer, or adrenal insufficiency
• Medications, paying particular attention to hypoglycemic agents
69Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Assessment
• Note hypoglycemic agents, prescribed dose, and the time last dose taken
• Functional assessment: information about current diet, exercise, alcohol intake, and the effects of symptoms on daily activities
• Important aspects of the physical examination include general behavior, appearance, pulse, and blood pressure
70Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.
Interventions
• Deficient Knowledge• Risk for Injury• Impaired Adjustment