Download Rehab Quiz 2 Review

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Rehab Quiz 2 Review
TBI, & musculoskeletal, stroke & brain tumors
1. Rheumatoid arthritis & pt education
2.
Hip fractures (several questions)
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3. S & s
4. Treatment
5. Risk factors post op
Fractures of the Hip
Hip fracture is the most common injuries in older adults and one of the most frequently seen
injuries in any health care setting or community. It has a high mortality rate as a result of
multiple complications related to surgery and prolonged immobility. Osteoporosis is the biggest
risk factor for hip fractures (see Chapter 53). This disease weakens the upper femur (hip),
breaks, and then causes the person to fall. The number of people with hip fracture is expected to
continue to increase as the population ages, and the associated health care costs will be
tremendous.
CONSIDERATIONS FOR OLDER ADULTS
Teach older adults about the risk factors for hip fracture including physiologic aging changes,
disease processes, drug therapy, and environmental hazards. Physiologic changes include
sensory changes such as visual acuity and diminished hearing; changes in gait, balance, and
muscle strength; and joint stiffness. Disease processes like osteoporosis, foot disorders, and
changes in cardiac function increase the risk for hip fracture. Drugs, such as diuretics,
antihypertensives, antidepressants, sedatives, opioids, and alcohol are factors that increase the
risks for falling in older adults. Use of three or more drugs at the same time drastically increases
the risk for falls. Throw rugs, loose carpeting, inadequate lighting, uneven walking surfaces or
steps, and pets are environmental hazards that also cause falls.
The older adult with hip fracture usually reports groin pain or pain behind the knee on the
affected side. In some cases, the patient has pain in the lower back or has no pain at all.
However, the patient is not able to stand. X-ray or other imaging assessment confirms the
diagnosis. Hip fractures include those involving the upper third of the femur and are classified as
intracapsular (within the joint capsule) or extracapsular (outside the joint capsule). These
types are further divided according to fracture location (Fig. 54-8). In the area of the femoral
neck there is concern with disruption of the blood supply to the head of the femur, which can
result in ischemic or avascular necrosis (AVN) of the femoral head. AVN causes death and
necrosis of bone tissue and results in pain and decreased mobility. This problem is most likely in
patients with displaced fractures. Prompt surgical repair can prevent this complication and
decrease pain.
The treatment of choice is surgical repair, when possible, to allow the older patient to be out of
bed and ambulatory. Buck's traction may be applied before surgery to help decrease pain
associated with muscle spasm. Depending on the exact location of the fracture, open reduction
with internal fixation (ORIF) may include an intramedullary rod, pins, prostheses (for femoral
head or neck fractures), or a compression screw.
Epidural or general anesthesia is used. Figs. 54-9 and 54-10 illustrate examples of these devices.
Occasionally a patient will be so debilitated that surgery cannot be done. In these cases,
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nonsurgical options are Buck's traction, pain management, and bedrest to allow natural fracture
healing (Altizer, 2005; Watters & Moran, 2006).
Patients usually receive PCA morphine or other opioid or epidural analgesia after surgery.
Chapter 5 discusses the nursing care associated with these pain management modalities in detail.
The patient begins ambulating with assistance the day after surgery to prevent complications
associated with immobility (e.g., pressure ulcers, atelectasis, venous thromboembolism). Early
movement and ambulation also decrease the chance of infection and increase surgical site
healing.
EVIDENCE-BASED PRACTICE
What are the major factors that influence functional status after hip surgery?
Folden, S., & Tappen, R. (2007). Factors influencing function and recovery following hip
repair surgery. Orthopaedic Nursing, 26(4), 234-241.
The purpose of this small descriptive study was to determine which factors predicted the
functional ability of patients who had hip repair surgery by 3 months after hospital discharge.
Previous studies had suggested many contributing factors, including age, balance, cognitive
ability, gender, fatigue, pain, and complications from surgery. Functional status before surgery
had also been found to be a factor.
A convenience sample of 73 men and women was evaluated by self-report in an inpatient
rehabilitation setting after hospital discharge and again in 3 months. Balance and cognitive
ability before surgery were the best predictors of recovery and return to baseline functional
status. Fatigue also played a role. Men reported higher functional levels than women and were
more likely to return to their presurgical activities. The authors concluded that gender did
influence recovery from hip repair surgery.
Level of Evidence—6. This research was a small descriptive study using a convenience sample.
Commentary: Implications for Practice and Research. Although this study was descriptive, it
confirmed previous findings of other researchers about which factors predict return to functional
ability among patients having hip repair. Physicians can use this information in making decisions
about who are the best candidates for surgery. Nurses and rehabilitation therapists can use these
findings to plan interventions to improve balance and reduce fatigue as patients recover from
surgery during their rehabilitation period.
Patients who have an ORIF are at risk for hip dislocation or subluxation. Be sure to prevent hip
adduction and rotation to keep the operative leg in proper alignment. Regular pillows or
abduction devices can be used for patients who are confused or restless. If straps are used to
hold the device in place, check the skin for signs of pressure. Perform neurovascular assessments
to ensure that the device is not interfering with arterial circulation or peripheral nerve
conduction.
Special considerations for the patient having a hip repair also include careful inspection of skin
including areas of pressure, especially the heels. Use of Buck's traction and periods of bedrest
before surgical intervention can increase the risk for pressure injury in this area within 24 hours.
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Be sure that the patient's heels are up off the bed at all times. Inspect the heels and other highrisk bony prominence areas every 8 to 12 hours. Delegate turning and repositioning every 1 to 2
hours to unlicensed assistive personnel (UAP), and supervise this nursing activity. Other
measures to decrease the risk for pressure ulcers are described elsewhere in this text and in
fundamentals textbooks.
Other nursing and interdisciplinary care is similar to that described for fracture in other sites.
Specific interventions are similar to those for total hip replacement (see Chapter 20).
Many patients recover fully from hip fracture repair and regain their functional ability. However,
some patients are not able to return to their pre-fracture ADLs and mobility level. These patients
usually do not return to their homes and are placed in long-term care facilities. Folden and
Tappen (2007) conducted a small descriptive study that identified predictors for patients who are
likely to fully recover. They found that balance and cognitive ability were the best predictors (see
the Evidence-Based Practice box above).
6. Risk factors for elderly r/t osteoporosis & osteoarthritis
Although the exact etiology of primary OA has not been identified, the disease may be triggered
by aging, genetic changes, obesity, smoking, and/or trauma.
Other factors that can lead to OA are obesity and smoking. Obesity causes joint degeneration,
particularly in the knees. Smoking leads to knee cartilage loss, especially in patients with a
family history of knee OA. This finding shows a geneenvironment interaction in the cause of
knee OA (Ding et al., 2007).
Trauma to the joints from excessive use or abuse predisposes a person to OA. Certain heavy
manual occupations(e.g., carpet laying, construction, farming) cause high-intensity or repetitive
stress to the joints. The risk of hip and knee OA is also increased in professional athletes,
especially football and soccer players, runners, and gymnasts. Lack of exercise can contribute to
muscle loss. Muscle tissue helps support joints, particularly those that bear weight (e.g., hips,
knees).
In a small percentage of people, congenital anomalies, trauma, and joint sepsis can result in
secondary OA. For example, injuries from motor vehicle accidents can cause OA in later years.
Certain metabolic diseases (e.g., diabetes mellitus, Paget's disease of the bone) and blood
disorders (e.g., hemophilia, sickle cell disease) can also cause joint degeneration. Inflammatory
joint diseases such as rheumatoid arthritis can lead to secondary OA.
OSTEOPOROSIS
Pathophysiology
Osteoporosis is a chronic metabolic disease in which bone loss causes decreased density and
possible fracture. It is often referred to as a “silent disease” because the first sign of osteoporosis
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in most people follows some kind of a fracture. The hip, spine, and wrist are most often at risk,
although any bone can fracture (National Osteoporosis Foundation, 2007a).
Bone is a dynamic tissue that is constantly undergoing changes in a process referred to as bone
remodeling. Osteoporosis and osteopenia (low bone mass) occur when osteoclastic (bone
resorption) activity is greater than osteoblastic (bone building) activity. The result is a decreased
bone mineral density (BMD). BMD determines bone strength and peaks between 25 and 30
years of age. Before and during the peak years, osteoclastic activity and osteoblastic activity
work at the same rate. After the peak years, bone resorption activity exceeds bone-building
activity, and bone density decreases. BMD decreases most rapidly in postmenopausal women as
serum estrogen levels diminish. Although estrogen does not build bone, it helps prevent bone
loss. Trabecular, or cancellous (spongy), bone is lost first, followed by loss of cortical
(compact) bone. This results in thin, fragile bone tissue that is at risk for fracture (National
Osteoporosis Foundation, 2007b).
Standards for the diagnosis of osteoporosis are based on BMD testing that provides a T-score for
the patient. A T-score represents the number of standard deviations above or below the average
BMD for young, healthy adults. Osteopenia is present when the T-score is at −2 1 and above
−22.5. Osteoporosisis diagnosed in a person who has a T-score at or lower than −22.5.
Medicare reimburses for BMD testing every 2 years in people age 65 years and older who
(National Osteoporosis Foundation, 2007c):
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Are estrogen deficient
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Receive long-term steroid therapy
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Have hyperparathyroidism
•
Are being monitored while on osteoporosis drug therapy
The exact pathophysiology of osteoporosis is unclear, but two broad theories of disease
development have been advocated. First, osteoporosis may result from increased osteoclastic
(bone resorption) activity and decreased osteoblastic (bone building) activity related to changes
in hormone levels or other disease processes. This theory has resulted in treatment directed
toward measures to prevent rapid bone resorption. The second theory is that osteoblasts, or boneforming cells, may have a shortened life span or may be less efficient in the patient with
osteoporosis.
Osteoporosis can be classified as generalized or regional. Generalized osteoporosis involves
many structures in the skeleton and is further divided into two categories, primary and
secondary. Primary osteoporosis is more common and occurs in postmenopausal women and in
men in their seventh or eighth decade of life. Even though men do not experience the rapid bone
loss that postmenopausal women have, they do have decreasing levels of testosterone (which
builds bone) and altered ability to absorb calcium. This results in a slower loss of bone mass in
men, especially those older than 75 years. Secondary osteoporosis may result from other medical
conditions, such as hyperparathyroidism; long-term drug therapy, such as with corticosteroids; or
prolonged immobility, such as that seen with spinal cord injury (Table 53-1). Treatment of the
secondary type is directed toward the cause of the osteoporosis when possible.
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Regional osteoporosis, an example of secondary disease, occurs when a limb is immobilized
related to a fracture, injury, or paralysis. Immobility for longer than 8 to 12 weeks can result in
this type of osteoporosis. Bone loss also occurs when people spend prolonged time in a gravityfree or weightless environment (e.g., astronauts). The United States and other countries are
studying this problem during trips into space.
Etiology and Genetic Risk
Primary osteoporosis is probably caused by a combination of risk factors and genetic changes
(Chart 53-1). Peak bone mass is achieved by about 30 years of age in most women. Building
strong bone as a young person may be the best defense against osteoporosis in later adulthood
(National Osteoporosis Foundation, 2007a). Young women need to be aware of appropriate
health and lifestyle practices that can prevent this potentially disabling disease.
TABLE 53-1
Causes of Secondary Osteoporosis
DISEASES/CONDITIONS
• Diabetes mellitus
• Hyperthyroidism
• Hyperparathyroidism
• Cushing's syndrome
• Growth hormone deficiency
• Metabolic acidosis
• Female hypogonadism
• Paget's disease
• Osteogenesis imperfecta
• Rheumatoid arthritis
• Prolonged immobilization
• Bone cancer
• Cirrhosis
• HIV/AIDS
• Chronic airway limitation
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DRUGS (CHRONIC USE)
• Corticosteroids
• Heparin
• Anticonvulsants (phenobarbital, phenytoin)
• Ethanol (alcohol)
• Drugs that induce hypogonadism (decreased levels of sex hormones)
• High levels of thyroid hormone
• Cytotoxic agents
• Immunosuppressants
• Loop diuretics
AIDS, Acquired immune deficiency syndrome; HIV, human immune
deficiency virus.
Chart 53-1
BEST PRACTICE FOR PATIENT SAFETY & QUALITY CARE
Assessing Risk Factors for Primary Osteoporosis
Assess for:
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Age 65 years and older in all women
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Age 75 years and older in men
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Family history of osteoporosis
•
History of low-trauma fracture after age 50 years
•
Caucasian or Asian ethnicity
•
Low body weight, thin build
•
Chronic low calcium intake
•
Estrogen or androgen deficiency
•
Women with other risk factors
•
Smoking history
•
High alcohol intake
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•
Lack of physical exercise or prolonged immobility
Primary osteoporosis most often occurs in women after menopause as a result of decreased
estrogen levels. Women lose about 2% of their bone mass every year in the first 5 years after
natural or surgical (ovary removal) menopause. For women of any age who do not take estrogen
replacement, the risk for osteoporosis increases.
In addition, body build seems to influence who gets the disease. Osteoporosis occurs more often
in thin, lean-built European-American and Asian women, particularly those who do not exercise
regularly. Obese women can store estrogen in their tissues for use as necessary to maintain a
normal level of serum calcium. Weight-bearing exercise reduces bone resorption (loss) and
stimulates bone formation. Prolonged immobility produces rapid bone loss.
The relationship of osteoporosis to nutrition is well established. For example, excessive caffeine
in the diet can cause calcium loss in the urine. A diet lacking enough calcium and vitamin D
stimulates the parathyroid gland to produce parathyroid hormone (PTH). PTH triggers the
release of calcium from the bony matrix. Activated vitamin D is needed for calcium uptake in the
body. Malabsorption of nutrients in the GI tract also contributes to low serum calcium levels.
Institutionalized or homebound patients who are not exposed to sunlight may be at a higher risk
because they do not receive adequate vitamin D for the metabolism of calcium.
Calcium loss occurs at a more rapid rate when phosphorus intake is high. (Chapter 13 describes
the normal relationship between calcium and phosphorus in the body.) People who drink large
amounts of carbonated beverages each day (over 40 ounces) are at high risk for calcium loss and
subsequent osteoporosis, regardless of age or gender.
Protein deficiency may also reduce bone density. Because 50% of serum calcium is protein
bound, protein is needed to use calcium. However, excessive protein intake may increase
calcium loss in the urine. For instance, people who are on high-protein, low-carbohydrate diets,
like the Atkins diet, may consume too much protein to replace other food not allowed. Dietary
protein intake in healthy adults is recommended at 0.8 grams per kilogram of body weight.
Protein is needed for bone healing when a fracture occurs.
Excessive alcohol and tobacco use are other risk factors for osteoporosis. Although the exact
mechanisms are not known, these substances promote acidosis, which in turn increases bone
loss. Alcohol also has a direct toxic effect on bone tissue, resulting in decreased bone formation
and increased bone resorption. For those people who have excessive alcohol intake, alcohol
calories decrease hunger and the need to take in adequate amounts of nutrients.
Osteoporosis also occurs in young adults who participate in excessive exercise or weight-loss
dieting or in those who have eating disorders, such as anorexia nervosa or bulimia nervosa.
Young females with these risk factors have a low body weight and absent menstruation, which
contribute to the development of osteoporosis. Dancers, gymnasts, and other athletes may
overtrain without sufficient caloric intake, which also results in severe weight loss. Young girls
and women may have an obsession with being slim. Particular attention must be paid to bone
health for these groups.
GENETIC CONSIDERATIONS
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The genetic and immune factors that cause osteoporosis are very complex and unclear. Family
history often reveals that the patient's mother had the disease. Many genetic changes have been
identified as possible causative factors, but there is no agreement about which ones are most
important or constant in all patients. For example, changes in the vitamin D receptor (VDR) gene
and calcitonin receptor (CTR) gene have been found in some patients with the disease. Receptors
are essential for the uptake and use of these substances by the cells.
The bone morphogenetic protein-2 (BMP-2) gene has a key role in bone formation and
maintenance. Some osteoporotic patients who have had fractures have changes in their BMP-2
gene. Alterations in growth hormone-1 (GH-1) have been discovered in petite Asian-American
women, those who are likely to have osteoporosis (Lui et al., 2006).
Hormones, tumor necrosis factor (TNF), interleukins, and other substances in the body help
control osteoclasts in a very complex pathway. The recent identification of the importance of the
cytokine receptor activator of nuclear factor kappa-B ligand (RANKL), its receptor RANK, and
its decoy receptor osteoprotegerin (OPG) has helped researchers understand more about the
activity of osteoclasts in metabolic bone disease. Disruptions in the RANKL, RANK, and OPG
system can lead to increased osteoclast activity in which bone is rapidly broken down (McCance
& Huether, 2006).
Incidence/Prevalence
Osteoporosis is a major health problem in the United States and many other countries. Iacono
(2007) stated that the disease is a national public health priority. The estimated cost for
osteoporosis-related health care alone in the United States is more than $18 billion each year in
2002 dollars with continual cost increases each year (National Osteoporosis Foundation, 2007a).
Osteoporosis is a potential health problem for more than 44 million Americans. About 10 million
persons in the United States have the disease, and about 34 million persons 50 years of age and
older experience osteopenia and are at risk for development of osteoporosis. Women remain the
largest group affected by osteoporosis (8 million). Two million men (especially those older than
75 years) also have the disease. People of all ethnic backgrounds are at some risk (National
Osteoporosis Foundation, 2007a), but white, thin women are likely to get primary osteoporosis at
an earlier age.
CULTURAL AWARENESS
Although there is some advantage of increased bone density in dark-skinned women, lifestyle
and health beliefs about prevention may put all women at an equal risk for osteoporosis. Dietary
preferences or the ability to afford high-nutrient food may influence the woman's rate of bone
loss. For example, many blacks have lactose intolerance and cannot drink milk or eat other dairybased foods. Milk and cheese are good sources of protein, a nutrient needed to bind calcium for
use by the body.
Osteoporosis results in more than 1.5 million fractures each year. Of these, 300,000 are hip
fractures, 700,000 are vertebral fractures, and 250,000 are wrist fractures (National Osteoporosis
Foundation, 2007a). A woman who experiences a hip fracture has a four times greater risk for a
second fracture. Fractures as a result of osteoporosis can decrease a patient's mobility and quality
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of life. The mortality rate for older patients with hip fractures is very high, especially within the
first 6 months, and the debilitating effects can be devastating
Health Promotion and Maintenance
A study by Giangregorio et al. (2007) found that health care professionals, including nurses, who
worked with older patients could not identify ways to prevent osteoporosis. (See the EvidenceBased Practice box below). Nurses can play a vital role in patient education to prevent and
manage osteoporosis. Teaching should begin with young women who begin to lose bone after 30
years of age.
The focus of osteoporosis prevention is to decrease modifiable risk factors. For example, teach
patients who do not include enough dietary calcium which foods should be included, such as
dairy products and dark green, leafy vegetables. Teach them to read food labels for sources of
calcium content. Explain the importance of sun exposure (but not so much as to get sunburned)
or adequate vitamin D in the diet. Teach the need to limit the amount of carbonated beverages
consumed each day. People who have sedentary lifestyles should be taught about the importance
of exercise and what types of exercise builds bone tissue. Weight-bearing exercises are preferred.
Teach people to avoid activities that cause jarring, such as horseback riding, to prevent potential
vertebral bone damage.
7. Fat emboli syndrome:
a circulatory condition characterized by the blocking of an artery by a plug of fat. The plug
enters the circulatory system after the fracture of a long bone or, less commonly, after
traumatic injury to adipose tissue or to a fatty liver. Fat embolism usually occurs suddenly 12
to 36 hours after an injury and is characterized by symptoms related to the site occluded,
such as severe chest pain, pallor, dyspnea, tachycardia, delirium, prostration, and in some
cases coma. Anemia and thrombocytopenia are common. Systemic fat embolism may occur
after extensive trauma, since lipid metabolism is altered by the injury and free fatty acids are
released, resulting in vasculitis with obstruction of many small pulmonary and cerebral
arteries. Classic signs of systemic fat embolism are petechial hemorrhages on the neck,
shoulders, axillae, and conjunctivae that appear 2 or 3 days after the injury. Radiographic
findings include patchy diffuse opacities throughout the lungs. There is no specific therapy
for systemic fat embolism. The patient is placed in a high Fowler's position and given
oxygen, corticosteroids, blood transfusion, respiratory assistance, or other supportive care as
needed.
8. DVT complications
a disorder involving a thrombus in one of the deep veins of the body, most commonly the
iliac or femoral vein. Symptoms include tenderness, pain, swelling, warmth, and
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discoloration of the skin. A deep vein thrombus is potentially life threatening. Treatment,
including bed rest and use of thrombolytic and anticoagulant drugs, is directed to preventing
movement of the thrombus toward the lungs. See also pulmonary embolism.
observations
It may be asymptomatic or manifest as tenderness, pain, warmth, and swelling in the affected
extremity with deep reddish or blue color. There is a positive Homans’ sign in about 10% of
cases, which affects a lower extremity. Serial compression ultrasonography is the initial test
used for diagnosis. Magnetic resonance direct thrombus imaging may be used for thrombi
undetectable on ultrasound. Contrast venography remains the gold standard for detection of
lower extremity DVT. Chronic venous insufficiency and pulmonary embolus are the most
common complications of thrombosis.
interventions
Initial treatment is heparin or enoxaparin followed by warfarin for maintenance treatment for
3 to 6 months. Continued monitoring of prothrombin time and partial thromboplastin time is
done during anticoagulant therapy. Ligation, clipping, plication, and thrombectomy are
surgical alternatives when thrombus fails to respond to anticoagulant therapy. An
extravascular vena cava interruption with possible placement of intracaval filter is used for
cases involving probable emboli. Analgesics are given for pain; however, aspirin is
contraindicated because it interferes with platelet function. Enoxaparin may be used with
patients at high risk for DVT to prevent thrombus formation.
nursing considerations
Acute care nursing goals focus on prevention of pulmonary emboli, pain relief, prevention of
skin breakdown, and prevention of complications related to anticoagulant therapy. Bed rest is
instituted for the first several days after beginning anticoagulant with elevation of affected
extremity above the level of the heart and use of warm, moist packs. When ambulation is
resumed, compression stockings are used to support vein walls and reduce pain and swelling.
Individuals are closely observed for signs of bleeding (e.g., gums, nasal mucosa, stool, and
urine). Safety precautions are instituted to prevent bruising while on anticoagulants and to
prevent skin ulceration of affected extremity. Individuals are monitored for manifestations of
pulmonary emboli, including sudden dyspnea, tachypnea, and pleuritic chest pain. Education
is important and includes effects and side effects of anticoagulant therapy; need for ongoing
blood tests to monitor clotting and regulate anticoagulant dosage; avoidance of activities that
may precipitate bleeding; avoidance of anticoagulant over-the-counter medications that may
interfere with clotting (e.g., aspirin/aspirin products, NSAIDs, and herbal products).
Education is needed about signs of pulmonary embolus and the need for immediate medical
attention should they occur. Instruction is provided to prevent pooled blood in the lower
extremities, including regular use of compression garments and avoidance of prolonged
standing, sitting, or walking. Teaching also includes prevention of future thrombosis
episodes, such as avoidance or correction of modifiable risk factors (e.g., tobacco use or
alcohol abuse, use of oral contraceptives or hormone replacement therapy, and prolonged
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periods of inactivity), regular exercise program, proper posture, and balanced diet with
weight loss if indicated.
9. Skeletal traction
one of the two basic kinds of traction used in orthopedics for the treatment of fractured bones
and the correction of orthopedic abnormalities. Skeletal traction is applied to the affected
structure by a metal pin or wire inserted into the structure and attached to traction ropes.
Skeletal traction is often used when continuous traction is desired to immobilize, position,
and align a fractured bone properly during the healing process. Infection of the pin tract is
one of the complications that may develop with skeletal traction, and careful scrutiny of pin
sites is an important precaution. Some common signs of infection of the pin tracts are
erythema, drainage, noxious odor, pin slippage, temperature elevation, and pain. Superficial
infection of pin tracts is often treated with antibiotic therapy. Deeper infections usually
require pin removal and antibiotic therapy
10. Couple questions… care of elderly delirium, dementia & depression
11. s/s of Increased intercranial pressure
12. ischemic stroke, incidence & treatment
An ischemic stroke is caused by the occlusion of a cerebral artery by either a thrombus or an
embolus. A stroke that is caused by a thrombus (clot) is referred to as a thrombotic stroke,
whereas a stroke caused by an embolus (dislodged clot) is referred to as an embolic stroke.
Most strokes are ischemic.
Thrombotic Stroke.
Thrombotic strokes account for more than half of all strokes and are commonly associated with
the development of atherosclerosis of the blood vessel wall. Atherosclerosis is the process by
which plaques develop on the inner wall of the affected arterial vessel. Chapter 38 describes this
health problem, including its pathophysiology, in more detail.
Rupture of one or more plaques exposes foam cells to clot-promoting elements in the blood. The
end result is clot formation. If the clot is of sufficient size, it may interrupt blood flowto the brain
tissue supplied by the vessel, causing an occlusive stroke. This process may occur over many
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years because collateral circulation to the involved area develops to compensate for the
occlusion. The bifurcation (point of division) of the common carotid artery and the vertebral
arteries at their junction with the basilar artery are the most common sites involved. Because of
the gradual occlusion (blockage) of the arteries, thrombotic strokes tend to have a slow onset.
Embolic Stroke.
An embolic stroke is caused by an embolus or a group of emboli that break off from one area of
the body and travel to the cerebral arteries via the carotid artery or vertebrobasilar system. The
usual source of emboli is the heart. Emboli can occur in patients with nonvalvular atria
fibrillation, ischemic heart disease, rheumatic heart disease, and mural thrombi after a
myocardial infarction (MI) or insertion of a prosthetic heart valve. Another source of emboli may
be plaque that breaks off from the carotid sinus or internal carotid artery. Emboli tend to become
lodged in the smaller cerebral blood vessels at their point of bifurcation or where the lumen
narrows.
The middle cerebral artery (MCA) is most commonly involved in an embolic stroke. As the
emboli occlude the vessel, ischemia develops and the patient experiences the clinical
manifestations of the stroke. However, the occlusion may be temporary if the embolus breaks
into smaller fragments, enters smaller blood vessels, and is absorbed. For these reasons, embolic
strokes are characterized by the sudden development and rapid occurrence of neurologic deficits.
The symptoms may resolve over several hours or a few days. Conversion of an occlusive stroke
to a hemorrhagic stroke may occur because the arterial vessel wall is also vulnerable to ischemic
damage from blood supply interruption. Sudden hemodynamic stress may result in vessel
rupture, causing bleeding directly within the brain tissue.
13. s/s of osteoarthritis
14. gouty arthritis, scenario, history, treatment
a disease associated with an inborn error of uric acid metabolism that increases production or
interferes with excretion of uric acid. Excess uric acid is converted to sodium urate crystals
that precipitate from the blood and become deposited in joints and other tissues. Men are
more often affected than premenopausal women. The great toe is a common site for the
accumulation of urate crystals. The condition can cause exceedingly painful swelling of a
joint, accompanied by chills and fever. The symptoms are recurrent. Episodes become longer
each year. The disorder is disabling and, if untreated, can progress to the development of
destructive joint changes, such as tophi. Treatment usually includes administration of
colchicine, phenylbutazone, indomethacin, or glucocorticoid drugs and a diet that excludes
purine-rich foods such as organ meats. It may include surgical removal of ulcerated tophi.
Chronically, probenecid, allopurinol, or cholchicine may be used to decrease uric acid levels.
Acquired gout is a condition having the signs and symptoms of gout but resulting from
another disorder or treatment for a different condition. Diuretic drugs can alter the
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concentration of uric acid so that uric acid salts precipitate from the blood and are carried to
the joints.
15. side effects of NSAIDS
16. cardinal signs for neurovascular assessment
17. diff between viral & bacterial meningitis (key difference)
any infection or inflammation of the membranes covering the brain and spinal cord. It is usually
purulent and involves the fluid in the subarachnoid space. The most common causes in adults are
bacterial infection with Streptococcus pneumoniae, Neisseria meningitidis, or Haemophilus
influenzae. Aseptic meningitis may be caused by nonbacterial agents such as a high dose of
intravenous immunoglobulin, chemicals, neoplasms, or viruses. Many of these diseases are
benign and self-limited, such as meningitis caused by strains of coxsackievirus or echovirus.
Others are more severe, such as those involving arboviruses, herpesviruses, or poliomyelitis
viruses. Yeasts such as Candida and Cryptococcus may cause a severe, often fatal meningitis. A
kind of meningitis is tuberculous meningitis. Compare encephalitis. Also called
cerebromeningitis.
observations
The onset of meningitis is usually sudden and characterized by severe headache, stiffness of the
neck, irritability, malaise, and restlessness. Nausea, vomiting, delirium, and complete
disorientation may develop quickly. Temperature, pulse rate, and respirations are increased.
Residual damage may include deafness, blindness, paralysis, and mental retardation.
Hydrocephalus also may develop.
interventions
Bacterial meningitis is treated promptly with antibiotics specific for the causative organism.
They are administered intravenously or intrathecally. Antifungal medications, such as
amphotericin B, given intravenously or intrathecally for several weeks, may prevent death from
fungal meningitis, but serious neurologic sequelae may occur.
nursing considerations
Constant skilled nursing attention is necessary to ensure early recognition of rising intracranial
pressure, to prevent aspiration in the event of convulsive seizures, and to prevent airway
obstruction. Except for the first day or two of meningococcal disease, strict isolation procedures
are unnecessary. IV fluids and nasogastric tube feeding may be necessary for a prolonged period.
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Sedatives and narcotic analgesics should not be used because they may obscure important
neurologic signs in addition to depressing vital functions.
18. diff between// types of injuries assoc w/ shoulder pain, strain
19. for fractures, review material on different types, hallmarks of diff types, green stick, spiral,
simple, open, etc…
20. know diff between ligaments & tendons
21. review charac of elder abuse
22. charact of CNS coma
23. risk factors assoc w/ stroke
24. TBI, sequale that can follow as persons get over acute brain injury
25. Couple drug questions… one will be IV drug (2 questions them)
26. Paget’s disease
a common nonmetabolic disease of bone of unknown cause, usually affecting middle-aged and
elderly people and characterized by excessive bone destruction and unorganized bone repair.
Paget's disease, or osteitis deformans, is a chronic metabolic disorder in which bone is
excessively broken down (osteoclastic activity) and re-formed (osteoblastic activity). The result
is bone that is structurally disorganized, causing bones to be weak with increased risk for bowing
of long bones and fractures. Two types of Paget's disease can occur—familial and sporadic.
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In the first phase (the active phase), a rapid increase in osteoclasts (cells that break down bone)
causes massive bone destruction and deformity. The osteoclasts of pagetic bone are large and
multinuclear, unlike the osteoclasts of normal bone tissue.
In the mixed phase, the osteoblasts (bone-forming cells) react to compensate in forming new
bone. The result is bone that is vascular, structurally weak, and deformed. Paget's disease occurs
in one bone or in multiple sites. The most common areas of involvement are the vertebrae,
femur, skull, clavicle, humerus, and pelvis.
Paget's disease is second only to osteoporosis as one of the most common bone diseases in the
United States, but its occurrence is rapidly declining around the world. The disease is seen more
frequently in people age 50 years and older. The risk for developing Paget's disease increases as
a person ages, particularly in those 80 years old and older.
27. Amputation
the surgical removal of a part of the body, a limb, or part of a limb to treat recurrent infection
or gangrene in peripheral vascular disease; to remove malignant tumors; and to treat severe
trauma. The part is removed, and a shaped amputation flap is cut from muscular and
cutaneous tissue to cover the end of the bone. A section may be left open for drainage if
infection is present. After surgery, a lower leg amputation is elevated on a pillow for no more
than 24 to 48 hours and if necessary, protected with plastic from urinary and fecal
contamination. Vital signs are monitored carefully. If a dressing is used, it is watched for
excessive bleeding. The stump is moved frequently to prevent circulatory complications,
contractures, and tissue necrosis. If a cast is used, it must remain in place for 8 to 14 days. If
the cast comes off accidentally, the stump must be wrapped tightly at once with an
amputation-stump bandage, and plans must be made to replace the cast. The patient is fit for
a prosthesis, either delayed or immediately. Medication may relieve incisional pain and
phantom limb syndrome.