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Rehab Quiz 2 ReviewTBI, & musculoskeletal, stroke & brain tumorsRheumatoid arthritis & pt educationHip fractures (several questions) S & sTreatment Risk factors post opFractures of the HipHip 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 ADULTSTeach 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, 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 PRACTICEWhat 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 mentary: 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. Be sure that the patient's heels are up off the bed at all times. Inspect the heels and other high-risk 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).Risk factors for elderly r/t osteoporosis & osteoarthritisAlthough 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.OSTEOPOROSISPathophysiologyOsteoporosis 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 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):?Are estrogen deficient?Receive long-term steroid therapy?Have hyperparathyroidism?Are being monitored while on osteoporosis drug therapyThe 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 bone-forming 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.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 gravity-free or weightless environment (e.g., astronauts). The United States and other countries are studying this problem during trips into space.Etiology and Genetic RiskPrimary 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 OsteoporosisDISEASES/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 limitationDRUGS (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 diureticsAIDS, Acquired immune deficiency syndrome; HIV, human immune deficiency virus.Chart 53-1 BEST PRACTICE FOR PATIENT SAFETY & QUALITY CAREAssessing Risk Factors for Primary OsteoporosisAssess for:?Age 65 years and older in all women?Age 75 years and older in men?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?Lack of physical exercise or prolonged immobilityPrimary 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 CONSIDERATIONSThe 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/PrevalenceOsteoporosis 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 AWARENESSAlthough 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 dairy-based 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 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 devastatingHealth Promotion and MaintenanceA 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 Evidence-Based 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.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.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 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.observationsIt 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.interventionsInitial 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 considerationsAcute 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 periods of inactivity), regular exercise program, proper posture, and balanced diet with weight loss if indicated.Skeletal tractionone 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 therapyCouple questions… care of elderly delirium, dementia & depression s/s of Increased intercranial pressureischemic 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 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.s/s of osteoarthritis 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 concentration of uric acid so that uric acid salts precipitate from the blood and are carried to the joints. side effects of NSAIDS cardinal signs for neurovascular assessmentdiff 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.observationsThe 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.interventionsBacterial 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 considerationsConstant 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. Sedatives and narcotic analgesics should not be used because they may obscure important neurologic signs in addition to depressing vital functions.diff between// types of injuries assoc w/ shoulder pain, strainfor fractures, review material on different types, hallmarks of diff types, green stick, spiral, simple, open, etc…know diff between ligaments & tendons review charac of elder abuse charact of CNS comarisk factors assoc w/ strokeTBI, sequale that can follow as persons get over acute brain injuryCouple drug questions… one will be IV drug (2 questions them) Paget’s diseasea 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.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.Amputationthe 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. ................
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