Test Number 2-Adult Health

Front 1

1/3 systolic pressure + 2/3 diastolic pressure

Back 1

MAP equation

Front 2

1/3 systolic pressure + 2/3 diastolic pressure

Back 2

CPP

Front 3

occurs as a result of periventricular diffusion of ventricular CSF in a patient with uncontrolled hydrocephalus. It can be caused by enlargement of the extracellular space as a result of systemic water excess (hyponatremia). Fluid moves into the cells to equilibriate with the hypoosmotic interstitial fluid.

Back 3

interstitial cerebral edema

Front 4

The partial pressure of anterial CO2 is a potent vasoactive agent. An increase in PaCO2 relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance and increases CBF. Alternately, a decrease in PaCO2 reverses this process and decreases CBF. Cerebral oxygen tension below 50 mmHg results in cerebral vascular dilation. This dilation decreases cerebral vascular resistiance, increases CBF and raises oxygen tension. If oxygen tension is not raised, anaerobic metabolism begins, resulting in an accumulation of lactic acid. As lactic acid increases and hydrogen ions accumulate, the environment becomes more acidic. The more acidic the environment is the more vasodilation occurs in a continued attempt to increase blood flow. The combination of a severely low arterial oxygen pressure (PaO2) and an elevated hydrogen ion concentration (acidosis), which are both potent vasodilators, may produce a state where in autoregulation does not work and compensatory mechanisms fail to meet tissue metabolic demands.

Back 4

contributes to increased ICP and cerebral edema

Front 5

increase in size of normal blind spot, papiledema, decreased visual acuity, unilateral papillary dilation, altered LOC

Back 5

early signs of increased ICP

Front 6

headache, vomiting, elevated temp,focal signs, seizures, altered LOC, alteration in level of consciousness

Back 6

variable signs of increased ICP

Front 7

decreased LOCàstuporàcoma(very late),
change in pupil size, equality, reactivityàpupils dilated and fixed (very late)
decorticate postureàdecerebrate postureàabsence of motor response(very late)
bilateral pupillary dilation-àpupils dilated and fixed (very late)
decreased consciousnessàstuporàcoma (very late)
increased systolic pressure, decreased pulse rate, altered respiratory patternàdecreased respiratory rateàdecreased systolic blood pressure, increased pulse rate, respiratory arrest (very late)
rigidity; unilateral decerebrate postureàbilateral decerebrate posturingàabsence of motor response (very late)

Back 7

late-very late signs of increased ICP

Front 8

includes systolic HTN, with an increased pulse pressure, bradycardia and irregular respiratory rate.

Back 8

cushings triad

Front 9

results in dilation of the pupil ipsilateral to the mass of lesion, sluggish or no response to light, inability to move the eye upward, and ptosis of the eyelid. These signs can be the result of a shifting of the brain from the midline, a process that compresses the trunk of CN III, paralyzing the pupil sphincter. (uncal herniation may cause a dilated unilateral pupil).

Back 9

compression of the oculomotor nerve

Front 10

internal rotation and adduction of the arms with flexion of the elbows, wrists, and fingers as a result of interruption of voluntary motor tracts Extension of the legs may also be seen.

Back 10

decorticate posturing

Front 11

may indicate more serious damage and result from disruption of motor fibers in the midbrain and brainstem. In this position the arms are stiffly extended, adducted, and hyperpronated. There is also hyperextension of the legs with plantar flexion of the feet

Back 11

decerebrate posturing

Front 12

A low PaO2 and a high hydrogen ion concentration (acidosis) are potent cerebral blood vasodilators that increase cerebral blood flow and may increase the ICP; therefore, maintaining mild hyperventilation will help to decrease the need for increased cerebral blood flow and help to decrease the ICP

Back 12

rational for MILD hyperventilation for treatment of increased ICP

Front 13

acts by increasing osmolarity of glomerular filtrate, which raises osmotic pressure of fluid in renal tubules; decrease in reabsorption of water, electrolytes; increase in urinary output, sodium, chloride excretion. keeps the sodium and fluid levels lower so to prevent increase in ICP.
There is evidence that, in prolonged dosage, may pass from the blood into the brain, where it might cause reverse osmotic shifts that increase intracranial pressure.

Back 13

mannitol mechanism of action for increased ICP

Front 14

EYES OPEN: spontaneous response: 4
Opening of eye to name or command:3
Lack of opening of eyes to previous stimuli but opening to pain: 2
Lack of opening of eyes to any stimulus: 1
Untestible: U

BEST VERBAL RESPONSE
Appropriate orientation, conversant, correct identification of self, place, year and month: 5
Confusion, conversant, but disorientation in one or more spheres: 4
Inappropriate or disorganized use of words (e.g cursing), lack fo sustained conversation: 3
Imcomprehensible words, sounds (e.g. moaning): 2
Lack of sound, even with painful stimulus: 1

BEST MOTOR RESPONSE
Obedience ofLocalization of pain, lack of obedience but presence of attempts to remove offending stimulus: 5
Flexion withdrawal, flexion of arm in response to pain without abnormal flexion posture: 4
Abnormal flexion, flexing of arm at elbow and pronation, making a fist: 3
Abnormal extension, extension of arm at elbow usually with adduction and internal rotation of arm at shoulder: 2
Lack of response: 1
command: 6

Back 14

Glascow coma scale

Front 15

Consider proper positioning and appropriate care activities and what activities are avoided.
Respiratory function: maintenance of patient airway is critical in the patient with increased ICP and is a primary nursing responsibility. Accumulated secretions should be removed by suctioning. The nurse must use proper measures to prevent hypoxia, hypercapnia, proper positioning is important. Elevation of the HOB should be 30 degrees-enhancing the respiratory exchange and aids in decreasing cerebral edema. Keep suctioning to a minimum( so as to not increase ICP). Abdominal distention can interfere with respiratory function and should be prevented ; inserting an NG tube to aspirate the stomach contents can prevent distention( no NG in pt. with facial or skull fractures). Pain anxiety and fear from the initial injury, thereapuetic procedures, or noxious stimuli can increase ICP, and blood pressure, complicating the management and recovery of the brain-injured person-use combination of sedatives, paralytics and analgesics for symptom management (choice, dose and combination should be chosen based on the patient’s history, neurologic state, and overall clinical presentation). ABGs should be measured and evaluated regularly.

Back 15

appropriate nursing interventions for patient with or at risk for increased iCP

Front 16

Fluid and Electrolyte balance: IV fluids should be closely monitored with the use of a limited volume device or a volume control apparatus for accuracy. I & O with insensible losses and daily wts. taken into account. Electrolyte determination should be made daily and any abnormal values should be discussed with the physician. It is especially important to monitor serum glucose, sodium, potassium and osmolality.
Monitoring intercranial pressure: ICP monitoring is used in combination with other physiologic parameters to guide the care of the patient and assess the patient’s response to routine care. Valsalva maneuver, coughing, sneezing,hypoxemia and arousal from sleep are factors that can increase ICP-minimize them as much as possible.
Body position: maintain HOB position, prevent extreme neck flexion which can cause venous obstruction and contributed to elevated ICP.tradtional practice has been to elevate HOB 30 degrees, unless a concurrent cervical neck injury has been Identified. Care should be taken when turning the patient with slow, gentile movements b/c rapid changes in position may increase ICP. Avoid extreme hip flexion should be avoided to decrease the risk of raising the intraabdominal pressure. Attempts should be made to provide needed physical care activities to minimize complications of immobility.
Protection from injury: restraints should be used judiciously in the agitated patient. Patient can benefit from quiet, nonstimulating environment. Nurse should always use a calm, reassuring approach, touching and talking to the patient even one who is in a coma.
Psychologic considerations: short simple explinations are appropriate and allow the patient and family to acquire the amount of information they desire. There is a need support, information an deducation of both patients and families. Assess the family members desire and need to assist in providing care for the patient and allow for their participation as appropriate.

Back 16

nursing interventions for increased ICP

Front 17

First method: test the leaking fluid with Dextrostix or Tes-Tape strip to determine whether glucose is present. CSF fives a positive reading for glucose. If blood is present in the fluid, testing for the presence of glucose is unreliable because blood contains glucose. In this event the nurse should look for the “halo” or “ring” sign. To perform this test the nurse allows the leaking fluid to drip onto a white pad or towel and observes the drainage. Within a few minutes the blood coalesces into a center, and a yellowish ring encircles the blood if CSF is present. The color appearance and amt of leaking fluid must be noted because both tests can give false-positive results. The major potential complications of skull fractures are intracranial infections and hematoma, as well as meningeal and brain tissue damage. Rhinorhhea (CSF leakage from the nose) and otorrhea (CSF leakage from the ear) generally confirm that the fracture has transverse the dura.
If CSF rhinorrhea or otorrhea occurs, the nurse should inform the physician immediately. The patient should lie flat in bed unless this is contraindicated because of increased ICP. The head of the bed may be raised to decrease the CSF pressure so that a tear can seal. A loose collection pad may be placed under the nose or over the ear. No dressingshould be placed into the nasal or ear cavities. The patient should be cautioned not to sneeze or blow the nose. NG tubes should not be used and nasotracheal suctioning should not be performed on these patients

Back 17

method is used to determine if rhinorrhea or otorrhea following head injury is CSF or mucus. interventions are absolutely contraindicated in the patient with CSF leak from the nose

Front 18

a sudden transient mechanical head injury with disruption of neural activity and a change in the LOC. It is considered a minor head injury; the patient may not lose total consciousness with this injury. Signs include a brief disruption in LOC, amnesia regarding the event and headache. The manifestations are generally of short duration. If the patient has lost consciousness or if the loss of consciousness lasts less than 5 minutes the patient is usually discharged from the care facility with instructions to notify if symptoms persist or if behavioral changes are noted. Postconcussion syndrome is seen anywhere form 2 weeks to 2 months after the concussion. Symptoms include persistent headache, lethargy, personality and behavioral changes, shortened attention span, decreased short term memory and changes in the intellectual ability. Although concussion is generally considered benign and usually resolves spontaneously, the symptoms may be the beginning of a more serious, progressive problem. At the dime of discharge, it is important to give the patient and the family instructions for observation and accurate reporting of symptoms or changes in nerulogic status.

Back 18

Concussion

Front 19

the bruising of the brain tissue within a focal area that maintains the integrity of the pia mater and arachnoid layers. develops areas of hemorrhage, infarction, necrosis and edema. frequently occurs at the site of fracture. the phenomenon of coup-contrecoup injury is often noted. Damage from coup-contrecoup injury occurs because of mass movement of the brain inside the skull. ____ or lacerations occur both at the site of the direct impact of the brain on the skull (coup) and at the secondary area of damage on the opposite side away from injury (contrecoup). Bleeding around the site is generally minimal, and the blood is reabsorbed slowly. Nerologic assessment demonstrates focal findings and a generalized disturbance in the LOC. Seizures are a common complication of

Back 19

Contusion

Front 20

involve actual tearing of the brain tissue and often occur in association with depressed and compound fractures and penetrating injuries. Tissue damage is severe, and surgical repair of the laceration is impossible because of the texture of the brain tissue. Internal hemorrhage is often associated with cerebral lacerations. The hemorrhage manifests as a space occupying lesion accompanied by unconsciousness, hemiplegia on the contralateral side, and a dilated pupil on the ipsilateral side. As the hematoma expanse symptoms of increased ICP become more severe. Prognosis is generally poor for the patient with a large intracerebral hemorrhage. Subarachnoid hemorrhage and intraventricular hemorrhage can also occur secondary to head trauma

Back 20

Laceration

Front 21

a widespread axonal damage occurring aftera mild, moderate or severe TBI. The damage occurs primarily around axons in subcortical white matter of the cerebral hemispheres, basal ganglia, thalamus and brainstem. DIA was believed to occur form the tensile forces of the trauma that sheared axons resulting in axonal disconnection. Clinical signs and symptoms include: a decreased LOC, increased ICP, decerebration and decortications and global cerebral edema

Back 21

difuse axonal injury

Front 22

results from bleeding between the dura and the inner surface of the skull. is a neurologic emergency and is usually associated with a linear fracture crossing a major artery in the dura, causing a tear. Venous ones are associated with a tear of the dural venous sinus and develop slowly. With arterial hematomas, the middle meningeal artery lying under the temporal bone is often torn. With arterial hematomas the middle meningeal artery lying under the temporal bone is often torn. Hemorrhage occurs into the epidural space, which lies between the dura and the inner surface of the skull. Because this is an arterial hemorrhage, the hematoma develops rapidly and under high pressure. Symptoms typically include unconsciousness at the scene, with a brief lucid interval followed by a decrease in LOC. Other symptoms may include a headache, N/V or other focal findings. Rapid surgical intervention to prevent cerebral herniation dramatically improves outcomes.

Back 22

epidural hematoma

Front 23

occurs form bleeding between the dura mater and the arachnoid layer of the meningeal covering of the brain. usually results from injury of the brain. usually results from injury to the brain substance and is parenchymal vessels. The veins that drain from the surface of the brain into the sagittal sinus are athe source of most. is usually venous in origin the hematoma is much slower to develop into a mass large enough to produce symptoms.

Back 23

subdural hematoma

Front 24

observation and management of increased ICP are the primary management strategies.
Treatment of skull fractures is usually conservative. For a depressed fracture and fractures with loose fragments, a craniotomy is necessary to elevate the depressed bone and remove the free fragments.
In cases of acute subdural and epidural hematomas the blood must be removed. A craniotomy is generally performed to visualize the bleeding vessels so that the bleeding can be controlled. Burr-hole openings may be used in an extreme emergency for a more rapid decompression. followed by a craniotomy to stop all bleeding. A drain is generally put into place postoperatively for several days to prevent reaccumulation of blood

Back 24

concussion and contusion

Front 25

Family members may be needed to sign the consent for surgery this is a difficult and frightening time for the patietn’s family and requires sensitive nursing management. The suddenness of the situation makes it especially difficult for the family to cope. Family needs to understand what is going on and taught appropriate interaction patterns. The nurse must give guidance and referrals for financial aid, child care and other personal needs and must assist the family in involving the patient in family activities whenever possible. Assisting the patient and family in maintaining communication and hope are strategies needed. The family must be prepared by the nurse for the emergence of the patient form coma and must explain that the process of awakening often takes several weeks as family may have unrealistic expectations.

Back 25

unique emotional/social challenges do family members of the head injured patient

Front 26

fever, severe headache, nausea, vomiting and nuchal rigidity ( resistance to flexion of the neck) are key signs of meningitis. Positive Kernig sign, a positive Brudzinksi sign, photophobia and decreased LOC, and signs of increased ICP may also be present. Seizures occur in 20%. With meningitis the headache becomes progressively worse and may be accompanied by vomiting and irritability. If the infecting organism is a meningococcal a skin rash is common and petechiae may be seen. Increased ICP occurs in more than 90%. Diagnosis often occurs with a lumbar puncture and analysis of CSF. Variatinos in the CSF depend on the causative organism. Protein levels in the CSF are usually elevated and are higher in bacterial than in viral meningitis. Decreased CSF glucose concnetration is common in bacterial meningitis and may be normal in viral meningitis. The CSF is purulent and turbid in bacterial meningitis; it may be the same or clear in viral meningitis. The predominant white blood cell type in the CSF during bacterial meningitis is polymorph nuclear cells.

Back 26

bacterial meningitis clinical manifestations

Front 27

usually presents as a headache, fever, photophobia and stiff neck. Fever may be moderate to high. Usually no symptoms of brain involvment. CSF typically includes lymphocytes

Back 27

viral meningitis clinical manifestations

Front 28

WBC>1000/ul (mainly PMN),, protein >500mg/dl glucose: decreased appearance of CSF: turbid, cloudy

Back 28

bacterial meningitis

Front 29

WBC count:25-500/ul (mainly lymphocytes), protein: 50-500mg/dl, glucose: normal to low. Appearance of CSF: clear or cloudy

Back 29

viral meningitis

Front 30

an acute inflammatoin of the brain, it is serious and sometimes fatal disease. It is usually caused by a virus. Ticks and mosquitoes transmit epidemic _____. HSV ___ is the most common cause of acute no epidemic viral encephalitis. Many different viruses have been implicated in encephalitis, some of them associated with certain seasons of the year and endemic to certain geographic areas. no epidemic encephalitis may occur as a complication of measles, chickenpox or mumps.

Back 30

etiology of encephalitis

Front 31

onset of infection is typically nonspecific with fever, headache, nausea and vomiting. It can be acute or sub acute. Signs of encephalitis appear on day tow or three and may vary from minmal alterations in mental status to coma. Virtually any CNS abnormality can occur including hemi paresis, tremors, seizures, cranial nerve palsies, personality changes, memory impairment, amnesia, and dysphasia

Back 31

clinical manifestations of encephalitis

Front 32

abnormalities in brain function are common, including altered mental status, motor or sensory deficits and speech or motor disorders.

Back 32

encephalitis

Front 33

age, gender, race and heredity. Stroke risk increases with age, double each decade after 55. Overall, incidence and prevalence of stroke is almost equal for men and women but women die more often from them then men. African Americans have a higher incidence as well as a higher death rate from stroke than whites. A family history , a prior transient ischemic attack, or a prior stroke also increases the risk

Back 33

nonmodifiable risk factors of stroke

Front 34

HTN (single most important), heart disease, including atrial fibrillation, MI, cardiomyopathy, cardiac valve abnormalities and cardiac congenital defects. Atrial fibrillation is the most important treatable cardiac related risk factor. Diabetes mellitus, increased serum cholesterol, risk associated with smoking, asymptomatic carotid stenosis, lifestyle habits such as excessive alcohol consumption, obesity, physical inactivity, poor diet and drug use. Migraine headaches, inflammatory states, and hyperhomocyteinemia. High dose estrogen oral contraceptives

Back 34

modifiable risk factors of stroke

Front 35

occurs in relation to injury to a blood vessel wall and formation of a blood clot. Thrombosis develops readily where atherosclerotic plaques have already narrowed blood vessels. is the result of thrombosis or narrowing of blood vessel, is the most common cause of stroke. 2/3 are associated with hypertension, or diabetes mellitus.

Back 35

thrombotic stroke

Front 36

occurs when an embolus lodges in and occludes a cerebral artery, resulting in infarction and edema of the area supplied by the involved vessel. Embolism is the second most common cause of stroke; majority of emboli originate in the endocardial (inside) layer of the heart, with plaque breaking off form the endocardium and entering circulation. Heart conditions associated with emboli include atrial fibrillation, myocardial infarction, infective endocarditic, rheumatic heart disease, valvular prosthesis, and atrial septal defects. Less common causes of emboli include fat from long bone (femur) fractures

Back 36

embolic stroke

Front 37

bleeding from the brain tissue itself (intercerebral or intraparenchymal hemorrhage) or into the subarachnoid space or ventricles (subarachnoid hemorrhage or intraventricular hemorrhage)

Back 37

hemorrhagic stroke

Front 38

primary diagnostic test used after a stroke. can indicate the size and location of the lesion and differentiate between ischemic and hemorrhagic stroke. CT angiography provides visualization of vasculature and can be performed at the same time as the CT scan. CTA allows detection of intracranial or extra cranial occlusive disease.

Back 38

CT scan

Front 39

the gold standard for imaging the carotid arteries. can identify cervical and cerebrovascular occlusion, atherosclerotic plaques, and malformation of vessels.

Back 39

Angiography

Front 40

Drugs that prevent platelet aggregation such as aspirin, ticlopidine (Ticlid), clopidogrel (plavix), dipyridamole (persantine) and anticoagulant drugs (e.g. warfarin (coumadin)), may be prescribed for long-term therapy after TIA

Back 40

pharmacologic management can the nurse expect for the patient with TIA

Front 41

TIAs are a temporary focal loss of neruologic function caused by ischemia of one of the vascular territories of the brain, lasting less than 24hrs. And often lasting less than 15 minutes.
The signs and symptoms of a TIA depend on the blood vessel that is involved and the area of the brain that is ischemic. If the carotid system is involved, patietns may have a temporary loss of vision in one eye (amaurosis fugax), a transient hemi paresis, numbness or loss of sensation, or a sudden inability to speak. Signs of a TIA involving the vertebrobasilar system may include tinnitus, vertigo, darkened or blurred vision, diplopia, ptosis, dysarthria, dysphasia, ataxia and unilateral or bilateral numbness or weakness

Back 41

prodromal (warning signs) symptoms are common with different types of strokes

Front 42

paralized right side: hemiplegia, impaired speech/language aphasias, impaired right/left discrimination, slow performance, cautious, aware of deficits; depression anxiety, impaired comprehension related to language, math

Back 42

Left brain damage (stroke on left side of the brain):

Front 43

paralyzed left side: hemiplegic, left sided neglect, spatial perceptual deficits, tends to deny or minimize problems, rapid performance, short attention span, impulsive, safety problems, impaired judgment, impaired time concepts.

Back 43

Right brain damage (stroke on right side of brain)

Front 44

irreversible inhibition of platelet aggregation through antagonism of ADP. Therapuetic response: absence of stroke. (hemorrhagic stroke

Back 44

Ticlopidine

Front 45

inhibits first and second phases of ADP-induced effects in platelet aggregation. Therapuetic response: absence of stroke, MI. used for embolic stroke and thrombotic stroke.

Back 45

Clopidogrel (plavix

Front 46

blocks pain impulses in CNS, reduces inflammation by inhibition of prostaglandin synthesis, antipyretic action results from vasodilation of peripheral vessels; decreases platelet aggregation. (ischemic stroke: thrombotic stroke, embolic stroke)

Back 46

asprin

Front 47

surgical interventions for the patient with ___ from carotid disease include carotid endarterectomy, transluminal angioplasty, stenting, and extra cranial-intracranial (ECIC) bypass.
In a carotid endarterectomy the athermanous lesion is removed from the carotid artery to improve blood flow.
Transluminal angioplasty-the insertion of a balloon to open a stenosed artery and improve blood flow. Stenting involves intravascular placement of a stent in an attempt to maintain patency of the artery.
ECIC bypass involves anatomizing (surgically connecting) a branch of an extra cranial artery to an intracranial artery beyond an area of obstruction with the goal of increasing cerebral perfusion.

Back 47

TIA surgical therapy

Front 48

surgical interventions include immediate evacuation of aneurysm included hematomas or cerebella hematomas larger than 3cm. Subarachnoid hemorrhage is usually caused by a ruptured aneurysm. Treatmetns of aneurysm involve clipping, wrapping, or coiling the aneurysm to prevent rebleeding. Treatment of atrioventricular malformation is surgical resection and or radio surgery. Both may be preceded by interventional neuropathology to embolize the blood vessels that supply the AVM. Subarachnoid and intracerebral hemorrhage can involve bleeding into the ventricles of the brain this situation produces hydrocephalus which further damages the brain tissue from increased ICP-insertion of a ventriculostomy for cerebrospinal fluid drainage can result in dramatic improvement

Back 48

stroke surgial therapy/interventions

Front 49

Elevated blood pressure is common immediately after a stroke and may be protective response to maintain cerebral perfusion. Immediately following ischemic stroke use of drugs to lower blood pressure is recommended only if blood pressure is markedly increased. Oral antihypertensive drugs are generally preferred. Hyervolemic hemodilution using crystalloids and colloids and durg-induced hypertension may be used in patients with ischemia caused by vasospasm following subarachnoid hemorrhage once the aneurysm has been successfully clipped or coiled. Fluid and electrolyte balance must be controlled carefully. IV solutions with glucose and water are avoided because they are hypotonic and may further increase cerebral edema and ICP. In addition, hyperglycemia may be associated with further brain damage and should be treated. Patient is usually given Normal Saline during initial interventions. Adequate fluid intake during acute care should be 1500-2000ml per day. In general decisions regarding fluid and electrolyte replacement therapy are based on the extent of intercranial edema, sympotoms of increased ICP, central venous pressure levels, lab values for electrolytes and I & Os

Back 49

initial management of blood pressure and fluid therapy can the nurse expect for the patient experiencing a stroke

Front 50

used to reestablish blood flow through a blocked artery to prevetn cell death in patients with the acute onset of ischemic stroke symptoms. Thrombolytic drugs such as tPA produce localized fibrinolysis by binding the fibrin in the thrombi. Because it is clot specific in its activation of the fibrinolytic system, tPA is less likely to cause hemorrhage compared to streptokinase or urokinase. No anticoagulant or ant platelets are given for 24 hours after tPA treatment.
may be administered within 3 hours of the onset of clinical signs of ischemic stroke. Therefore the single most important factor is timing.

Back 50

indications and contraindications for tPA

Front 51

stroke affecting the Worneke’s area of the brain; neither the sounds of speech nor its meaning can be understood. This results in impairment of the patient’s comprehension of both spoken and written language

Back 51

receptive aphasia

Front 52

strokes affecting the Broca’s area of the brain cause difficulty in speaking and writing

Back 52

expressive aphasia

Front 53

decrease environmental stimulation, treat patient as adult, present one thought or idea at a time, keep questions simple or ask yes/no questions, let person speak, do not interrupt, make use of gestures or demonstration as an acceptable alternative, say show me or point to what you want, do not pretend to understand the person if you don’t, speak with normal volume and tone, give patient time to process information and generate a response before repeating, allow body contact as much as possible, organize patient’s day by preparing and following a schedule, do not push communication if person is tired or upset.

Back 53

communicating with patient who has aphasia

Front 54

The nurse and speech therapist must assess the ability of the patient to swallow solids and fluids to adjust the diet appropriately. The dietitian plans the diet type, texture, calorie count, and fluids to meet the patients nutritional needs. Interventions to promote self feeding include using the unaffected upper extremity to eat; employing assitive devices such as rocker knives, plate guards, and nonslip pads for dishes, removing unnecessary items from the tray or table which can reduce spills; and providing a nondistracting environment to decrease sensory overload and distraction.

Back 54

feeding assistance is appropriate for the patient with stroke during the rehabilitation phase

Front 55

The chair is placed beside the bed so that the patient can lead with the stronger arm and leg.the patient sits on the side of the bed, stands, places the strong hadn on the far wheelchair arm and sits down. The nurs may either supervise the transfer or provide minimal assistance by guiding the patient’s strong hand to the wheelchair arm, standing in front of the patient blocking the patient’s knees with the nurses knees to prevent buckling, and guiding the patient into a sitting position

Back 55

assisting patient with hemiperisis to move from bed to chair

Front 56

The first oral feeding should be approached carefully because the gag reflex may be impaired. Before initiation of the feeding, the gag reflex may be assessed by gently stimulating the back of the throat with a tongue blade. To assess swallowing ability the nurse should elevate the head of the bed to an upright position and give the patient a small amount of crushed ice or ice water to swallow. If the gag reflex is present and the patient is able to swallow safely, the nurse may proceed with feeding. The patient should remain in high fowler’s position preferably in a chair with the head flexed forward for the feeding and for 30 minutes following. Foods should be easy to swallow and provide enough texture, temperature (warm or cold), flavor to stimulate a swallow reflex. Crushed ice can be used as a stimulant. The patient is instructed to swallow and then swallow again. Food should be placed on the unaffected side of the mouth. Pureed foods are non usually the best choice they are often bland and too smooth. Thin liquids are often difficult to swallow and may promote coughing. Milk products should be avoided because they tend to increase the viscosity of mucus and increase salvation. The nurse should ensure an unrushed, nonstressful atmosphere. Feedings must be followed by scrupulous oral hygiene because food may collect on the affected side of the mouth

Back 56

actions by the nurse are used to prevent aspiration during initial feeding for patient with dysphagia

Front 57

Efforts should be made to promote normal bladder function and avoid the use of indwelling catheters. If an indwelling catheter must be used initially, it should be removed as soon as the patientis medically and neurologically stable. An intermittent catheterization program may be used for patient with urinary retention because of the lower incidence of UTIs. A bladder retraining program consists of 1. Adequate fluid intake with the majority given between 8am and 7pm, 2. Scheduled toileting every 2hrs. Using bedpan, commode, or bathroom and 3. Noting signs of restlessness which may indicate the need for urination.

Back 57

bladder retraining following a stroke

Front 58

Assending paralysis could cause respiratory or cardiac arrest.
Assessment of the patient is the most important aspect of nursing care during the acute phase. The nurse must monitor the ascending paralysis; assess respiratory function; monitor arterial blood gases (ABGs) and assess the gag, corneal and swallowing reflexes during the routine assessment. Reflexes are usually decreased or absent. Monitoring blood pressure and cardiac rate and rhythm is also important during the acute phase because transient cardiac arrhythmias have been reported. Autonomic dysfunction is common and usually takes the form of bradycardia and arrhythmias. Orthostatic hypotension secondary to muscle atony may occur in severe cases. Vasopressin agents and volume expanders may be needed to treat low blood pressure.

Back 58

priority assessment of the patient with Guillain-Barre syndrome

Front 59

characterized by decreased reflexes, loss of sensation, and flaccid paralysis below the level of the injury. This syndrome lasts days to months and may mask post injury neurologic function

Back 59

spinal shock

Front 60

due to the loss of vasomotor tone caused by injury and is characterized by hypotension, bradycardia, and warm dry extremities. Loss of Sympathetic innervation causes perihperal vasodilation, venous pooling, and decreased cardiac output. Bradycarida and hypotension are caused by loss of vasomotor tone which does not allow you to control the muscles and nerves that control blood vessels thus not allowing you to control your blood pressure

Back 60

neurologic shock

Front 61

By 24 hours or less permanent damage may occur because of the development of edema. Edema secondary to the inflammatory response is particularly harmful because of lack of space for tissue expansion. Therefore resultant compression of the cord and extension of edema above and below the injury increase the ischemic damage. The extent of neurologic damage caused by a spinal cord injury results from primary injury damage (actual physical disruption of axons) and secondary injury damage (ischemia, hypoxia, microhemorrhage and edema). Because secondary injury processes occur over time the extent of injury and prognosis for recovery are most accurately determined at 72 hours or more after spinal injury

Back 61

progression of SCI in the first 72 hours post injury

Front 62

C1-C3-often fatal injury, movement of neck and above, loss of innervation to diaphram, absence of independent respiratory function.
C4: sensation and movement of neck and aboce, may be able to breathe without a ventilator
C5-full neck, partial shoulder, back and biceps, gross elbow, inability to roll over or use hands; decreased respiratory reserve
C6: shoulder and upper back abduction and rotation at shoulder, full biceps to elbow flexion, wrist extension, weak grasp of thumb, decreased respiratory reserve.
C7-8: all triceps to elbow extension, finger extensors and flexors, good grasp with some decreased strength, decreased respiratory reserv

Back 62

Cervical injury(tetraplegia)

Front 63

T1-T6-fullinnervation fo upper extremities, back ,essential intrinsic muscles of hands, full strength and dexterity of grasp; decreased trunk stability, decreased respiratory reserve.
T6-T12-full stable thoracic muscles and upper back, functional intercostals, resulting in increased respiratory reserve.
L1-L2: varying control of legs and pelvis, instability of lower back.
L3-L4: quadriceps and hip flexors, absence of hamstring function, flail ankles.

Back 63

paraplegia

Front 64

when administered early and in a large does, resulted in greater recovery of neurologic function. MP a blocker of lipid per oxidation by products improves blood flow and reduces edema in the spinal cord. MP produces a number of effects that may account for the overall improvement noted in the spinal-cord ischemia, improvement of energy balance, restoration of extra cellular calcium, improvement of nerve impulse conduction and repression fo the release of free fatty acids from spinal cord tissues.

Back 64

methylprednisone

Front 65

Immediately after injury urine is retained b/c of the loss of autonomic and relex control of the bladder and sphincter. overdistention of the bladder can result in reflux into the kidney with eventual renal failure. An indwelling catheter is placed as a result. After the patient is stabilized the best means of managing long term urinary function is assessed. Usually the patient is started on intermittent catheterization program. The patient is often maintained on a fluid restriction of 1800-2000ml per day to facilitate a bladder training program. Catheterization should be done ever 3-4 hours to prevent bacterial overgrowth resulting from urinary stasis. Constipation is generally a problem during spinal shock because no voluntary or involuntary evacuation of the bowel occurs. A bowel program should be started during acute care this consists of choosing a rectal stimulant (suppository or mincemeat) to be inserted daily at a regular time followed by gentle digital stimulation or manual evacuation done by the nurse until evacuation is complete.

Back 65

bladder and bowel management following SCI

Front 66

a massive uncompensated cardiovascular reaction mediated by the sympathetic nervous system. It occurs in response to visceral stimulation once spinal shock is resolved in patients with spinal cord lesions above T7. The condition is a life threatening situation that requires immediate resolution. Manifestations include: HTN, blurred vision, throbbing headache, marked diaphoresis above the level of the lesion, bradycardia (30-40 bpm) piloerection ( erection of the body hair) as a result of pilomotor spasm, flushing of the skin above the level of the lesion, blurred vision or spots in the visual fields, nasal congestion, anxiety and nausea. It is important to measure BP when a patient with spinal injury complains of headache. Nursing interventions are elevation of the head of the bed 45 degrees or sitting the patient upright, notificatio of the physician, and assessment to determine the cause. The most common cause is bladder irritation; immediate catheterization may be necessary to relieve bladder distention. If a catheter is already in place it shold be checked for kinks or folds, if plugged small volume irrigation should be performed slowly and gently to open a plugged catheter, or a new cath. May be inserted. Stool impaction can also result in autonomic dysreflexia-digital rectal examination should be performed only after application of an anesthetic ointment to decrease rectal stimulation and to prevent an increase of symptoms. The nurse should remove all skin stimuli such as constrictive clothing and tight shoes. Blood pressure should be monitored frequently during the episode. If symptoms persist after the source has been relieved an alpha adrenergic blocker or an arteriolar vasodilator is administered. Careful monitoring must continue until vitals are stable.

Back 66

Autonomic dysreflexia

Front 67

Coordinate care with patient and encourage self-care. Support family members; prevent alleviation fo guilt by supporting dependency. Use humor liberally, allow patient outbursts, do not allow fixation on injury

Back 67

nursing actions are appropriate for the patient experiencing anger following SCI

Front 68

are the best drugs for treatment of allergic rhinitis and urtiaria. They act by competing with histamine for H1 receptor sites and thus blocking the effect of histamine. Antihistamines can be used effectively to treat edema and pruritus but are relatively ineffective in preventing bronchoconstriction

Back 68

antihistamines

Front 69

treatment of anaphylactic shock. It is a hormone produced by the adrenal medulla that stimulates alpha and beta adrenergic receptors. Stimulation of the alpha adrenergic receptors causes vasoconstriction of peripheral blood vessles and beta receptor stimulation relaxes bronchial smooth muscles. also acts directly on mast cells to stabilize them against further degranulation

Back 69

Epinephrine

Front 70

effectively used to treat allergic rhinitis. Prednisone: decreases inflammation by suppression of migration of polymorph nuclear leukocytes, fibroblasts, reversal to increase capillary permeability and lysosomal stabilization.

Back 70

Corticosteroids

Front 71

causes bronchodilation by acting on B2 (pulmonary) receptors by increasing levels of cAMP, which relaxes smooth muscle; produeces bronchodilator CNS, cardiac stimulation, as well as increased diuresis and gastric acid secretion; longer acting than isoproterenol

Back 71

B2-agonist inhalers (albuterol):

Front 72

depresses subcortical levels of CNS, including limbic sytem, reticular formation; competes with H1-receptor sites

Back 72

Antipuritics (hydroxyzine)

Front 73

The cardinal principle in therapuetic management is speed in (1) recognition, 2) mainfenance of a patent airway, (3) prevetion of spread of the allergen by using a tournaquet, (4) administration of drugs and (5) treatment of shock.
Ensure patent airway, remove insect stinger if present, epinephrine 1:1000 for mild symptoms repeat at 20 min. interventions, administer high flow oxygen via non-rebreather mask, place recumbent and elevate legs, keep warm, administer histamine H2 blockers such as tegamet, maintain blood pressure with fluids, volume expanders, vasopressin(dopamine, nor epinephrine). Monitor vital signs, respiratory efforts, oxygen saturation, level of consciousness and cardiac rhythm, anticipate intubation with severe respiratory distress, anticipate cricothyrotomy or tracheotomy with severe laryngeal edema.

Back 73

priority nursing interventions for the person experiencing anaphylaxis

Front 74

The nurse must teach the patient about allergen recognition and lifestyle adjustments so that there is minimal exposure to offending allergens, the nurse must reinforce that even with drug therapy and immunotherapy the patient will never be desensitized or completely symptoms free, the need to identify the offending allergen is of primary importance, the patient should wear a medic alert bracelet listing the allergies patient has.

Back 74

teaching needs for the person with severe allergies

Front 75

Drug induced immunosuppressant is the most common. Stress may alter the immune response, hypo functional state of the immune system exists in young children and older adults, malnutrition alters cell-mediated immune responses. When protein is deficient over a prolonged period atrophy of the thymus gland occurs and lymphoid tissue decreases. Radation destroys lumphocytes either directly or through depletion of stem cells. Surgical removal of lymph nodes, thymus or spleen can supress the immune system. Hodgkin’s disease greatly impairs the cell-mediated immune response and patients may die from severe viral or fungal infections. Viruses especially rubella may cause immunodeficiency by direct cytotoxic damage of lymphoid cells. Systemic infections can place such a demand on the immune system that resistance to a secondary or subsequent infection is impaired

Back 75

common causes of secondary immune deficiencies

Front 76

involve an imparement of one or more immune mechanism which include: phagocytosis, humoral response, cell mediated response, complement and a combined humoral and cell mediated deficiency. Immunodeficiency disorders are primary if the cells are improperly developed or absent and secondary if eh deficiency is caused by illness of treatment.

Back 76

Immunodeficiency disorders

Front 77

identify the HLA antigens for both donors and potential recipients. A serologic test is used to type for the antigens of all five loci. Lymphocytes are isolated from peripheral blood and then combined with serum and contains antibodies to HLAs. The total time required for HLA typing is about 4-6hrs. Crossmatching is done at the time a living donor is being evaluated and just before surgery for cadaver donors. A crossmatch uses serum form the recipient mixed with donor lymphocyte to test for any preformed cytotoxic antibodies to the potential donor organ. A positive crossmatch indicates that the recipient is catatonic antibodies to the donor and is an absolute contraindication to transplantation. The potential recipient may have been exposed to antigens similar to those of the donor by means of previous blood transfusions, pregnancy, or a previous organ transplant. Crossmatching is also performed to detect preformed catatonic antibodies in the recipient serum to HLAs on lymphocytes from random donor. A high PRA indicates that the person has a large number of catatonic antibodies which means that there is a poor chance of finding a crossmatch negative donor. In patients awaiting transplantation a PRA panel is usually done on a regular basis.

Back 77

histocompatibility testing

Front 78

By using a combination of medications that work in different phases of the immune response, lower doses of each drug produce effective immunosuppression while minimizing side effects. It is important to take medications daily and to take all meds especially those that cause immunosuppression to prevent rejection. The most common drugs include: prednisone (corticosteroids), tacrolimus (prograf), cyclosporine (neoral), mycophenolate mofetil (cellcept), birdlimes (rapamune), muromonab-CD3 (OKT3), daclizumab (zenapax), basiliximab (simulect), polyclonal antibody serums: ATG, ALG (thymoglobulin, ATGAM)

Back 78

immunosuppression

Front 79

The organ does not function properly
General discomfort, uneasiness, or ill feeling
Pain or swelling in the location of the organ (rare)
Fever (rare)
The symptoms vary depending on the transplanted organ or tissue. For example, patients who reject a kidney may have less urine, and patients who reject a heart may have symptoms of heart failure

Back 79

possible signs of organ rejection

Front 80

may occur as an idiopathic (formerly primary) or secondary disorder. The cause of idiopathic ___ is unknown. Secondary ___ is caused by a known event or condition that directly damages cartilage or causes joint instability (trauma, mechanical stress, inflammation, joint instability, neurologic disorder, skeletal deformities, hematologic/ endocrine disorders, use of selected drugs, the increase in incidence of __ in aging women is believed to be due to estrogen reduction role in the occurrence of ____.___results from cartilage damage that triggers a metabolic response at the level of the chondrocytes, progression of ___ causes the normally smooth white translucent articular cartilage to become dull, yellow and granular. The body’s attempt at cartilage repair cannot keep up with the destruction that is occurring. Continued changes in the collagen structure of the cartilage lead to fissuring, fibrillation and erosion of the articular surface. While inflammation is not a characteristic of __ a secondary synovitis may result when phagocytic cells try to rid the joint of small pieces of cartilage torn from contact between exposed bony joint surfaces after the articular cartilage has completely deteriorated.

Back 80

Osteoarthritis

Front 81

is a chronic systemic disease characterized by inflammation of connective tissue int eh diarthrodial (synovial) joints, typically with periods of remission and exacerbation. frequently accompanied by extraarticular manifestations. Cause is unknown.

Back 81

Rheumatiod Arthritis

Front 82

usually > 40yrs. Old before age 50 more men than women, after age 50 more women than men. Often overweight, localized disease with variable progressive course weight bearing joints (knee, hips), MCPs, DIPs, PIPs, cervical and lumbar spine effected; often asymmetric. Effusions are uncommon. Clinical manifestations: mild discomfort to significant disability, joint pain is the predominant symptom, in early stages joint pain is relieved by rest, in advanced disease pateitn may complain of pain with rest or experience sleep disruption caused by increasing joint discomfort. Pain may also become worse as barometric pressure falls. Pain of OA may be referred to the groin, buttock or medial side of the thigh or knee, sitting down becomes difficult, joint stiffness occurs after periods of rest or static position. usually effects jionts asymmetrically. Crepitation-indicates the loss of cartilage and is present in more than 90% patietns with knee OA. Collaborative therapy focuses on managing pain and inflamamtion preventing disability and maintaining and improving joint fuction. Rest and joint protection, heat and cold application-short term relief, nurtional therapy (weight reduction) and exercise, complementary alterative therapies, drug therapy (acetaminophen, no steroidal anti-inflammatory drugs, intraarticular hyaluronic acid), reconstructive therapy.
Nursing management would include acute interventions -the person who often complains of pain, stiffness, limitation of function, and the frustration of coping in these physical difficulties on a daily basis.

Back 82

osteoarthritis clinical manifestations and interventions

Front 83

onset is typically insidious, nonspecific manifestations such as fatigue, anorexia, weght loss, and generalized stiffness may precede the onset of arthritic complaints. Stiffness becomes more localized in the following weeks to months. Specific articular involvement is manifested clinically by pain, stiffness, limitation of motion, and signs of inflammation. Joint symptoms occur symmetrically and frequently affect the small joint of the hands and feet. Larger peripheral joints such as the wrists, elbows, shoulders, knees, hips and ankles, and jaw may also be involved. can affect nearly every system in the body. Joint symptoms occur symmetrically and frequently. Often experience joint stiffness after periods of inactivity, morning stiffness may last from 60 minutes to several hours or more. Joints become tender, painful and warm to the touch. Joint pain increases with motion, varies in intensity, may not be proportional to degree of inflammation inflammation and fibrosis of the joint capsule and supporting structures may lead to deformity and disability. Rheumatoid nodules: when high RF factor, Sjorgen syndrome and Felty syndrome-inflammatory eye disorders, splenomegaly, lymphadenopathy, pulmonary disease, blood dyscrasias

Back 83

Rheumatoid arthritis clincal manifestations and interventions

Front 84

physical therapy: joint motion and muscle strength, occupational therapy: upper extremity function, assistive devices and strategies. Drug therapy: cornerstone of RA treatment, disease modifying antirhematic drugs: plaquinil(1st line), methyltrexate, gold therapy injection, pain control-cox2 inhibitors, NSAIDS. Nutritional therapy: balanced nutrition important, weight loss may result from lack of appeptite. Nursing management: rest, joint protection, psychologic support, heat and cold therapy and exercise.

Back 84

collaborative care of RA

Front 85

drug therapy based on severity of symptoms: acetaminphen (1000mg every 6hrs.) calculates (aspercreme), NSAIDS, nonopioid analgesics, opioid analgesics, corticosteroids-intraarticular injection, antibiotics

Back 85

drug therapy for Osteoarthritis

Front 86

1st line: plaquinil-safest drugs fro mild disease SE: rash, methyltrexate-depresses immune system SE: bone marrow suppression, hard on liver, Gold therapy-injection, pain control: COX2 inhibitors, NSAIDS

Back 86

drug therapy for rheumatoid arthritis

Front 87

A major challenge in treatment is to manage the active phase of the disease while preventing complications of treatments tha cause long term tissue damage. Drug therapy: NAIDS continue to be an important intervention, especially for patients with mild polyarthralgias or polyarthritis. Corticosteroid exposure should be limited, but tapering doses of intravenous methylprednisolone may be useful in controlling severe exacerbations of polyarthritis. During exacerbation the patient may become abruptly and dramatically ill. Fever pattern, joint inflammation, limitation of motion, location and degree of discomfort, and fatigability should be specifically assessed, the patient’s weight and fluid intake and output should be monitored if corticosteroids are prescribed because of the fluid-retention effect of these drugs and the possibility of renal failure. Collection of 24 hour urine samples for protein and creatnine clearance may be ordered. The nurse should observe signs of bleeding that may result from drug therapy, such as palor, skin bruising, petechiae, or tarry stools. careful assessment of neurologic status includes observation for visual disturbances, headaches, personality changes, seizures, and forgetfulness. Psychosis may indicate CNS disease or may be the effect of corticosteroid therapy. The nurse must explain the nature of the disease modes of therapy and all diagnostic procedures.

Back 87

nursing interventions for the person with acute exacerbation of Systemic Lupus Erythematosus

Front 88

cutaneous vascular lesions can appear in any location but are most likely to develop in sun exposed areas. Severe skin reactions can occur in persons who are photosensitive. Classic butterfly rash over the cheeks and bridge of the nose occurs in 50% of patients with SLE. Small number of patients have persistent lesions, photosensitivity, and mild systemic disease in a syndrome referred to as sub acute cutaneous lupus. Ulcer of oral or nasopharyngeal membranes occur in up to 1/3 of patients with SLE. The scalp becomes dry, scaly, and atrophied. Polyarthralgia with morning stiffness is often the patient’s first complaint and may precede the onset of multisystem disease to many years. Arthritis occurs in more than 90% patients with SLE. Diffuse swelling is accompanied by joint and muscle pain, and some stiffness may be experienced. Tachyon and cough in patients with SLE are suggestive of restrictive lung disease. Pleurisy with or without pleural effusion is also possible. Cardiac involvement may include arrhythmias resulting from fibrosis of the senatorial and atrioventricular nodes. Clinical factors such as HTN and hypercholesterolemia require aggressive therapy and careful monitoring. SLE accelerates coronary artery disease (CAD) and the risk of developing CAD also increases. Lupus nephritis occurs in about 50% of patients within 1 year of diagnosis with SLE. Manifestations of LN vary from mild proteinuria to rapid, progressive glomerulonephritis. Nearly all patietns with SLE show renal histologic abnormalities in renal biopsy studies or autopsy results. Along with renal involvement neurologic effects are the most prevalent in SLE. Generalized or focal seizures are the most common manifestation involving the central nervous system, and occur in as many as 15% of patients with SLE at the time of diagnosis.

Back 88

clinical manifestations of systemic Lupus erythematosus.

Front 89

Mular rash, discoid rash, photosensitivity, oral ulcers, arthritis: nonerosive, involvement of two or more joints characterized by tenderness, swelling and effusion. Serositis: pleuritis, or pericarditis, renal disorder: persistent proteinuria or cellular casts in urine, Neurologic disorder: hemolytic anemia, leucopenia, lymphopenia, or thrombocytopenia, immunologic disorder: protein LE preparation; anti-DNA antibody or antibody to Sm nuclear antigen; or false-positive serologic test for syphilis, antinuclear antibodies

Back 89

clinical manifeststaion of SLE

Front 90

The patient must understand that even perfect adherence to the treatment plan is not a guarantee against exacerbation because of the course of the disease is unpredictable. However, a variety of factors may increase disease activity such as fatigue, sun exposure, emotional stress, infection, drugs and surgery.

Back 90

nursing responsibilities in assisting a person control symptoms of SLE and learn to cope with the illness

Front 91

a non surgical, manual realignment of bone fragmetns to their previous anatomic position. Traction and countertraction are manually applied to the bone fragments to restore position, length, and alignment. Closed reduction usually performed with the patietn under local or general anesthesia. After reduction the injured part is immobilized by traction, casting, external fixation, splints or orthoses to maintain alignment until healing occurs.

Back 91

close reduction

Front 92

is the correction of bone alignment through surgical incision. It often includes internal fixation of the fracture with the use of a wire, screws, pins, plates, intramedullary rods or nails. The chief disadvantage of this form is the possibility of infection and the complications associated with anesthesia

Back 92

open reduction

Front 93

traction devices apply a pulling on the fractured extremity to attain realignment while countertraction pulls in the opposite direction. The two most common types include skin traction and skeletal traction. When traction si used to treat fractures the forces are usually exerted on the distal fragment to obtain alignment with the proximal fragment. Several types of traction are used for this purpose. It is imperative that the nurse maintain the traction constantly and not interrupt the weight applied to the traction

Back 93

traction

Front 94

a temporary circumferential immobilizatoin device. It is often a common treatmetn following closed reduction it allows the patient to perform many normal activities of daily living while providing sufficient immobilization to ensure stability. The plaster hardens within 15 minutes so the patient may move around without difficulty; however, it is not strong enough for weight bearing until about 24-72 hours. A fresh cast should never be covered with a blanket because air cannot circulate and heat builds up in the cast. During the drying process the cast should not be subjected to any wetness, soiling or abnormal stressess that can cause weakening or a break in the cast. It should be carefully handled by the palms of the hands rather than the fingertips to avoid indentations that can become potential pressure areas

Back 94

cast

Front 95

consists of peripheral vascular assessment (Color, temperature, capillary refill, peripheral pulses, and edema) and a peripheral neurologic assessment (sensation, motor function and pain) throughout the neurovascular assessment both extremities are compared to obtain and accurate assessment.

Back 95

neurovascular assessment of an injured extremity

Front 96

The majority of fractures heal without complications. Complications of fractures may be either direct or indirect, direct complications include problems with bone infection, bone union, and avascular necrosis. Indirect complications of fractures are associated with blood vessel and nerve damage resulting in conditions such as compartment syndrome, venous thrombosis, fat embolism, and traumatic or hypovolemic shock. Although most musculoskeletal injuries are not life threatening, open fractures or fractures accompanied by severe blood loss and fractures that damage vital organs are medical emergencies requiring immediate attention

Back 96

complications associated with facture injury and fracture healing

Front 97

Postoperative procedures such as turning, deep breathing use of bedpan and bedside commode, and use of abductor pillows should be explained and opportunities for practice provided. The patietn should be reassured that pain relief will be available; PCA can be helpful. A preoperative visit from a physical therapist allows practice for postoperative exercises and measurement for crutches or other assistive devices. Discharge planning begins immediately. Patietn teaching includes instructions on reporting complications, including infection, dislocation of prosthesis

Back 97

postoperative management of the patient having joint replacement surgery

Front 98

used to treat infections caused by viruses other than HIV
Guanines:

Back 98

antiviral

Front 99

drug of choice for herpes-oral, IV or topical, HSV1, HSV2, VZV
Adverse reaction: N/V/D

Back 99

acyclovir

Front 100

CMV retinitis and systemic CMV infection IV or PO

Back 100

Acyclovir (DHPG)

Front 101

most common for RSV influenza type A and B, RSV, LV, HV

Back 101

Rebavirin (RTCD)

Front 102

influenza A
Foscarnet (Foscavir)-CMV (retinitis and systemic), HSV infection

Back 102

Amantadine(symmetrel) and rimantadine (Flumadine)-

Front 103

uncomplicated influenza decreasing severity of illness and length of time and zanamivir (relenza)

Back 103

Oseltamivir (tamiflu)-

Front 104

HSV-1, and HSV-2, VZV(chickenpox or shingles)
ganciclovir (cytovene)-CMV infections

Back 104

Acyclovir (zovirax)-

Front 105

CMV infections

Back 105

ganciclovir (cytovene)-

Front 106

lower respiratory RSV infections in infants (oral or nasal spray)

Back 106

Ribavirin(copegus)-

Front 107

burning when topically applied, N/V/D, headache

Back 107

Acyclovir side effects

Front 108

anticholinergic effects, lightheadedness, anorexia, nausea, others

Back 108

Amantadine and rimantadine side effects

Front 109

pancreatitis, peripheral neuropathies, seizures

Back 109

Didanosine: side effects

Front 110

bone marrow suppression, nausea, headache

Back 110

Zidovudine side effects

Front 111

headache, seizures, acute renal failure, N/V/D, others

Back 111

Foscarnet side effects

Front 112

bone marrow toxicity, nausea, anorexia, vomiting

Back 112

Ganciclovir side effects

Front 113

IV systemic funcal infection. Side effects: fever, headache, malaise, hypotension, msucle and joint pain, lowered potassium and magnesium levels, chills, dysrhthmias, nausea and anxiety. Main concerns: renal toxicity, nuerotoxicity: seizures and parestheisas. (mechanism of action: bind to sterols in cell membrane lining Result: fungal death.)

Back 113

Amphotericin B (ambisome):

Front 114

PO/IV, elevated liver function tests, nasuea (mechanism of action: taken up by fungal cells and interferes with DNA synthesis result: fungal cell death.
SE: N/V/D , stomach pain, increased liver function studies

Back 114

Fluconazole (diflucan)-

Front 115

hepatotoxic, given for ochymosis toenails, takes a long time to work, can be given or IV. casogfungin-IV
(mechanism of action: inhibit an enzyme, resulting in cell membrane leaking, lead to altered cell membrane result fungal cell death)
SE: N/V/anorexia headache, dizziness, others

Back 115

Ketoconazole, intraconazole

Front 116

disrupts cell division
Result: inhibited fungal mitosis (reproduction)
SE: rash, urinary, headache, nausea, vomiting, anorexia,others

Back 116

Griseofulvin