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91 Cards in this Set
- Front
- Back
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What is Guillain-Barre Syndrome (GBS)?
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An acute infectious neuronitis of the cranial and peripheral nerves. Rapidly progressive and potentially fatal motor neuropathy
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What is Guillain-Barre Syndrome the result of?
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A variety of related immune mediated pathological processes that DESTROY THE MYELIN SHEATH IN THE AXONS OF THE PERIPHERAL NERVES.
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Most clients report having what acute illness before the development of Guillain-Barre Syndrome symptoms?
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Gastroenteritis caused by an upper respiratory infection.
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Signs and symptoms of Guillain-Barre Syndrome?
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Ascending symmetric muscle weakness leading to flaccid paralysis without muscle atrophy; decreased or absent deep tendon reflexes, ataxia, incontinence, DYSPNEA, DIMINISHED BREATH SOUNDS, RESPIRATORY FAILURE, parestesias, muscle cramps, dysarthria, dysphagia, diplopia, cardiac dysrhythmias
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What is the major concern with GBS?
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The major concern with GBS is DIFFICULTY BREATHING
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What tests are used to diagnose GBS?
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CSF analysis by lumbar puncture (will reveal elevated protein levels); CBC count will show leukcytosis with immature cells and increased immunoglobulin; Electromyography shows repeated firing of the same motor unit instead of widespread sectional stimulation; Nerve conduction tests will show slowing
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Treatments for GBS?
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Usually self limiting- PERIPHERAL NERVES HAVE THE ABILITY TO REGENERATE; may need endotracheal intubation or tracheotomy with mechanical ventilation; plasmapheresis (to remove autoantibodies); continuous ECG monitoring, IV immunoglobulin; corticosteroids; rehabilitation; pain management for neuropathy
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Most important nursing considerations for GBS?
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ASSESS RESPIRATORY STATUS EVERY 1-2 HRS; ELEVATE HOB 45 DEGREES; SUCTION AS NEEDED; PLACE CLIENT ON CARDIAC MONITOR B/C AT HIGH RISK FOR DYSRHYTHMIAS; ASSESS MOTOR FUNCTION EVERY 2-4 HRS; MONITOR SKIN INTEGRITY
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What is Myasthenia Gravis?
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Neuromuscular disorder that is characterized by considerable weakness and abnormal fatigue of the voluntary muscles.
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Who does Myasthenia Gravis occur in more often?
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Occurs slightly more often in women, women are commonly affected in their 20s and 30s while men are usually affected in their 60s and 70s.
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Pathophysiology of Myasthenia Gravis
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AUTOANTIBODIES ATTACK THE ACETYLCHOLINE RECEPTORS (AChR) in the muscle end plate membranes
--> decreased numbers of receptors --> failure of the nerve impulses to be transmitted to the skeletal muscle at the neuromuscular junction --> inability of the muscles to contract |
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Causes of Myasthenia Gravis?
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Insufficient secretion of acetylcholine, excessive secretion of cholinesterase, and unresponsiveness of the muscle fibers to acetylcholine, however, the exact cause is unknown.
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Risk factors//Predisposing factors for Myasthenia Gravis?
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AUTOIMMUNE response; small familial incidence; THYOMA (encapsulated thymus gland tumor); HYPERTHYROIDISM; bone marrow transplant
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S/S of Myasthenia Gravis?
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WEAKNESS AND FATIGUE (CLIENT IS THE STRONGEST IN THE MORNING), PTOSIS, weak eye closure, diplopia, difficulty chewing, dysphagia, RESPIRATORY PROBLLEMS DUE TO INEFFECTIVE COUGH, weak hoarse voice, diminished breath sounds
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Diagnostic testing for Myasthenia Gravis?
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TENSILON TEST CONFIRMS THE DIAGNOSIS; Electromyography with repeated neural stimulation shows progressive decrease in muscle fiber contraction; Chest x-ray reveals thyoma; Increased serum anti-acetylcholine antibody titer
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Nursing considerations for Myasthenia Gravis
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Monitor RESPIRATORY STATUS and ability to cough and deep breathe adequately; Monitor for respiratory failure; Keep Ambu bag, oxygen, suctioning equipment and endotracheal intubation tray at bedside; Avoid excessive fatigue, stress and infection; Assess muscle strength; Rest is critical because increased fatigue can precipitate a crisis; MONITOR FOR SUDDEN INCREASE IN WEAKNESS AND INABILITY TO CLEAR SECRETIONS, SWALLOW, OR BREATHE (INDICATES SOME FORM OF CRISIS); APPLY ARTIFICIAL TEARS, TAPES EYES AT NIGHT (PTOSIS); determine ability to communicate, dysarthria can occur; Assist with plasmapheresis.
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Treatments/Medications for Myasthenia Gravis
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ANTICHOLINESTERASE DRUGS (these increase levels of acetylcholine at the myoneural junction) such as: NEOSTIGMINE, PYRIDOSTIGMINE AND EDROPHONIUM; Immunosuppressant therapy with corticosteroids, azathioprine, cyclosporine, and cyclophosphamide; Plasmapheresis; Immunoglobulin G; Thymectomy; Tracheotomy, mechanical ventilation
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What is the Tensilon test and how is it performed?
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Temporarily improves muscle function within 30-60 seconds after IV injection of edrophonium or neostimine and lasts up to 30 minutes. It is performed to diagnose Myasthenia Gravis and to differentiate between Myasthenic crisis and Cholinergic crisis.
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Tensilon test- What indicates a positive diagnosis of Myasthenia Gravis?
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Positive for MG: the client shows improvement in muscle strength after the administration of Tensilon.
Negative for MG: client shows no improvement in muscle strength, and strength may even deteriorate after injection of Tensilon. |
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Tensilon test- How to differentiate between Myasthenic crisis and Cholinergic crisis?
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To differentiate crisis:
Myasthenic crisis: Tensilone is administered, and if strength improves, the client needs more medication. Cholinergic crisis: Tensilon is administered, and if the client's weakness is more severe, then the client is overmedicated; administer atropine sulfate (the antidote) as prescribed. |
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What is a Cholinergic crisis?
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CAUSES BY OVERMEDICATION WITH ANTICHOLINERASE. With this crisis, MUSCLE TONE DOES NOT IMPROVE AFTER GIVING TENSILON. Cholinergic crisis results in depolarization of the motor end plates
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What should be readily available in the case of a Cholinergic crisis?
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Atropine sulfate (the antidote for anticholinesterase drugs)
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What are the S/S of a Cholinergic crisis?
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ABDOMINAL CRAMPS, N/V, diarrhea, BLURRED VISION, pallor, FACIAL MUSCLE TWITCHING, hypotension, papillary miosis, bradycardia
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What is Myasthenic Crisis?
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Myasthenic crisis is an acute exacerbation of the disease (Myasthenia Gravis)
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What causes a Myasthenic crisis?
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Caused by a rapid, unrecognized progression of the disease; an inadequate amount of medication; infection; fatigue or stress
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What intervention should be done in the case of a Myasthenic crisis?
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If this crisis occurs, increase anticholinesterase medication, as prescribed
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S/S of Myasthenic crisis
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Increased pulse, respirations and B/P; RESTLESSNESS, DYSPNEA, anoxia, cyanosis, total incontinence, decreased urine output, INCREASED SALIVATION/TEARING, absence of cough or swallow reflex
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What is the definition of mydriasis?
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Mydriasis- prolonged abnormal dilation of the pupil.
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What is the definition of xerostomia?
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Xerostomia- abnormal dryness of the mouth resulting from decreased secretion of saliva.
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What other term is Trigeminal Neuralgia refered to as?
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Tic douloureaux
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What cranial nerve does Trigeminal Neuralgia affect?
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Disease that affects the trigeminal, or cranial nerve V.
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What does Trigeminal Neuralgia result in?
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Trigeminal Neuralgia results in severe, recurrent, sharp, facial pain or facial spasms along the trigeminal nerve.
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What provokes Trigeminal Neuralgia?
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Provoked by minimal stimulation such as cold, washing the face, chewing, or food or fluids of extreme temperatures.
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S/S of Trigeminal Neuralgia
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Classic syndrome: UNILATERAL, EXCRUCIATING, sharp, shooting, piercing, burning, and stabbing PAIN lasting seconds to minutes, with remissions, with no sensory or motor deficits on examination. Atypical syndrome: continuous burning sensation that involves the entire face with or without remission periods.
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Treatments for Trigeminal Neuralgia
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Drug therapy with antiepileptic drugs:CARBAMAZEPINE (TEGRETOL) AND GABAPENTIN (NEURONTIN) IS USED FIRST; glycerol injection; Phenytoin (Dilantin); Muscle relaxants such as Baclofen (Lioresal); Percutaneous rhizotomy (needle is inserted and nerve root resected); Radiofrequency (creates nerve lesions); Balloon microcompression of the nerve root; microvascular decompression.
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Nursing considerations for Trigeminal Neuralgia
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PAIN MANAGEMENT IS THE PRIORITY OF CARE; administer medications as prescribed; Instruct the client to AVOID TALKING, SMILING, SHAVING, WASHING FACE, AND BRUSHING THE TEETH (modify oral hygiene, rinse mouth); AVOID WALKING SWIFTLY PAST THE CLIENT; NO FANS; DISCOURAGE CHEWING ON THE AFFECTED SIDE; PROVIDE SMALL FEEDINGS OF LIQUID OR SOFT FOODS; NO HOT OR COLD FLUIDS
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What is Transient ischemic attack (TIA) also known as
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TIA is also called a silent stroke or a reversible ischemic neurologic deficit
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What is a transient ischemic attack?
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A temporary neurologic dysfunction resulting from a BRIEF INTERRUPTION IN CEREBRAL BLOOD FLOW
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How long does a TIA usually last?
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TIA usually lasts a few minutes to fewer than 24 hours. Typically, symptoms of a TIA resolve within 30-60 minutes
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S/S of Transient Ischemic Attack
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S/S: Blurred vision, diplopia, blindness in one eye, tunnel vision; unilateral weakness in the arm, hand, or leg; Gait distubance (ataxia); Unilateral numbness in the face, arm, or hand; Vertigo; Aphasia; DYSARTHRIA (SLURRED SPEECH)
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What can repeated TIAs cause?
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Repeated TIAs may damage the brain tissue, as seen on MRI or CT scans, and indicate HIGH RISK FOR STROKE
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Upon discharge from the emergency department following a TIA what is the client usually placed on?
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At discharge the client is usually placed in anticoagulant therapy (ASA, Plavix) unless conraindicated.
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What does the National Stroke Association now refer to stroke as?
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The term brain attack is used to describe a stroke
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What is a stroke cause by?
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A stroke is caused by a change in the normal blod supply to the brain (altered cerebral perfusion)
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Why is a stroke that strikes suddenly a medical emergency?
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A stroke that strikes suddenly is a medical emergency, and should be treated immediately to prevent neurologic deficit and permanent disability.
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Where does stroke rank on causes of death worldwide?
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Stroke is the 2nd most common cause of death and major disability worldwide
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Pathophysiology of a stroke
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Regardless of the cause (thrombosis, embolism, or hemorrhage), the underlyin event is deprivation of oxygen and nutrients
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Pathophysiology of a thrombotic or embolic stroke?
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Thrombotic or embolic stroke --> ischemia --> cerebral infarction, cellular injury, and edema --> further damage
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Pathophysiology of a hemorrhage stroke?
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Hemorrhage --> occupation of space; body attempts to maintain equilibrium by increasing B/P --> increased intracranial pressure --> further ischemia --> tissue death
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Pathophysiology of a stroke
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Regardless of the cause (thrombosis, embolism, or hemorrhage), the underlyin event is deprivation of oxygen and nutrients
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Risk factors for stroke (brain attack)?
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Risk factors: ATRIAL FIBRILATION, arteriosclerosis, HTN, brain trauma, atherosclerosis, artervenous malformation; previous stroke, TIA, heart surgery; DIABETES MELLITIS, SMOKING, COCAINE, ALCOHOL, OBESITY, SEDENTARY LIFESTYLE, CONTRACEPTIVES; hyperlipidemia, migraines, OLDER AGE; MALE, AFRICAN AMERICAN, hispanic or American Indian, sickle cell anemia
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S/S of a stroke?
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S/S: HEMIPARESIS, HEMIPLEGIA, altered LOC; Sudden SEVERE HEADACHE (HEMORRHAGIC; ANEURYSM), dizziness, and anxiety; Ataxia, vertigo, and coordination problems; Aphasia (EXPRESSIVE, RECEPTIVE, OR BOTH WHICH IS GLOBAL), dysarthria, dysphagia; HEMIANOPIA, DIPLOPIA, FACIAL ASYMMETRY
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Pathophysiology of a thrombotic or embolic stroke?
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Thrombotic or embolic stroke --> ischemia --> cerebral infarction, cellular injury, and edema --> further damage
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Pathophysiology of a stroke
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Regardless of the cause (thrombosis, embolism, or hemorrhage), the underlyin event is deprivation of oxygen and nutrients
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S/S of a left hemisphere stroke?
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Left hemisphere: APHASIA, possible memory impairment, reading problems, right hemianopia, SLOW, CAUTIOUS, depression, right hemiplegia
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Pathophysiology of a hemorrhage stroke?
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Hemorrhage --> occupation of space; body attempts to maintain equilibrium by increasing B/P --> increased intracranial pressure --> further ischemia --> tissue death
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S/S of a right hemisphere stroke
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Right hemisphere: Disorientation, left hemianopia, IMPULSIVENESS, POOR JUDGEMENT, confabulation, euphoria, constant smiling, hearing problems, left hemiplegia
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Risk factors for stroke (brain attack)?
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Risk factors: ATRIAL FIBRILATION, arteriosclerosis, HTN, brain trauma, atherosclerosis, artervenous malformation; previous stroke, TIA, heart surgery; DIABETES MELLITIS, SMOKING, COCAINE, ALCOHOL, OBESITY, SEDENTARY LIFESTYLE, CONTRACEPTIVES; hyperlipidemia, migraines, OLDER AGE; MALE, AFRICAN AMERICAN, hispanic or American Indian, sickle cell anemia
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Proprioception alterations
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Proprioception alterations: unaware of body position in space
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Pathophysiology of a thrombotic or embolic stroke?
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Thrombotic or embolic stroke --> ischemia --> cerebral infarction, cellular injury, and edema --> further damage
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S/S of a stroke?
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S/S: HEMIPARESIS, HEMIPLEGIA, altered LOC; Sudden SEVERE HEADACHE (HEMORRHAGIC; ANEURYSM), dizziness, and anxiety; Ataxia, vertigo, and coordination problems; Aphasia (EXPRESSIVE, RECEPTIVE, OR BOTH WHICH IS GLOBAL), dysarthria, dysphagia; HEMIANOPIA, DIPLOPIA, FACIAL ASYMMETRY
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Expressive aphasia
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EXPRESSIVE APHASIA: INABILITY TO SPEAK
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Pathophysiology of a hemorrhage stroke?
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Hemorrhage --> occupation of space; body attempts to maintain equilibrium by increasing B/P --> increased intracranial pressure --> further ischemia --> tissue death
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S/S of a left hemisphere stroke?
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Left hemisphere: APHASIA, possible memory impairment, reading problems, right hemianopia, SLOW, CAUTIOUS, depression, right hemiplegia
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Risk factors for stroke (brain attack)?
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Risk factors: ATRIAL FIBRILATION, arteriosclerosis, HTN, brain trauma, atherosclerosis, artervenous malformation; previous stroke, TIA, heart surgery; DIABETES MELLITIS, SMOKING, COCAINE, ALCOHOL, OBESITY, SEDENTARY LIFESTYLE, CONTRACEPTIVES; hyperlipidemia, migraines, OLDER AGE; MALE, AFRICAN AMERICAN, hispanic or American Indian, sickle cell anemia
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S/S of a right hemisphere stroke
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Right hemisphere: Disorientation, left hemianopia, IMPULSIVENESS, POOR JUDGEMENT, confabulation, euphoria, constant smiling, hearing problems, left hemiplegia
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Receptive aphasia
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RECEPTIVE APHASIA- INABILITY TO UNDERSTAND SPOKEN WORK
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S/S of a stroke?
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S/S: HEMIPARESIS, HEMIPLEGIA, altered LOC; Sudden SEVERE HEADACHE (HEMORRHAGIC; ANEURYSM), dizziness, and anxiety; Ataxia, vertigo, and coordination problems; Aphasia (EXPRESSIVE, RECEPTIVE, OR BOTH WHICH IS GLOBAL), dysarthria, dysphagia; HEMIANOPIA, DIPLOPIA, FACIAL ASYMMETRY
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Proprioception alterations
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Proprioception alterations: unaware of body position in space
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Expressive aphasia
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EXPRESSIVE APHASIA: INABILITY TO SPEAK
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S/S of a left hemisphere stroke?
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Left hemisphere: APHASIA, possible memory impairment, reading problems, right hemianopia, SLOW, CAUTIOUS, depression, right hemiplegia
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S/S of a right hemisphere stroke
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Right hemisphere: Disorientation, left hemianopia, IMPULSIVENESS, POOR JUDGEMENT, confabulation, euphoria, constant smiling, hearing problems, left hemiplegia
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Receptive aphasia
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RECEPTIVE APHASIA- INABILITY TO UNDERSTAND SPOKEN WORK
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Proprioception alterations
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Proprioception alterations: unaware of body position in space
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Expressive aphasia
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EXPRESSIVE APHASIA: INABILITY TO SPEAK
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Receptive aphasia
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RECEPTIVE APHASIA- INABILITY TO UNDERSTAND SPOKEN WORK
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Agraphia
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Agraphia: difficulty writing
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Hemiplegia
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Hemiplegia: Paralysis on one side
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Hemiparesis
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Hemiparesis: Weakness on one side
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Agnosia
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Agnosia: Inability to use object correctly
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Apraxia
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Apraxia: inability to carry out a purposeful activity
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Hemianopia
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HEMIANOPIA (ALSO CALLED HEMIANOPSIA) BLINDNESS IN HALF OF THE VISUAL FIELD
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Homonymous hemianopia
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Homonymous hemianopia: blindness in the same visual field of both eyes
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Neglect syndrome (unilateral neglect)
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Neglect syndrome (unilateral neglect): unaware of the existence of paralyzed side
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Pyramid point
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Pyramid point: with visual problems, client must turn the head to SCAN THE COMPLETE RANGE OF VISION
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What are data collection findings in a stroke?
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Proprioception alterations; EXPRESSIVE APHASIA; RECEPTIVE APHASIA; Agraphia; Hemiplegia; Hemiparesis; Agnosia; Apraxia; HEMIANOPIA; Homonymous hemianopia; Neglect syndrome (unilateral neglect); Pyramid point
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Diagnostics for a stroke?
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CT scan identifies ischemic result within first 72 hours of symptom onset and evidence of hemorrhagic stroke (>1 cm lesion) immediately; MRI identifies area of ischemia or infarction, and edema; Arteriography reveals disruption of cerebral circulation; carotid duplex scan identifies stenosis
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Treatment for ischemic stroke?
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Treatment for ischemic stroke: Thrombolytic therapy with tissue plasminogen activator within 3 hours of symptom onset; ASA, warfarin, heparin; Carotid endarterectomy; cerebral angioplasty and stents
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Treatment for hemorrhagic stroke:
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Aneurysm clipping, coiling (aneurysm embolization) - blocks blood flow to the aneurysm
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Stroke- nursing considerations in the acute phase?
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Priority is the ABCs; MAINTAIN AIRWAY and administer oxygen as prescribed; Monitor VS, maintain a B/P of 150/100 mm Hg or as prescribed to maintain cerebral perfusion; NO B/P ON AFFECTED SIDE (DECREASES MUSCLE TONE --> INACCURATE LOW READING) Suction as ordered, but NEVER SUCTION NASALLY or for > than 10 seconds; Monitor for increased ICP (client at greatest risk during the first 72 hrs after stroke); Assist with ICP monitoring device insertion; HOB should be flat or elevated no > than 30 degrees to increase blod flow to the brain; position on side; Monitor LOC, pupillary response, motor and sensory respose, CN function, and reflexes; Maintain a QUIET ENVIRONMENT, and provide MINIMAL HANDLING of the client to prevent further bleeding (hemorrhagic); insert a foley catheter as prescribed; Monitor prescribed IV fluids; maintain fluid and electrolyte balance; prepare to administer thrombolytic therapy as prescribed; Prepare to administer anticoagulants, antiplatelets, diuretics, antihypertensives, and anticonvulsants as prescribed; establish a form of communication
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Stroke- nursing considerations in post-acute phase?
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Continue with interventions from acute phase; position the client 2 hours on unaffected side, 20 minutes on affected side; posistion the client in prone position, if prescribed, for 30 minutes 3 times daily; provide skin, mouth and eye care; perform PASSIVE ROM exercises and PROPER POSITIONING TO PREVENT CONTRACTURES; PLACE ANTIEMBOLISM STOCKING on client; SPLINTS AND FOOTBOARD to prevent foot drop; Measure thighs and calves for increased in size (DVT); Monitor GAG REFLEX, SWALLOW, AND LUNG SOUNDS; Provide sips of fluids and slowly advance diet to foods that are easy to chew and swallow; Provide soft and semisoft foods, provide thickened liquids; When the client is eating, POSITION UPRIGHT, WITH HEAD AND NECK POSITIONED SLIGHTLY FORWARD AND FLEXED; place food in the back of the mouth on the unaffected side to prevent trapping of food in the buccal pocket of the affected cheek; Start scheduling toileting; encourage use of canes and walkers for stability
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