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69 Cards in this Set
- Front
- Back
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What is Amyotrophic Lateral Sclerosis (Lou Gehrigs Disease)
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rapidly progressing, fatal, degenerative, disease of the upper and lower motor neurons. Has no effect on intellectual ability, sensory function, vision, hearing, or bowel and bladder
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where do degenerative changes occur in ALS
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motor nuclei of brain stem, anterior horn cells of spinal cord and corticospinal tracts
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what does upper motor neuron involvement mean in ALS
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spasticity and decreased muscle strength
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what does lower motor neuron involvement mean in ALS
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flaccidity, paralysis, and muscle atrophy
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what is the cause of ALS
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unknown. Possible: genetic, slow acting virus, nutritional deficiency, metabolic, autoimmune disorder
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what are the symptoms of ALS
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muscle weakness and atrophy, muscle spasticity and hyperreflexia, fatigue, dysarthria and dysphagia, dyspnea, mental/ emotional
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how does muscle weakness spread
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hands to shoulders to upper arms to legs
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how do you diagnose ALS
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history, neuro exam, EMG, muscle biopsy, nerve conduction studies
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what are the treatments for ALS
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no know cure. Do PT/OT, speech therapy, have G tube/nutritional support, monitor respiratory funciton, counseling/support groups, patient/family teaching
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what is guillian- barre syndrome
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acute, progressive and potentially fatal inflammatory polyneuropathy affecting the peripheral nervous system.
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what does guillian-barre syndrome do to the peripheral nerves
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causes segmental demyelination, prevents normal transmission of electrical impulses along sensori-motor nerve roots. Autonomic nerve transmission may be impaired (bradycardia, hypo/hypertension, sweating)
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what is the cause of guillian barre syndrome
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majority report recent infection within 2 weeks prior to onset (URI, viral pneumonia, GI infection)
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what are the 3 phases of guillian barre syndrome
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acute-1-3 weeks
plateau-days- 2 weeks recovery- 4-6 months, may last 2-3 years |
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what are the symptoms of guillian barre syndrome
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ascending from legs to arms to face or descending from arms to legs or simultaneously. Return of function in reverse order
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what are complications of guillian barre syndrome
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thrombophlebitis, pressure ulcers, muscle wasting, sepsis, joint contractures, aspiration, resp. tract infections, resp. failure, sinus tachy/brady, hypertension/postural hypotension, loss of bowel and bladder control, SIADH
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how do you diagnose guillian barre syndrome
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elevated CSF protein-peaks in 7-10 days at 700 mg/dl (normal=15-45)
EMG Decreased NCV |
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what are the treatments for guillian barre syndrome
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primarily supportive, respiratory- patient airway, intubation, tracheostomy. Steroids, plasmaphoresis, IVIG, EKG monitoring, nutritional support, pain management, prevention of immobility problems, monitor lytes, bowel regime, psych/emotional needs, rehab, support services
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what is plasmaphoresis
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blood is removed a little at a time a separeted into RBCs and plasma, plasma discarded and replaced with fresh frozen plasma, albumin or plasma substitute and reconstituted blood infused
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what is the goal of plasmaphoresis
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temporary reduction of antibodies which are attacking the neuromuscular junction, leave enough antibodies so that overall immunity is not compromised.
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what are the risks of plasmaphoresis
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hypotension, allergic reaction, intolerance, requires central line
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what are the benefits of plasmaphoresis
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not a cure, helps with relief of symptoms, accelerated rate of recovery.
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what is an IVIG
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provides passive immunity through presence of injected antibodies
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when do you used an IVIG
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patient is deteriorating at time of diagnosis, patient is non-ambulatory at time of diagnosis, any evidence of respiratory dysfunction at time of diagnosis
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what are special considerations for an IVIG
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need to start infusion rate slow, continuous infusion of 1,3, or 5 days, do not mix with other meds, have epinephrine 1:1000 available
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what are advantages of IVIG
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simple to use, only requires peripheral IV access
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what are side effects of IVIG
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anaphylaxis, chemical meningitis, hypotension, renal failure, urticaria, angioedema, N/V, chills/ fever
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what is huntington's chorea
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hereditary disorder in which degeneration of cerrebral corex and basal ganglia causes chronic progressive chorea (involuntary and irregualr movements) and cognitive deterioration resulting in dementia
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what is the patho of huntingtons
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disturbance in neurotransmitter substances-primarily GABA deficiency and dopamine excess causing abnormal neurotransmission
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how is huntingtons transmitted
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autosomal dominant trait
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how do you diagnose huntingtons
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medical history, neuro assessment, MRI, CT, genetic testing,
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what are the signs and symptoms of huntingtons
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onset is insidious, progresses until totally dependent emotionally and physically. Progressive severe choreic movements secondary to excess dopamine, initially unilateral. Dysarthria,dysphagia, dementia, decreased short term memory, decreased impulse control, depression, mania, personality change
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what are compications of huntingtons
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chocking aspiration pneumonia, heart failure
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what is the treatment of huntingtons
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no know cure, symptom based. Haloperidol/diazepam, psychotherapy, nutritional (high caloric diet)
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what is myasthenia gravis
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chronic disease of failure in transmission of nerve impulses at the neuromuscular junction
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what is the patho of myasthenia gravis
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autoimmune response destroys a variable number of acetylcholine receptor sites at the post-synaptic muscle membrane
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what are the causes of myasthenia gravis
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unknown. Can be autoimmune response, thymus gland involvement.
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what are exacerbating factors of myasthenia gravis
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menstruation, pregnancy, infections, extremes in temp, exposure to sun (UV), emotional stress, drugs.
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what are the signs of myasthenia gravis
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usually gradual onset, ocular (ptosis, diplopia), facial/masticator/speech/swallow/neck, general weakness or fatigue, respiratory.
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how do you diagnose myasthenia gravis
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history, neuro exam, cholinesterase inhibitor drug testing, repetitive muscle stimulation, antibody titer for AChR, single fiber EMG, mediastinal MRI, pulmonary function tests
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what is the treatment for myasthenia gravis
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cholinesterase inhibitors-mestinon and protigmin
immunosuppression -glucocorticoids, azathioprine, cyclosporine -thymectomy -plasmaphoresis -IVGI |
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what is a myasthenic crisis
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sudden exacerbation of muscle weakness. May have swallowing difficulty, respiratory distress, tensilon test positive
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what is the causes of myasthenic crisis
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infection, missed meds
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what is the treatment for myasthenic crisis
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supportive until ChE-inhibitor drugs can be restarted
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what causes a cholinergic crisis
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precipitated by overmedication of ChE-inhibitor drugs
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what are symptoms of cholinergic crisis
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abdominal cramping/diarrhea, profound weakness, increased respiratory secretions and respiratory distress. tensilon test negative
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what is the treatment for a cholinergic crisis
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hold Che-inhibiting drugs
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what is the nursing interventions for myasthenia gravis
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monitor respiratory function, assessment of activity tolerance, monitor swallowing, teach family about rest periods and support and medic alert
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what is multiple sclerosis
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a demyelinating disease of the white matter of the brain and spinal cordd characterized by exacerbations and remissions
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what is the patho of multiple sclerosis
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demylination of white matter of brain and spinal cord with damage to nerve fibers. Prevent conduction of normal nerve impulse. Remissions =myelins heath regeneration
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what are the risk factors of multiple sclerosis
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family history, living in cold, damp, climate.
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what is the life expectancy of multiple sclerosis
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25 years
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what is the cause of multiple sclerosis
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viral infeciton or immunologic abnormalities
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what are the classifications of multiple sclerosis
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relapsing-remitting MS
primary-progressive MS secondary-progressive MS progressive-relapsing MS stable MS |
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what are the exacerbating factors of multiple sclerosis
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fatigue, excessive exertion, excessive heat or cold, infections, hot baths, fever, emotional stress, pregnancy, ocular, vestibular, sensory, motor, neurobehavioral, GI/GU, fatigue
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how do you diagnose multiple sclerosis
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made on the clinical grounds by exclusion of other disorders. No test definitive. MRI, SSEPs, CSF-elevated protein, elevated IgG.
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what is the drug therapy for multiple sclerosis
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corticosteroids, ACTH, interferon, Co-polymer 1, imuran, cytoxan, baclofen, diazepam, dantrolene Na
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how do you manage symptoms of multiple sclerosis
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PT, OT, patient/family teaching
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what is a seizure
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single event caused by a localized, discharge focus in the brain
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what is epilepsy
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chronic, recurrent seizures
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what is the cause of epilepsy
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unknown. Some genetic influence
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what are the causes of acute seizures
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fever, head injury, CNS infections, CNS tumors, cerebrovascular disease, hypoglycemia, hyponatremia, ETOH, drug overdose, vitamin deficiency, poisons (lead)
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what are the precipitating factors or triggers of a seizure or epilepsy
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odors, photo stimuli, music, lack of sleep, fatigue, medication non-compliance, emotional stress, constipation, menstruation, hyperventilation
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what are the classifications of epilepsy
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partial-simple or complex
generalized-generalized tonic/clonic (grand Mal) or absence Status epilepticus |
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how do you diagnose epilepsy
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history, toxicology screen, EEG, CT/ MRI, lumbar puncture
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what are the drug therapies of seizures and epilepsy
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phenytoin, phenobarbitol, carbamazepine, valproic acid, clonazepam, primidone, ethosuximide
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what is the surgical management of a seizure or epilepsy
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resection of epileptogenic focus
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what are the nursing interventions with a seizure
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safety-prevent injury, do not put anything in the mouth, turn to side
family teaching, sensory and motor assessment |
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what do you do in the sensory assessment
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light touch/pain, sharp/dull, eyes closed, recored highest level, dermatomes, proprioception, paresthesias
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What do you do in a motor assessment
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strength, upper extremities-hand grasps, biceps, triceps, pronator drift
lower extremities- dorsiflexion, plantar flexion, straight leg raising |
