neuro stressors 3 student
TRANSCRIPT
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Neurological Stressors III
Chronic Neurological DisordersJoy Borrero, RN, MSN
AndNUR240 Nursing Students
12/11
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Topics
Multiple Sclerosis Amyotropic Lateral Sclerosis (ALS)
Parkinsons Disease Myasthenia Gravis Guillain-Barre Syndrome
Huntingtons Disease
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Chronic Neuromuscular Dysfunction
Some commonalities in adaptations are: Altered motor activity Altered coordination Altered sensory function Altered urinary/bowel patterns Altered role/self perception Altered speech/swallowing
Impaired physical mobility Risk for injury Nutrition less than body requirements Risk for aspiration
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Multiple Sclerosis (MS)
Etiology:Types:S&S:
Dx:Triggers:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/ -
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Multiple Sclerosis
Chronic autoimmune disease affecting the myelinsheath and conduction pathway of the CNS
Characterized by periods of remission and
exacerbation Inflammatory response resulting in random or patchy areas of plaque in the white matter of theCNS
Demyelination of brain and spinal cord, affectsconduction pathway of CNS Two major courses: relapsing and remitting, and
chronic and progressive
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Multiple Sclerosis (MS)
Exact cause unknown, may be defective immuneresponse, early viral infection.
More common in people living in northern
temperate climate. Affects twice as many women than men. Typically occurs between ages 20-40 Family hx of MS in 15% of cases No cure for the disease Dx- McDonald criteria http://www.nmss.org/
http://www.nmss.org/http://www.nmss.org/ -
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MSPrimary Symptoms: Fatigue, weakness, numbness Difficulty in coordination, loss of balance Visual disturbances: blurring, diplopia, patchy or total
blindness, change in peripheral vision, nystagmus Speech defects Dysarthria, dysphagia Spastic weakness, ataxia, tremors, dysmetria Emotional lability, depression/euphoria. Bladder/bowel dysfunction Tinnitus, vertigo, decreasing hearing acuity Cognitive changes-memory loss, impaired judgement
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MS
Secondary symptoms-Problems/complications that occur a/r/oprimary symptoms
Repeated UTIs Loss of muscle tone and disuse weakness Poor posture and control of torso
Decreased bone density Shallow inefficient breathing Pressure ulcers from immobility
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PharmacologyBiological response modifiers- InteferonMonoclonal antibody- NatalizumabSynthetic protein-Glatiramer acetate
Immunosuppressives-CyclosporineCorticosteroids-PrednisoneAntispasmodic drugs-Dantrolene, BaclofenAnticonvulsants-Dilantin
Stool softeners-ColaceAnticholinergics-ProbanthineBeta-blockers- Inderal (tremors)CAM Therapy
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Biological Response Modifiers
Interferon Betaseron- blocks replicationof viruses and stimulates hostimmunoregulatory activities.
Reduce frequency of exacerbations Dose 0.25 mg sc every other day. Adverse effects: Dizziness, confusion,
anorexia, hypotension, leukopenia, flu likesymptoms, depression,suicidal ideation Thrombocytopenia
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Amytropic Lateral Sclerosis ALS
Etiology:Types:S&S:
Dx:Triggers:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/ -
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Amyotrophic Lateral Sclerosis(ALS)
Deteriorating disease of motor neurons inanterior horn of spinal cord and motor nuclei of lower brain stem
AKA Lou Gehrigs disease Etiology unknown. More common men 50-60. Manifestations: Depends on location of affected
motor neurons, atrophy and twitching. Death occurs within 2-5 years after onset of
symptoms.
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Diagnostic Procedures
Creatine kinase (CK)- increased Electromyography (EMG)- Muscle
fasciculations
http://www.youtube.com/watch?v=k0uSpYd_Ics
Muscle biopsy- Muscle atrophy
Serial muscle testing- Loss of musclestrength Pulmonary function tests
http://www.youtube.com/watch?v=k0uSpYd_Icshttp://www.youtube.com/watch?v=k0uSpYd_Icshttp://www.youtube.com/watch?v=k0uSpYd_Icshttp://www.youtube.com/watch?v=k0uSpYd_Ics -
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Assessments & Interventions
Assess airway, resp status Assess speech patterns, skin integrity
No known cure, no treatment, nopreventive measures Riluzole, only drug approved by FDA to
extend survival time Exercise and mobility program Management of swallowing difficulties
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Interventions
Teach swallowing technique Maintain resp. function- assess lung
sounds,suction prn, C&DB Administer Quinine for muscle cramps Antispasmotics: baclofen, dantrolene, diazepam
www.als.org for pt/family support and education
http://www.als.org/http://www.als.org/ -
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Parkinsons Disease
Etiology:Types:S&S:
Dx:Triggers:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/ -
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Parkinsons disease Cause unknown-progressively debilitating disease
that affects gross motor function.Degeneration of the nerves that control voluntary
movement.Occurs in the part of the brain called the substantia
nigraNeurons here communicate with other neurons in the
brain using a neurotransmitter called dopamine.
When these neurons that make dopamine die,signaling between neurons is severely hampered,causing a loss of controlled movement
Risk factors
Dx Procedures
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Manifestations
Manifestations: Stooped posture, postural instability , head
bent forward Tremors of head and hand, pill rolling Akinesia , Bradykinesia Rigid stance, shuffling and propulsive gait
Mask like facial expression
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Parkinsons disease
Impaired physical mobility r/t musclerigidity and weakness.
Self care deficit r/t to tremor and motor disturbance.
Risk for falls Risk for imbalanced nutrition: Less than
body requirements, r/t tremor, slowness ineating, difficulty in chewing andswallowing.
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Drug Therapy for Parkinsons Goal: Increase patients functional abilities
PDMeds
Levodopa
COMTInhibitors
MAOI:
Eledepryl
Amantadine:Symmetrel
Dopamine Agonists:
Mirapex
Anticholinergics:
Cogentin
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Parkinsons disease
levodopa (Dopar, Laradopa)- antiparkinsonagent, precursor of dopamine that cancross the blood brain barrier, then istransformed to dopamine.
levodopa and carbidopa ( Sinemet )- GOLDSTANDARD, antiparkinsonian combo med-dosage is adjusted to patients symptoms
Adverse effects involuntary movements,ataxia, increased tremor, anorexia
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Parkinsons disease
Amantadine hydrochloride (Symmetrel) Antiviral and Antiparkinsonian Therapeutic actions thought to increase
dopamine release, helpful in treatingbradykinesia, rigidity and tremor.
Dose 100 mg po bid (up to 400 mg)
Adverse- dizziness, insomnia, dry mouth,confusion, constipation, urinary retention,orthostatic hypotension.
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Parkinsons Disease
Complications: Aspiration pneumonia Altered cognition, dementia
Additional therapeutic options:ThalamotomyStereotactic PallidotomyDeep Brain Stimulation
http://www.parkinsons.org
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Myasthenia Gravis
Etiology:Types:S&S:
Dx:Triggers:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/ -
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Myasthenia Gravis
Progressive autoimmune disease resulting insevere muscle weakness.Women 15-35 or men over 40.
Exacerbations and remissionsManifestations:Extreme muscle weakness and fatiguability.Diplopia and ptosis are early signsSleepy, mask like expression, dysphonia.Problems chewing and swallowing aspirationProgressive weakness of diaphragm- resp. distress.
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Myasthenia Gravis
Diagnostic tests pt. history and exam,Tensilon testing
IV tensilon relieves symptoms within 30seconds. Positive result.
AChR-Acetylcholine receptor antibodiesfound serum of 90%.
EMG- shows neuromuscular transmissioncharacteristics.
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Therapeutic Procedures
Plasmapheresis Thymectomy
http://www.myasthenia.org
http://www.myasthenia.org/http://www.myasthenia.org/ -
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Medications
Anticholinesterase meds- pyridostigmine(Mestinon) and ambenonium (Mytelase)
Administer with small amount of food toavoid GI upset and eat within 45 minutes.
Must be administerd on time and sametime each day.
Potential SE is cholinergic crisisCotricosteroidsImmunosuppressants
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ComplicationsMyasthenic Crisis
Undermedication
Cholinergic Crisis
OvermedicationResp muscle weakness-mechanical ventilation
Muscle twitching results inresp muscle weakness, mechventilation
Myasthenic symptoms-weakness,incontinence,fatigue
Cholinergic symptoms-hypersecretions,hypermotility
Hypertension Hypotension
Temp improvement of symptoms with Tensilon
Tensilon has no positive effecton symptomsSymptoms improve with
anticholinergic meds
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Guillain-Barre Syndrome
Etiology:Types:S&S:
Dx:Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/ -
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Guillian Barre Syndrome
Acute inflammatory disease of unknownorigin
Usually preceeded by a viral infection (URIor GI) 1-4 weeks
Degeneration of the myelin sheath of peripheral nerves
Manifestations: paresthesias, ascendingweakness in legs progresses toparalysis,autonomic dysfunction
Diagnosis by H&P, CSF exam.
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Facts
Most people reach the stage of greatestweakness within 2 weeks after symptomsappear, and by the 3 rd week 90% of all
patients are at their weakest. Recovery may be from a few weeks to a
few years
30% will have residual weakness after 3yrs 3% may suffer a relapse
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Huntingtons Disease
Etiology:S&S:Dx:
Tx:
http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/http://www.nmss.org/ -
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MANAGEMENT
Dx: made on basis of symptoms and familyhx
Genetic counseling and testingTx: Haldol and Navane
Riluzole Antidepressants