Peripheral Neurological Disorders & Central Nervous Center Slideshow Transcript
Slide 1: Peripheral Neurological Disorders MG, GB
Slide 2: Common Nursing Diagnoses(there are more…) Mobility, Impaired Physical Self Care Deficit Disturbed Self Esteem Fatigue Respiratory Function, risk for impaired Risk for Injury Pain
Slide 3: Myasthenia Gravis: “grave muscle weakness” Affects about one of every 7,500 people, all ethnic groups affected Onset usually between age 20 to 40 for women. Later age of onset tends to include more men.
Slide 4: Pathophysiology Autoimmune response: decreases the number of available acetylcholine receptors at the nerve to muscle junction. Antibodies bind to the receptor sites, render them useless. Without Ach receptors there is muscle weakness. Frequently goes with Thymus abnormalities
Slide 5: Symptoms of MG: gradual onset common Weakness in muscles needed to talk, chew, swallow. Ptosis Drooling Later, limb weakness, respiratory muscle weakness
Slide 6: High Risk Nursing Care Issues Choking and/or aspiration during eating and drinking Insufficient breathing effort due to muscle weakness leads to respiratory crisis Falling
Slide 7: Diagnosis of Myasthenia Gravis H & P: for signs and symptoms of muscle weakness, patterns MRI or CT of Thymus Labwork: look for increased antibody levels in blood Tensilon Test. Tensilon is a short acting anticholinesterase inhibitor. Give to patient, if see dramatic but short lived improvement in symptoms, + for MG. When physician is doing test, have atropine available.
Slide 8: Myasthenic Crisis Patient with MG can present with a severe bout of symptoms, especially respiratory— may present like anxiety. Prevention involves taking care re precipitants: menses, pregnancy (read in Lewis), stress, infection, over-exertion. Since overmedication can also cause problems (cholinergic crisis), differentiate carefully.
Slide 9: Treatment with Medication Anticholinesterase drugs: inhibit the destruction of acetylcholine and thus make more acetlycholine available at receptor sites. Two common ones are Prostigmin (neostigmine) and Mestinon (pyridostigmine). Best taken about an hour prior to meals. Also use prednisone (decrease inflammatory response), other immunosuppressants, plasmapheresis, thymectomy
Slide 10: Guillain-Barre’ Syndrome Acute inflammatory process with varying degrees of motor weakness and paralysis Immune system destroys the myelin sheath – affects cranial, motor, and sensory neurons
Slide 11: Epidemiology 0.4-1.7 cases per 100,000 Affects all races and ages, but more often seen among those over 45 and Caucasian
Slide 12: Symptoms of GB Flaccid paralysis with absent reflexes Respiratory weakness/failure Pain and paresthesias Facial weakness with double vision and trouble speaking
Slide 13: Respiratory Care
Slide 14: Medications
Slide 15: Other nursing care issues
Slide 19: Unit 8 CNS Problems: Read about Headaches and treatment Read about Huntingtons Disease and treatment Read about different types of Seizures In this unit we will discuss Parkinson Disease, Alzheimer’s Disease, MS, and SCI in class
Slide 20: Multiple Sclerosis: “Many areas of patchy destruction” About 250,000 to 300,000 people with MS in the USA. More common among those living in the North, Caucasian descent. Typical onset is in young and middle adult years.
Slide 21: Destruction of Myelin Sheath
Slide 22: MS Symptoms: Early and Later Early: Nystagmus, diplopia, blurry vision, mild weakness, poor sensation, paresthesias. Pattern is quite variable, which makes diagnosis difficult Middle/Later: More serious weakness of limbs, and can include paralysis, spasticity, ataxia. Numbness/tingling worsened. Continued eye, ear problems. Bowel and Bladder function may be affected Emotionally difficult disease, Labile mood.
Slide 23: Diagnosis of MS is Difficult No definitive test for MS H & P remains central MRI – look for plaques on neurons Evoked potential study CSF analysis, labwork
Slide 24: Medical Treatment of MS: medication therapy Bethanecol Glucocorticoids Immunosuppressants Skeletal muscle relaxants, eg Baclofen and Dantrolene
Slide 25: MS: Multiple Nursing Care Issues Help the client avoid triggers to exacerbation and to moderate activity level Later, immobility becomes a real issue, and the complications of immobility require vigilant care Read your text re care plan.
Slide 26: Assessment of seizure activity Observe, time and document carefully Body movements, character, type progression, include eye movements Loss of consciousness, incontinence Precipitating factors you note Post seizure (ictal) response. Confusion, sleepiness common.
Slide 27: Issues in Seizure Precautions Tongue blade is outdated Suction equipment nearby, IV or hep. lock if risk is high for venous access Padding on bedrails/Observe client often Avoid precipitants Notify MD of new seizure, injury, unrelenting seizure activity If client seizes, move objects away, side lying if possible, loosen tight clothing, ease to floor or bed if possible
Slide 28: Status Epilepticus Defined as seizure over 4 minutes or in rapid succession Life threatening due to brain damage mainly Response involves ABC’s, IV administration of anticonvulsants in a particular order. Usually valium first, if no response, dilantin and later a third drug are used. NG to control vomitus possibly. Review Anticonvulsant drugs discussed earlier
Slide 29: Parkinson’s Disease: Triad 1. Tremor: hands, feet, steady rate, resting, “pill rolling” 2. Rigidity: stiffening up, cogwheeling 3. Bradykinesia: less movement inc. trunk, masklike face, moving “en bloc” and festinating gait (shuffling with accelerations)
Slide 30: More Parkinson’s Symptoms Decreased volume and variability of voice Micrographia Depression 50% Dementia 10-40% Psychosis 10% Chronic, progressive disease
Slide 31: Pathophysiology Pathway for disposing of flawed proteins (Uch-Ll) is disturbed, leading to neuron death in substantia nigra. There is less dopamine available, symptoms don’t occur until about 80% destroyed. Gene on chromosome 4 is implicated in the disease
Slide 32: Nursing Care of PD FASE: avoid fatigue, anxiety, stimulation, and exertion Multiple care issues: injury prevention, self care, nutrition, dysphagia, activity and rest, mobility, communication deficit, despair/grief, altered thought process, and knowledge deficit
Slide 33: Surgical Treatment of PD Pallidotomy: globus pallidus (which is overactive in PD) is partly ablated—SE is occasional speech impairment Electronic Stimulator placement: Small wire is set into brain and has a device placed in chest wall that can be stimulated to control increased tremors
Slide 34: Meds for Parkinson’s D. Levodopa—the precursor to dopamine This drug chemically reverses the effect of PD, enhances amt. of dopamine SE: nausea, hypotension, agitation and hallucinations After several years, efficacy may decline Don’t take with B-6 or if you have narrow angle glaucoma
Slide 35: Sinemet: levodopa and carbidopa Adding carbidopa to levodopa allows smaller dose of levodopa and fewer side effects Carbidopa prevents the breakdown of levodopa When taking: have LFTs, RFTs, CBC Many meds reverse the effect: antipsychotics, dilantin, reserpine
Slide 36: Selegiline: Eldepryl MAOB inhibitor: decreases the degradation of dopamine (note similarity to MAOIs) Careful use: many serious interactions (opiods, SSRI’s, TCA’s) Limit tyramine rich foods in diet (You will need to get familiar with list)
Slide 37: Other meds in PD Tasmar Mirapex TCA’s Requip Antihistamines For test know sinemet, eldepryl Symmetrel and be aware of Parlodel others Pergolide
Slide 38: Dementia: Basic Definitions Progressive deterioration in intellectual functioning – MEMORY, LEARNING, and JUDGEMENT Onset insidious, chronic, and may be a primary disorder
Slide 39: Types of Dementias-some Alzheimers DAT—see pathophys. Picks; prominent emotional disinhibition Huntington’s Chorea: inherited, choreiform movement plus confusion Infarct Dementias Korsakoffs slow starvation of brain tissue ass. W/ alcoholism HIV encephalopathy
Slide 40: Pathophysiology of DAT
Slide 41: Progression of Alzheimer’s Stage I: mild—forgetful. Short term memory loss, aware of problem, depression common Stage II: moderate—confused. Progressive memory deficits, Instrumental ADL’s decline, Cover with confabulation, denial Stage III: Severe—ambulatory dementia. Thinking and communicating decrease, all ADLs decrease, depression resolves, person not aware of deficits Stage IV: Late. Loss of basic human abilities, identity of self and family gone, physical deterioration
Slide 42: Treatment of Alzheimers Recent advances—correlation with head trauma, disuse, large families 3 genes cause over production of alpha beta Some possible protective factors- vitamin E, antiinflammatory drugs, estrogen supp. Med: Tacrine/Cognex
Slide 43: Nursing Diagnosis (some) Confusion, acute and chronic Caregiver role strain Memory, impaired Wandering
Slide 44: Spinal Cord Injury Epidemiology About 10-12,000 new cases per year, has stayed stable over past 20 years. 80% male/20% female; 60% are young adult males Currently about ¼ million paralyzed individuals in the US Most frequent causes: MVA, gunshot (17%), falls, diving, skiing, contact sport 50% paraplegia; 50% quadriplegia
Slide 45: Pathophysiology Injury leads to: lactate and chemical release causing vasospasm edema, hemorrhage All within a closed space: decreased circulation (decreased O2/glucose), build up of lactic acid
Slide 46: More Patho By limiting compression and edema, cell death is minimized This can affect the level of injury. Even a small gain in level of injury, can mean the preservation of function of a group of muscles that can directly affect rehabilitation
Slide 47: Shock in SC Injury: acute period Spinal Shock Neurogenic shock Flaccid paralysis High level of injury No bowel or bladder hypotension, no persp. tone bradycardia No reflex activity peripheral vasodilation Poikelothermia NSG: dopamine, atropine, NSG: keep temp WNL, MAST boots, tilt table, foley catheter, IV fluids, gradual position change Skin care, positioning, bowel regimen (suppositories)
Slide 48: When Spinal and Neurogenic shock subsides Typically see improvement in shock symptoms after 1-6 weeks. Note: see spasticity, spastic bladder Stabilization of VS. A small percentage of clients continue to have “flaccid” paralysis
Slide 49: Some treatment issues in acute period Time is important. Medical CNS tissue does not management with survive for long. methylprednisone, Stabilization of spine mannitol, meds to on site stabilize BP Techniques for CPR Surgical –jaw thrust decompression and Transfer to neuro fixation/stabilization center asap
Slide 50: Nursing Issues: Acute period Spinal / Neurogenic shock Altered respiratory function Prevent DVT, skin breakdown and other complications of immobility Body alignment Post op infection risk
Slide 51: Levels of Spinal Cord Innervation C-4 to C-6 Phrenic Nerve: diaphragm function Upper Limbs C-7, C-8 T-1 to T-6 Intercostal muscles T-1to L-4 Sympathetic outflow (HR, bronchiole dilation, temp control) Bowel and Bladder at lowest level
Slide 52: Autonomic Dysreflexia (also called hyperreflexia) Excess reflex arc stimulation, which fails to be modified by messages from the brain, leads to a crisis. Sky high BP with bradycardia, headache, sweating, blurred vision Can result in a CVA NSG: raise HOB, Monitor VS, give antihypertensive if needed, eliminate source of excess reflex activity such as kinked catheter, full bowel, etc.
Slide 53: More Notes about Nursing Issues: Enduring Problems Depression and suicide are common About ¼ patients have chronic pain and spasticity (antispasmodics) About 1/10 patients have decubiti Altered respiratory function at higher levels of injury is a continued concern- aspiration, atelectasis
Slide 54: Nursing Care Concerns Triple logroll technique to maintain body alignment Skeletal/halo traction and care: pin care, skin care under brace, proper fit Read in text re level of injury and related ability and rehab potential
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