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NUR 335 - Exam 4 > Chronic Illness and Chronic Neurological Diseases > Flashcards

Chronic Illness and Chronic Neurological Diseases Flashcards

1
Q

Types of disability

A
  • Developmental
  • Acquired
  • Age-related
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2
Q

Autoimmune nervous system disorders

A
  • Multiple Sclerosis (MS)
  • Myasthenia Gravis
  • Guillain-Barré Syndrome
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3
Q

MS

Overview

A
  • Immune-mediated, progressive demyelinating disease of the CNS
  • Usually occurs between ages 20-40, affecting more women than men
  • Eventually, axons degenerate
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4
Q

MS

Primary symptoms

A
  • Fatigue
  • Depression
  • Weakness
  • Numbness
  • Coordination difficulties
  • Loss of balance
  • Pain
  • Visual disturbances include blurring, diplopia, scotoma, and total blindness.
  • Spasticity
  • Ataxia
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5
Q

MS

Secondary complications

A
  • UTI
  • Constipation
  • Pressure ulcers
  • Dependent pedal edema
  • Contractures
  • Pneumonia
  • Depression
  • Decreased bone density
  • Psychosocial issues
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6
Q

MS

Diagnosis and progression

A
  • MRI
  • Electrophoresis of CSF
  • Evoked potential studies (EPS)
  • Urodynamic studies
  • Neurophysiological testing
  • Sexual History
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7
Q

MS

Medical management

A

Aimed at delaying disease progression, management of chronic symptoms, and treatment of acute exacerbations.

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8
Q

MS

Disease-modifying medications

A
  • Interferon beta-1a (Rebif) SC q 3 days
  • Interferon beta-1b (Betaseron) SC qod
  • Interferon beta-1a (Avonex) IM q wk
  • Glatiramer acetate (Copaxone) SC qd
  • Methylprednisolone 1Gm IV x 3 days
  • Oral taper of Prednisone
  • Mitozanrone (Novanrone) IV infusion q 3 mo
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9
Q

MS
Symptom Management
Spasticity

A
  • Baclofen (Lioresal) – GABA agonist (PO or IT)
  • Benzodiazepines:
    • Diazepam
    • Tizanidine
    • Dantrolene
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10
Q

MS
Symptom Management
Fatigue

A
  • Fluoxetine (Prozac)
  • Amantadine
  • Pemoline
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11
Q

MS
Symptom Management
Ataxia

A
  • Inderal (β-blocker)
  • Neurontin (antiseizure)
  • Klonopin (benzodiazepine)
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12
Q

MS
Symptom Management
Bladder / bowel problems

A
  • α-blockers
  • antispasmodics
  • anticholinergics
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13
Q

MS
Symptom Management
UTI

A
  • Ascorbic acid

- Antibiotics PRN

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14
Q

MS

Nursing diagnoses

A
  • Impaired physical mobility
  • Risk for injury
  • Impaired urinary and bowel elimination
  • Impaired verbal communication
  • Risk for aspiration
  • Disturbed thought processes
  • Ineffective individual coping
  • Impaired home maintenance management
  • Potential for sexual dysfunction
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15
Q

MS

Nursing Interventions

A

TEACHING ASSISTIVE DEVICES
FEET APART-WIDE BASE OF SUPPORT
THEY ARE VERY HEAT SENTITIVE. HEAT CAN EXACERBATE SYMPTOMS. WARM vs. HOT SHOWERS.

  • Promoting Physical Mobility
    • Exercises
    • Minimizing spasticity and contractures
    • Activity and rest
    • Minimizing effects of immobility
  • Preventing Injury
  • Enhancing Bladder and Bowel Control
  • Enhancing Communication
  • Managing Swallowing Difficulties
  • Improving Sensory and Cognitive Function
    • Vision
    • Cognition and emotional responses
    • Strengthening coping mechanisms
  • Improving Home Management
  • Promoting Sexual Functioning
  • Promoting Home and Community-Based Care
    • Teaching patients self-care
    • Continuing care
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16
Q

Myasthenia Gravis

Overview

A
  • Autoimmune disorder affecting myoneural junction
  • Varying degrees of weakness of voluntary muscles
  • Women affected more and at earlier age 20-40
  • Men 60-70
  • Autoantibodies attack ACh receptor sites
  • Fewer ACh receptors available for transmission of impulses across myoneural junction
  • Results in voluntary muscle weakness; escalates with continued activity
  • Thymic hyperplasia or thymic tumor (80%)
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17
Q

Myasthenia Gravis

Clinical Manifestations

A
  • Usually starts with ocular muscles
    • Diplopia, Ptosis
  • Weakness of muscles of face and throat (bulbar symptoms)
    • Bland facial expression
  • Laryngeal involvement
    • Dysphonia
    • Risk for choking/aspiration
  • Generalized weakness
    • All extremities
    • Intercostal muscles
      > Decreased vital capacity
      > Respiratory failure
  • Motor Disorder
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18
Q

Myasthenia Gravis

Diagnostics

A
  • Anticholinesterase inhibitor test
    • Edrophonium chloride (Tensilon) IV
      > 2 mg administered, if no response after 2 minutes, up to 8 mg more may be administered
    • Positive result if immediate muscle improvement lasting about 5 minutes; confirms diagnosis
    • Atropine must be available to control SE’s of Tensilon (bradycardia, sweating, cramping)
  • Serum acetylcholine receptor antibodies elevated
  • Repetitive nerve stimulation (EMG)
    • Decrease in successive action potentials
  • MRI

AFTER ANTICHOLINERGIC CRISIS, ALWAYS HAVE ATROPINE AT HAND

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19
Q

Myasthenia Gravis

Medical Management

A

Goal is to improve function and reduce/remove circulating antibodies.

  • Anticholinesterase Medications (1st line)
    • Pyridostigmine bromide (Mestinon) – fewer SE’s
    • Neostigmine bromide (Prostigmin)
  • Immunosuppressant Medications
    • Corticosteroids
    • Cytotoxic medications
  • Exacerbation Treatment
    • Plasmapheresis
    • IVIG
  • Thymectomy
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20
Q

Myasthenic Crisis vs Cholinergic Crisis

A
  • Myasthenic Crisis
    • Exacerbation of disease
    • Undermedication or precipitating event (respiratory infection, med change, surgery, pregnancy)
    • Severe generalized muscle weakness
    • May result in respiratory failure
    • Airway/Respiratory support
    • Plasmapheresis or IVIG
    • Nutritional support with prolonged mechanical vent.
    • Avoid sedatives/tranquilizers
  • Cholinergic Crisis
    • Overmedication with cholinesterase inhibitors
    • Symptoms mimic disease exacerbation
    • Stop all cholinesterase inhibitors
    • Atropine to treat bradycardia and or respiratory distress
    • Airway/Respiratory support
    • Plasmapheresis or IVIG then gradually restart cholinesterase inhibitors
    • Nutritional support
    • Avoid sedatives/tranquilizers
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21
Q

Major difference between Myasthenia Crisis and Cholinergic Crisis

A

Myasthenia crisis is an exacerbation usually triggered by a respiratory infection or some type of infectious process. Cholinergic crisis is triggered by over medication.

22
Q

Myasthenia Gravis

Nursing Management

A
  • Medication management
    • Must be taken correctly and on time to avoid Myasthenic Crisis or Cholinergic Crisis
    • Patient keeps diary inclusive of fluctuation of symptoms and effects of medication to determine best times for daily dosing
  • Strategies to conserve energy
  • Minimize risk of aspiration
    • Suction should be available at home
    • Alternate nutritional strategies
  • Care of impaired vision
    • Corneal damage prevention by taping eyes closed for short periods; instilling artificial tears
    • Crutches to lift eyelids
    • Eye patches for double vision
  • Maintain health screening, health promotion, avoid exacerbations
  • Resources – Myasthenia Gravis Foundation
23
Q

Guillain-Barré Syndrome

Overview

A

USUALLY CAUSED BY A VIRAL INFECTION

  • AKA Infectious Polyneuritis
  • Autoimmune attack on peripheral nerve myelin
  • Produces ascending weakness (from legs upward) with dyskinesia, hyporeflexia, and paresthesia
  • Symptoms are usually symmetrical
  • Usually caused by viral exposure 2 weeks prior to symptom onset
  • More frequent in males ages 16-25 and 45-60
  • 60-75% of patients recover completely within 6-12 months
  • 20-25% of patients suffer residual deficits
  • Death occurs in 5% of patients
  • Schwann cell is spared, allowing remyelinization in recovery phase
24
Q

Guillian-Barré Syndrome

Clinical Manifestations

A
  • Muscle weakness and diminished reflexes of lower extremities progressing upwards
  • Maximum weakness usually includes respiratory failure and bulbar weakness
  • Cranial Nerve Demyelination
    • Optic – blindness
    • Glossopharyngeal + Vagus – inability to swallow or clear secretions
    • Vagus – cardiovascular instability
  • Complete functional recovery may take up to 2 years
  • Residual symptoms are permanent and reflect axonal damage from demyelination
25
Q

Guillain-Barré Syndrome

Diagnostics

A
  • Presentation with symmetric weakness, diminished reflexes, upward progression of motor weakness
  • Recent history of viral illness
  • Assessment of impending neuromuscular respiratory failure (NIF, Vital Capacity)
  • Elevated protein levels in CSF
  • Evoked potential studies – progressive loss of nerve conduction velocity
26
Q

Guillain-Barré Syndrome

Medical Management

A
  • Support pulmonary function / adequate oxygenation
    • Elective intubation to prevent autonomic dysfunction
  • Prevent complications of immobility
  • Plasmapheresis and IVIG
  • Continuous ECG monitoring
    • Tachycardia and HTN treated with short acting meds
    • Hypotension managed with IV fluids
    • Bradycardia managed with meds and may require temporary pacing
27
Q

Guillain-Barré Syndrome

Nursing Implications

A

DVT PROPHYLAXIS
PSYCHOSOCIAL AND EMOTIONAL SUPPORT

  • Maintain respiratory function
  • Enhance physical mobility
  • Provide adequate nutrition
  • Improve communication
  • Decrease fear and anxiety
  • Monitor and manage potential complications
    • Respiratory failure is major cause of mortality; reported to be as high as 20%
  • Promote home and community-based care
    • Teach self-care – Discharge planning
    • Continuing care – Rehab and follow-up
28
Q

Degenerative Nervous System Disorders

A
  • Parkinson’s Disease
  • Huntington’s Disease
  • Amyotrophic Lateral Sclerosis
29
Q

Parkinson’s Disease

Overview

A
  • Slowly progressing neurologic movement disorder leading to disability
  • Cause is generally unknown
    • Idiopathic
    • Suggested causative factors
  • Symptoms generally appear in 50’s
    • Cases have been diagnosed in 30’s
  • Affects men more frequently than women
  • Associated with decreased levels of dopamine due to destruction of pigmented neural cells in the substantia nigra in the basal ganglia.
  • Loss of dopamine stores results in more excitatory (acetylcholine) neurotransmitters than inhibitory (dopamine) neurotransmitters.
30
Q

Parkinson’s Disease

Cardinal signs

A
  • Tremor
  • Rigidity
  • Bradykinesia
  • Postural instability
31
Q

Parkinson’s Disease

Clinical Manifestations

A
  • Autonomic symptoms:
    • Excessive/uncontrolled sweating
    • Paroxysmal flushing
    • Orthostatic hypotension
    • Gastric and urinary retention
    • Constipation
    • Sexual dysfunction
  • Psychiatric changes:
    • Depression
    • Dementia (40-70%)
    • Sleep disturbances (75%)
    • Hallucinations (37%)
  • Mental Changes
    • Cognitive deficits
    • Perceptual deficits
    • Memory deficits
  • Other Manifestations:
    • Hypokinesia
    • Freezing phenomenon
    • Shuffling/decreased arm swing
    • Micrographia
    • Mask-like/expressionless face
    • Decreased blinking
    • Dysphonia
    • Dysphagia
    • Drooling
32
Q

Parkinson’s Disease

Diagnostics

A
  • Patient history and 2 of 4 Cardinal Signs
    • Tremor
    • Rigidity
    • Bradykinesia
    • Postural changes
  • Evaluation of:
    • Medical history
    • Presenting symptoms
    • Neuro exam
    • Response to pharmacologic management
33
Q

Parkinson’s Disease

Medical Management

A
  • Aimed at controlling symptoms and maintaining functional independence
  • Care is individualized based on patient needs
  • Pharmacologic therapy is mainstay of treatment
34
Q

Anti-parkinsonian Medications

A
  • LEVODOPA is most effective agent
  • Converts to dopamine in basal ganglia, producing symptom relief
  • Not initial treatment
  • May precipitate oxidation which causes further damage to substantia nigra, speeding disease progression
  • Usually administered with CARBIDOPA (SINEMET), amino acid decarboxylate inhibitor
    • Maximizes beneficial effects of levodopa by preventing breakdown outside the brain and reducing adverse effects
  • Within 5-10 years, dyskinesia develops
  • On-off syndrome
35
Q

Anti-parkinsonian Medications

Anticholinergic Therapy

A
  • Control tremor and rigidity
  • May be used in combination with Levodopa
  • Counteract the action of acetylcholine
  • Poorly tolerated in elderly due to SE’s of blurred vision, flushing, rash, constipation, urinary retention, and acute confusion
  • Contraindicated in narrow angle glaucoma
  • Monitor intraoccular pressure
36
Q

Anti-parkinsonian Medications

Antiviral Therapy

A
  • Amantadine hydrochloride (Symmetrel)
    • Reduces the 4 cardinal signs in early Parkinson’s Disease
  • Exact mechanism of action unknown
  • Low incidence of side effects
37
Q

Anti-parkinsonian Medications

Dopamine Receptor Agonists

A
  • ROPINIROLE HYDROCHLORIDE (REQUIP) and PRAMIPEXOLE (MIRAPEX)
    • 1st line treatment in early Parkinson’s
38
Q

Parkinson’s Disease

Surgical management

A
  • Palliative
    • Candidates – idiopathic form with max. doses of antiparkinsonian drugs
    • Dementia usually excluded
  • Stereotactic Procedures
    • Thalamotomy
    • Pallidotomy
  • Neural Transplantation
    • Limited by legal, ethical, and political concerns
  • Deep Brain Stimulation
39
Q

Parkinson’s Disease

Nursing Diagnoses

A
  • Impaired physical mobility
  • Self-care deficits
  • Constipation
  • Imbalanced nutrition, less than body requirements
  • Impaired verbal communication
  • Ineffective coping

May include:

  • Sleep pattern disturbances
  • Deficient knowledge
  • Risk for injury
  • Risk for activity intolerance
  • Disturbed thought processes
  • Compromised family coping
40
Q

Parkinson’s Disease

Nursing Interventions

A
  • Improve mobility
  • Enhance self-care activities
  • Improve bowel elimination
  • Improve nutrition
  • Enhance swallowing
  • Encourage use of assistive devices
  • Improve communication
  • Support coping abilities
  • Promote home and community-based care
    • Teach patients self-care
    • Continuing care
      > National Parkinson’s Foundation, Inc.
      > American Parkinson’s Disease Association
41
Q

Huntington’s Disease

Overview

A
  • Chronic, progressive, hereditary disease
  • Results in progressive involuntary choreiform movement and dementia
  • Autosomal dominant genetic disorder
  • 50% chance of inheriting disease
  • Premature death of cells in the striatum of the basal ganglia
    • Control of movement
  • Loss of cells in the cortex
    • Thinking, memory, perception, judgment
  • Loss of cells in cerebellum
    • Voluntary muscle activity coordination
  • Believed that glutamine (building block of protein) abnormally collects in cell nucleus and causes cell death
  • Onset usually ages 35-45
  • 10% of cases are children
  • Ravenous appetite yet, patients become emaciated and exhausted
  • Death in 10-20 years due to heart failure, pneumonia, infection, or from fall or choking
42
Q

Huntington’s Disease

Clinical Manifestations

A
  • Chorea of all body musculature which persists during sleep
  • Intellectual decline
  • Emotional disturbance
  • Speech declines to unintelligible
  • Disturbed gait becoming wheelchair to bed bound
  • Loss of bladder and bowel control
  • Cognitive decline, dementia
  • Personality changes
    • In early stages, uncontrolled fits of anger, suicidal, apathy, anxiety, psychosis, or euphoria
    • Most disturbing to patient and family
  • Psychotic symptoms may precede disjointed movements
  • Emotional and cognitive symptoms often less acute as disease progresses
43
Q

Huntington’s Disease

Diagnostics

A
  • Clinical presentation of characteristic symptoms, positive family history, exclusion of other causes
  • Genetic marker
  • CT/MRI
    • Cerebral atrophy in advanced stages
  • MRI/PET
    • Changes in brain activity before onset of physical symptoms
44
Q

Huntington’s Disease

Management

A
  • No cure
  • Medication to control chorea
    • Thiothixene HCl (Navane)
    • Haloperidol decanoate (Haldol)
      > Both block dopamine receptors, improving chorea
  • Akathisia in overmedicated patient may be overlooked
  • Hypokinetic motor impairment may temporarily respond to Levodopa
  • Antidepressants for emotional disturbances
  • Antipsychotics for psychosis
  • Psychotherapy for anxiety and stress reduction
  • Remotivation therapy and stimulating environment
45
Q

Huntington’s Disease

Nursing Implications

A
  • Patient and family teaching
    • Medications and effects
    • Management of chorea
    • Swallowing problems
    • Ambulation limitations
    • Loss of bowel and bladder function
  • Speech therapy consult
  • Genetic counseling and support
  • Palliative, respite, long-term care
  • Huntington Disease Foundation
46
Q

Huntington Disease

Nursing Diagnoses

A
  • Risk for injury and possible skin breakdown
  • Imbalanced nutrition, less than body requirements
  • Anxiety and impaired communication
  • Disturbed thought processes and impaired social interaction
47
Q

Amyotrophic Lateral Sclerosis (ALS)
aka Lou Gehrig’s Disease

Overview

A
  • Unknown cause
  • Loss of motor neurons in the anterior horns of the spinal cord and the motor nuclei of the lower brain stem
  • Corresponding muscle fibers atrophy
  • Neuronal degeneration may occur in upper and lower motor neuron systems.
  • Theories include autoimmune disease, free radical damage, oxidative stress
  • Overexcitation of nerve cells by neurotransmitter glutamate leads to cell injury and neuronal degeneration
  • Affects men more than women aged 50-60’s
48
Q

ALS

Clinical Manifestations

A
  • Dependent on location of affected motor neurons
  • If anterior horns of spinal cord affected:
    • Progressive weakness and atrophy of muscles of arms, trunk, or legs
    • Spasticity
    • Brisk/overactive deep tendon stretch reflexes
  • Weakness starts in muscles supplied by cranial nerves in ≈ 25% of patients
  • Difficulty talking
  • Difficulty swallowing
  • Difficulty breathing
  • Prognosis based on area of CNS involved and speed of disease progression
  • Death usually due to infection, respiratory failure, or aspiration
49
Q

ALS

Chief symptoms

A
  • Fatigue
  • Progressive muscle weakness
  • Cramps
  • Fasciculations
  • Incoordination
50
Q

ALS

Diagnostics

A
  • Based on S/S
  • No specific clinical or lab tests
  • EMG
  • Muscle Biopsy
  • MRI may show high signal density in corticospinal tracts
51
Q

ALS

Management

A
  • No specific therapy exists
  • Interventions to maintain or improve function, well-being, and quality of life
  • 25 months – mean survival from onset
  • RILUZOLE (RILUTEK) – glutamate antagonist slows deterioration of motor neurons
  • Symptomatic treatment and rehab
  • BACLOFEN (LIORESAL), DANTROLENE SODIUM (DANTRIUM), DIAZEPAM (VALIUM) for spasticity causing pain
  • Enteral feeding
  • Noninvasive positive pressure ventilation
  • Mechanical ventilation
  • End of Life issues – Code Status, Living Will
  • Resources: Amyotrophic Lateral Sclerosis Association

NUR 335 - Exam 4 (3 decks)

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