Med-Surg: Chapter 37: Multiple Sclerosis Flashcards

1
Q

Multiple Sclerosis (MS)

A

chronic neurological disorder in which the nerves of the CNS (brain and spinal cord) degenerate

  • derives its name from the build up of scar tissue (sclerosis) or plaques that for during demyelination (destruction of myelin sheath)
  • autoimmune disease; the immune system mistakenly identifies normal body substances and tissues as foreign and attacks them; the immune system attacks the brain and spinal cord (CNS)
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2
Q

Risk Factors

A
  • 20 to 50 years old
  • women
  • positive family hx
  • immunological factors
  • viral infections
  • higher in colder, more northern latitudes
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3
Q

4 Main types of MS

A
  • Relapsing-remitting
  • Secondary progressive
  • Progressive relapsing
  • Primary progressive
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4
Q

Types of MS: Relapsing-Remitting

A
  • most common form
  • characterized by relapses (exacerbations) during which new clinical manifestations appear and old ones worsen or reappear
  • relapses can last days or months
  • relapses are followed by periods of remission during which the patient has either a partial or total recovery; this can be slow or instantaneous
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5
Q

Types of MS: Secondary Progressive

A

the patient who initially had relapsing-remitting develops gradual worsening of the disease

  • in the early phase, the patient still may experience relapses, but these will progress into a general deterioration
  • no real recovery occurs
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6
Q

Types of MS: Progressive relapsing

A

progressive course with a gradual worsening of clinical manifestations from onset, and the relapses may or may not have recovery

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7
Q

Types of MS: Primary progressive

A

gradual progression with no remissions

  • may be temporary plateaus
  • affects women and men equally
  • occurs late 30’s early 40s
  • initial disease activity is in the spinal cord, not the brain, so these patients less likely to develop cognitive problems
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8
Q

Pathophysiology

A
  • myelin is the protective sheath that covers the spinal cord and nerves; it not only protects the nerve, but it also helps the impulses travel along the nerves at a faster rate; these impulses control muscle movements, as well as transmitting sensory data
  • the CNS contains the blood-brain barrier that separates circulating blood from the brain’s extracellular fluid; barrier is composed of tight junctions between endothelial cells in the CNS vessels that restrict the passage of solutes from the bloodstream
  • Demyelination is the loss of the myelin sheath; it begins with the breakdown of the blood-brain barrier that allows immune cells (T lymphocytes) to infiltrate and attack the myelin
  • in MS, the immune system attacks the brain and spinal cord (CNS)
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9
Q

Demyelination

A

the loss of the myelin sheath

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10
Q

Clinical Manifestation

A

the resulting inflammation in MS destroys the myelin, resulting in impaired sensation, movement, and thinking

  • nerves can regain myelin, but this occurs more slowly than deterioration in MS
  • nerve conduction is slowed or irregular due to loss of myelin that facilitates impulse transmission

> manifestations:

  • numbness or weakness in one or more limbs
  • partial or complete vision loss, often with pain during eye movement (optic neuritis)
  • double or blurred vision
  • tingling or pain
  • electric-shock sensations that occur with head movements
  • tremor, lack of coordination, or unsteady gait
  • fatigue
  • dizziness
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11
Q

Diagnosis

A

-no specific test; can be difficult to diagnose
-may not be diagnosed for months to years after onset of clinical manifestations
-diagnosis is made by ruling out conditions with similar presentations
-detailed hx, physical, and neurological examination are performed
-blood samples are sent to the laboratory to r/o other inflammatory or infectious diseases that may have the same clinical manifestations; vitamin B12 and E deficiencies, Lyme titer, antineutrophil antibodies (ANA) for autoimmune diseases, angio-tensin converting enzyme for sarcoidosis, HIV/HTLV (human T-lymphotropic virus), erythrocyte sedimentation rate (ESR) for inflammation, rapid plasma reagin (RPR) for neurosyphilis, anticardiolipin antibodies, and lupus anticoagulant for coagulopathy/vascular conditions
>a lumbar puncture performed to send CSF sample to be tested for abnormal levels of WBC or proteins and help r/o viral infections
-MRI scans for brain lesions (plaques)
-Electrophysiological tests, and evoked potentials to examine how quickly impulses are traveling through the nerves

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12
Q

For a definitive diagnosis

A

patient must have at least 2 separate symptomatic events or MRI changes in at least 2 separate locations

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13
Q

Treatment

A
  • no cure
  • focuses on improving the speed of recovery from attacks, reducing the number of attacks, and slowing the progression of the disease
  • lifestyle management: adequate rest, exercise, staying cool, healthy balanced diet, and relieving stress because these can all trigger exacerbation or flare of MS
  • physical therapy used to help strengthen muscles and improve daily function
  • Betaseron (Interferon beta-1b) modifies/slows the disease process
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14
Q

Medical Management

A

> First, medications used to modify the disease course; these are used to slow the progression of the disease

  • beta interferons: interferon beta-1a (Avonex, Betaseron, and Rebif); interferon beta-1b (Extavia)
  • glatiramer (Copaxone)
  • fingolimod (Gilenya)
  • immunosuppressive agents: natalizumab (Tysabri) and mitoxantrone (Novantrone)

> Second, strategies used to treat attacks include
-corticosteroids and plasma exchange (plasmapheresis) to decrease the inflammatory and immunologic factors involved in the exacerbation

> Final focus, treat clinical manifestations
-muscle relaxants such as baclofen (Lioresal and Kemstro) and tizanidine (Zanaflex) decrease spasticity

> medications may also be prescribed to help reduce fatigue and used to treat depression, pain, and bladder or bowel problems

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15
Q

Medication: Interferon beta-1a (Avonex, Refib)

A

immunomodulator

  • use to modify the disease course; slow the progression of the disease
  • alters the immune system by reducing the body’s ability to make antibodies; these antibodies are what attack the myelin; therefore, this slows the attack on myelin and slows disease progression
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16
Q

Medication: Interferon beta-1b (Betaseron, Extavia)

A

immunomodulator

  • used to modify the disease course; slow the progression of the disease
  • alters the immune system by reducing the body’s ability to make antibodies; these antibodies are what attack the myelin; therefore, this slows the attack on myelin and slows disease progression
17
Q

Medication: Glatiramer (Copaxone)

A

immunomodulator-synthetic protein

  • used to modify the disease course; slow the progression of the disease
  • alters the immune system by reducing the body’s ability to make antibodies; these antibodies are what attack the myelin; therefore, this slows the attack on myelin and slows disease progression
18
Q

Medication: Fingolimod (Gilenya)

A

immunomodulator-synthetic protein

  • used to modify the disease course; slow the progression of the disease
  • alters the immune system by reducing the body’s ability to make antibodies; these antibodies are what attack the myelin; therefore, this slows the attack on myelin and slows disease progression
  • first oral immunomodulator for MS
19
Q

What Medications are used to modify the disease course?

A
  • Interferon beta-1a (Avonex, Rebif)
  • Interferon beta-1b (Betaseron, Extavia)
  • Glatiramer (Copaxone)
  • Fingolimod (Gilenya)
  • Immunosuppressants (Natalizumab (Tysabri), Mitoxantrone (Novantrone)
20
Q

Medication: Immunosuppressants

A

-Natalizumab (Tysabri)
-Mitoxantrone (Novantrone)
>modify the disease process
-suppresses body’s immune response to prevent leukocytes from attacking each other

21
Q

Medication: Muscle relaxant and antispasmodic

A

-Baclofen (Lioresal, Kemstro)
-Tizanidine (Zanaflex)
>depress CNS to reduce pain and inhibit reflexes at the spinal level to decrease muscle spasm

22
Q

Medication: Corticosteroid

A
  • Prednisone
  • Cortisone
  • Hydrocortisone
  • Methylprednisolone sodium succinate (Solu-Medrol)

> mimic the effects of hormones produced in the adrenal glands; decrease inflammation by blocking the production of substances that trigger allergic and inflammatory reactions (e.g. prostaglandins)

23
Q

Medication: Anticholinergic; antispasmodic

A
  • Oxybutynin chloride (Ditropan)

- inhibits transmission of impulses through parasympathetic nerve fibers

24
Q

Medications: Analeptics

A
  • Modafinil (Provigil)
  • Armodafinil (Nuvigil)

> alter neurotransmitters to improve wakefulness

25
Q

Medications: Stool Softeners

A
  • Docusate (Colace)

- absorb water in the large intestine, increasing the bulk of the stool

26
Q

Medications: Antimuscarinics

A
  • Tolterodine (Detrol)

- reduces bladder spasms by inhibiting acetylcholine

27
Q

Medications: Laxatives (Osmotic)

A
  • milk of magnesia
  • Miralax
  • Lactulose

> pull fluids into the intestine from other tissue and blood vessels; the extra fluid makes the stool softer and easier to pass

28
Q

Medications: Laxatives (Stimulant)

A
  • Correctol
  • Dulcolax
  • Senokot

> irritates the intestinal lining and speeds up how quickly stool moves through the intestines

29
Q

Complications

A

-muscle stiffness or spasms
-paralysis, often in the legs
-problems with bladder, bowel, or sexual function
-mental status changes- memory loss, problems concentrating
-depression
-seizures
>other: pressure injuries resulting from immobility, skin breakdown caused by bladder and bowel incontinence, ataxic gait caused by weakness and loss of position sense in the legs; speech defects caused by muscle weakness; mood changes such as depression, euphoria, denial, and forgetfulness may be caused by both medications an demyelination process

30
Q

Nursing Management: Assessment and Analysis

A

because MS affects varying nerves throughout the body, the clinical presentation may change with each attack; clinical manifestations are the direct result of the demyelination process

  • numbness/weakness
  • complete or partial loss of vision
  • double or blurred vision
  • fatigue
  • dizziness
  • tremor
  • lack of coordination/balance
  • speech problems–especially articulation
  • memory loss

> other: depression, paranoia, reduce bowel or bladder control

31
Q

Nursing Assessments

A

> Neuromuscular function
-evaluate for changes in clinical presentation or for new symptoms to be addressed as the disease progresses and new areas of demyelination occur

> Vision/eye movement
-demyelination of cranial nerves can result in optic neuritis, causing visual changes

> Skin integrity
-immobility promotes breakdown as a result of compression of soft tissue between a bony prominence and an external surface; this compromises blood flow and decreases delivery of oxygen and nutrients to cells, resulting in cellular death and injury to the surrounding tissue

> Ability to perform ADLs
-evaluate need for assistive devices to decrease danger of falls

> Bowel and Bladder Function
-impaired innervation to the bladder and bowel may result in incontinence and constipation

32
Q

Nursing Actions

A

> Encourage ROM exercises
-increase venous return, prevent stiffness, and maintain muscle strength and endurance

> Administer interferon beta-1b (Betaseron)
-used to decrease exacerbations and slow disease progression

> Administer corticosteroids during exacerbations
-during an exacerbation of MS, typically a result of some type of stress, corticosteroids decreases the inflammatory process associated with the flare

> Implement Safety Measures
-b/c of changes in mobility, sensation, and vision, the patient is at increased risk for falls and injury

> Patch each eye daily as needed in patients with visual deficits and/or diplopia
-alternating the patching of each eye several times per day improves balance and vision

33
Q

Teaching

A

> Take Medications as prescribed
-decrease exacerbations/slow progression; to treat clinical manifestations

> Importance of rest periods and preventing fatigue and overheating
-fatigue, overexertion, and overheating stimulate MS exacerbations

> Clinical Manifestations of MS exacerbation
-to detect early signs to receive early tx

> Visual Scanning
-b/c peripheral vision may be decreased in patients with MS, visual environment scanning decreases risk of injury

> Check water temperature prior to entering the bathtub or shower
-decreased sensation secondary to demyelination makes the patient at risk of burn injuries if the water is too hot

> Maintain ideal body weight
-impaired immobility may increase weight gain and increased weight is associated with complications with mobility and fatigue in patients with MS

> Review disease process and prognosis
-helps increase understanding and enhance patient’s ability to make informed choices

34
Q

Evaluating Care Outcomes

A

patients with MS live their lives never knowing when the next exacerbation or attack will occur

  • compliance with medication regimen, specifically Betaseron, helps reduce these exacerbations
  • patient and family education important regarding medication regimen. clinical manifestations of exacerbation, and importance of getting rest and exercise
  • goals of care: keep patient as active and functional as possible, provide symptomatic relief, and provide continued support