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NCM116 > DEMYELINATING DISESASES > Flashcards

DEMYELINATING DISESASES Flashcards

1
Q

Cause of MS

A

*Unknown
*Autoimmune
*Demyelination of CNS (Myelin & Oligodendrocytes)

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2
Q

Multiple factors of MS

A

Viral infection
Genetic Predisposition

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3
Q

MS is common in

A

Women ages 20-40

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4
Q

Dx tests for MS

A

MRI -primary
CSF Immunoglobulin G

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5
Q

MS results from progressive demyelination of the —- and —– leading to widespread neurologic dysfunction

A

white matter of the brain and spinal
cord

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6
Q

The structures usually involved in MS

A

Optic
Oculomotor nerves
Spinal nerve tracts

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7
Q

Myelin sheath that wraps around the axon is destroyed by

A

inflammation and scarring

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8
Q

TYPES of MS

A

*Clinically isolated syndrome (CIS)
*Relapse-remitting MS (RRMS)
*Primary progressive MS (PMS)
*Secondary Progressive MS (SPMS)

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9
Q

This is a single , first episode. with symptoms lasting at least 24 hours

A

Clinically isolated syndrome (CIS)

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10
Q

This episodes of new or increasing symptoms, followed by periods of remission, during which symptoms go away partially or totally.

A

Relapse-remitting MS (RRMS)

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11
Q

Symptoms worsen progressively, without early relapses or remissions. Some people may experience times of stability and periods when symptoms worsen and then get better.

A

Primary progressive MS (PMS)

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12
Q

At first, people will experience episodes of relapse and remission, but then the disease will start to progress steadily.

A

Secondary Progressive MS (SPMS)

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13
Q

S/sx of MS

A

Nystagmus
Diplopia
Dysarthria
Dysphagia
Urinary retention
Spastic bladder
Constipation

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14
Q

The most common areas affected in MS are

A

Optic nerves and chiasm
Cerebellum
Cerebrum
Spinal cord

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15
Q

Medications for MS

A

*Corticosteroids
*Interferon beta-1a or interferon beta-1b
*Chlordiazepoxide
*Baclofen/Dantrolene
*Bethanechol or oxybutynin

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16
Q

med to reduce edema and inflammation of myelin sheath

A

Corticosteroid (Corticotropin, prednisone, dexamethasone)

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17
Q

med to decrease the frequency of relapses

A

Interferon beta-1a or interferon beta-1b

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18
Q

med to mitigate mood swings

A

chlordiazepoxide

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19
Q

med to relieve spasticity

A

Baclofen or dantrolene

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20
Q

med to relieve urine retention and minimize urinary freq and urgency

A

Bethanechol or oxybutynin

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21
Q

Nrsg intervention for MS

A

Exercise
Wheelchair
Aspiration precaution
Eye patch
Warm packs
Stress mgt.
Speech therapist

22
Q

is an acute
autoimmune disease marked by inflammation
of the peripheral nerves, affecting arms and legs

A

GBS

23
Q

involves destruction of the myelin sheath surrounding largest, most myelinated
sensory and motor fibers, resulting in disrupted
proprioception and weakness.

A

GBS

24
Q

is a rare disorder in which body’s immune
system attacks nerves and causes damage to the peripheral nerves.

A

GBS

25
Q

often causes muscle weakness, cause paralysis and sensitivity problems, including
pain, tingling or numbness

A

Nerve injury by GBS

26
Q

Cause of GBS

A

unknown origin commonly follows viral infection

27
Q

s/sx of GBS

A

*Demyelination of PNS (myelin only, intact Schwann cells thus
allowing recovery)
*Ascending weakness and paralysis
*diminished reflexes of the lower extremities
*paresthesia
*potential respiratory failure

28
Q

a result of a cell-mediated immune attack on peripheral nerve myelin proteins.

A

GBS

29
Q

contains an amino acid that mimics the peripheral nerve myelin protein

A

Infectious organism

30
Q

is the most likely target of the immune attack.

A

GM1b

31
Q

cause inflammation and destruction, and leave the axon unable to support nerve conduction

A

an influx of macrophages and other immune mediated agents that
attack myelin

32
Q

Clinical features of gbs

A

*pain in muscles
*Weakness of muscle
*onset is gradual and progresses over days or weeks
*Usually begins in the lower extremities and progressively involves the trunk, the upper
limbs, and finally the bulbar muscles (Landry ascending paralysis)
*Respiratory insufficiency due to intercostal and diaphragmatic muscle paralysis
*dysphagia and facial weakness
*Papilledema
*Oculomotor and other cranial neuropathies

33
Q

Nrgs mgt for GBS

A

*CPT
*Prevent complication of immobility
*Improve communication

34
Q

Medical mgt for GBS

A

*ICU admission
*Mechanical Ventilation
*PLASMAPHERESIS
*TPN and IVF
*IV IMMUNOGLOBULIN

35
Q

Chronic, progressive &
degenerative brain disorder

A

Alzheimer’s disease

36
Q

Profound effects on memory, cognition & ability for self care

A

Alzheimer’s disease

37
Q

Causes and potential factors of AD

A

Unknown
Amyloid plaques in the brain

38
Q

Other causes of AD

A

degeneration of brain neurons especially in the
cerebral cortex

presence of neurofibrillary tangles

plaques containing beta-amyloid cells.

39
Q

It is a chronic, irreversible disease that affects the cells of the brain and causes impairment of intellectual functioning.

A

Alzheimer’s Disease

40
Q

Alzheimer destroys ability to

A

reason, remember, imagine, and learn.

41
Q

Alzheimers disease attacks

A

nerves and brain cells
as well as neurotransmitters.

42
Q

The destruction of these parts causes clumps of
protein to form around the brain’s cells. These
clumps are known as

A

plaques and Bundles

43
Q

10 Warning Signs of
Alzheimer’s disease

A

*memory loss
*difficulty to perform familiar tasks
*problems with language
*disorientation to time and place
*Poor or decrease judgment
*Problems with abstract thinking
*Misplacing things
*Changes in mood or behavior
*Changes in personality
*Loss of initiative

44
Q

Clinical Manifestation of AD

A

Amnesia – loss of memory
Apraxia – unable to determine function & purpose of object
Agnosia – unable to recognize familiar object
Aphasia

45
Q

LATE CLINICAL
MANIFESTATION
S of AD

A

Difficulty in abstract thinking
Difficulty communicating
Severe deterioration in memory, language
and motor function
personality changes

46
Q

DIAGNOSTIC TEST OF AD

A

No definitive examination
Brain scan could help

Confirmatory test?
Autopsy results

47
Q

Drug therapy OF AD

A

Acetylcholinesterase inhibitors-

48
Q

prevent the breakdown of acetylcholine, a chemical messenger
important for learning and memory

A

Acetylcholinesterase inhibitors-

49
Q

Example of Acetylcholineterase

A

Donepezil (Aricept)

tacrine HCl (Cognex)

Rivastigmine (Exelon)

Galantamine (Razadyne)

50
Q

it is a compound
that binds to soluble amyloid-beta
peptide and inhibits the formation of neurotoxic aggregates that leads to
amyloid plaque deposition in the brain

A

Anti-amyloid therapy-

51
Q

Anti-amyloid therapy-

A

tramiprosate (Alzhemed)

52
Q

Nursing Interventions:

A

Use short simple sentences, words and gestures

Maintain a calm and consistent approach

Keep bed in low position

Provide adequate lightning

NCM116 (4 decks)

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