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MEDICAL-SURGICAL(MIDTERM) > NEURO04 > Flashcards

NEURO04 Flashcards

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1
Q

approximately 2 to 4 years short–term memory loss: forgets location and names of objects and has difficulty learning new information; long term is unaffected

A

STAGE 1 AD

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2
Q

○Decreased attention span
⚬ Subtle personality changes: lack spontaneity; denial,
irritability, and depression are possible.
⚬ Mild cognitive deficits: attempts to adjust to and cover
up memory loss.
⚬ Usually, family members are the first to notice lapses.

A

STAGE 1 AD

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3
Q

approximately 2 to 12 years

A

STAGE 2 AD

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4
Q

⚬ Memory deficits are more apparent, and less able to behave spontaneously,
loss of ability to tell time and orientation to place, loss of abstract thinking.
⚬ “sundowning”, behavioral changes, characterized by increased agitation,
time disorientation, and wandering behaviors during afternoon and evening
hours;
⚬ Language deficits; paraphasia, echolalia and scanning speech, total aphasia.
⚬ Sensorimotor deficits: apraxia; astereognosis; and agraphia
⚬ Impaired judgment: diminished social skills; inability to drive a car; inability to
make decisions
⚬ Sleep disturbances, malnutrition, and decreased fluid intake

A

STAGE 2 AD

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5
Q

approximately 2 to 4 years or longer
⚬ Cognitive abilities grossly decreased or absent: usually
disoriented to time, place, and person.
⚬ Communication skills usually absent: frequently mute
⚬ Motor skills grossly impaired or absent: limb rigidity and
posture flexion; bowel and bladder incontinence.
⚬ Complications: pneumonia, dehydration, malnutrition,
falls, depression, delusion, seizures, and paranoid
reactions

A

STAGE 3 AD

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6
Q

DIAGNOSTIC TESTS FOR AD

A

Postmortem examination of brain tissue
• Folstein Mini-Mental Status Examination

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7
Q

used to assess mental status, areas of function such as the client’s orientation to time, ability to repeat back a series of words, ability to name objects, and ability to follow written instructions

A

Folstein Mini-Mental Status Examination

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8
Q

first medication specifically
approved treatment of AD

A

Tacrine hydrochloride (Cognex)

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9
Q

– used to treat mild to moderate
AD dementia.

A

Donepezil hydrochloride (Aricept)

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10
Q

used to treat mild to moderate AD manifestations, improves the ability to carry out ADLs, decreases agitation and delusions, and improves cognitive function.

A

Rivastigmine tartrate (Exelon) –

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11
Q

used to increase the
concentration of Ach in the CNS.

A

Galantamine hydrobromide (Reminyl)

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12
Q

Improves cognitive function in moderate to
severe AD and mild to moderate vascular dementia, acts by blocking the receptors for glutamate, resulting in decreased calcium accumulation into neurons (increased calcium accumulation
damaged neurons).

A

Memantine (Namenda)

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13
Q

are usually avoided because they can increase AD manifestations – have high
anticholinergic activity.

A

Antihistamines and Tricyclic antidepressants

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14
Q

are thought to improve cognition.

A

Gingko Biloba and Vitamin E

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15
Q

• A chronic, progressive disease of the CNS (brain, optic nerves, anD spinal cord), associated characterized by the destruction of myelin.
• Typically affects young adults between the ages of 20 and 50 years.
• Women are more frequently affected than men.
• Characterized by periods of exacerbation, when manifestations are highly pronounced, followed by periods of remission, the result, however, is progressing with increasing loss of function.

A

MULTIPLE SCLEROSIS

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16
Q

RISK FACTORS OF MULTIPLE SCLEROSIS

A

• Geographic Prevalence ( Europe, New Zealand, southern Australia,
Northern USA, and Southern Canada)
• Genetic predisposition (Autoimmune), alteration in the immune
system
• Viral Infection (Epstein – Barr Virus)

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17
Q

Areas commonly affected by multiple sclerosis

A

• Optic Nerve - Vision
• Cerebrum - Intellect
• Cerebellum - Balance
• SC - weakness and paralysis
• Brainstem - sleep wake cycle

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18
Q

⚬ Most common clinical course, characterized by exacerbations
(acute attacks) with either full recovery or partial recovery
with disability.
⚬ 80 – 85 % of all MS

A

Relapsing-remitting course (RR)

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19
Q

⚬ Steady worsening of the disease from the onset with
occasional minor recovery.
⚬ 10% of RR develops into this course.

A

Primary Progressive

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20
Q

⚬ Begins as with relapsing-remitting, but the disease steadily becomes worse between exacerbations.

A

Secondary progressive course

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21
Q

⚬ Rare continues to progress from the onset but also
has exacerbations.
⚬ 5% of cases

A

Progressive - relapsing course

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22
Q

PATTERNS OF MULTIPLE SCLEROSIS

A

RELAPSING REMITTING COURSE
PRIMARY PROGRESSIVE
SECONDARY PROGRESSIVE COURSE
PROGRESSIVE-RELAPSING COURSE

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23
Q

Triad of MS

A

￭ I – ntentional tremors
￭ N – ystagmus – abnormal rotation of eyes Charcot’s triad
￭ A – taxia & Scanning speech

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24
Q

Clinical Manifestation of MS

A

●Fatigue
●Pain along with paresthesia, dysesthesias (impairment to sensitivity especially to touch), and proprioception loss (inability to sense stimulus)
●Spasticity of the extremities and loss of abdominal reflexes
●Cognitive changes like memory loss or decreased concentration
●Impaired cerebellar function;
Emotional lability and euphoria
●Visual disturbances such as blurring of vision, diplopia/ double vision, and
scotomas (blind spots)
●Bladder, bowel, and sexual dysfunctions
●Contracture, UTI, pressure sores are some complications

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25
measures brain activity, the scan reveals areas with changes in glucose metabolism
Positron emission tomography (PET) scan
26
Theories attributed to the development of PD
●Genetics • Encephalitis • Atherosclerosis • Poisoning/Toxicity (Carbon monoxide) • Degenerative changes in the basal ganglia resulting decreased dopamine level (Dopamine- Acetylcholine Disequilibrium) • Drugs (Phenothiazines (antipsychotic drugs), Reserpine, Haloperidol, Methydopa)
27
• A progressive disease, degenerative neurologic disease characterized by tremor (shaking), muscle rigidity, and bradykinesia (slowness movement). • Degeneration of dopamine • Usually develops after the age of 65 years, but 15% of those diagnosed are under 40 years of age. • Men and women are affected equally.
Parkinson’s disease (Paralysis Agitans or Parkinsonism)
28
reveals an increased number of T lymphocytes that are reactive with antigens, indicating the presence of immune response in the client
Cerebrospinal fluid (CSF) analysis
29
PHARMACOLOGIC THERAPY FOR MS
⚬ Combination of adrenal corticosteroid hormone (ACTH) and glucocorticoids ⚬ Immunosuppressive agents – Azathioprine (Imuran), and Cyclophosphamide (Cytoxan) ⚬ Interferon beta- 1a (Rebif) and interferon beta- 1b (Betaseron) and glatiramer acetate (Copaxone) ⚬ IV Methylprednisone ￭It exerts anti-inflammatory effects by acting on T cells and cytokines. ￭Given 1 gm daily IV for 3 days followed by oral prednisone. ￭S/E: mood swings, weight gain, and electrolyte imbalances
30
Clinical manifestations of PD
Tremor Rigidity and bradykinesia Abnormal posture Mood and cognition Increase salivation Autonomic and neuroendocrine effect
31
Anti-parkinsonian agents (e.g.
●Levodopa (L-Dopa), ●Carbidopa (Sinemet), ●Amantadine hydrochloride (Symmetrel)
32
Nursing considerations for pharmacologic tx of PD
￭ Take with meals – to decrease GIT irritation ￭ Inform client – urine/ stool may be darkened ￭ Instruct client- don’t take food Vitamin B6 (Pyridoxine) cereals, organ meats, green leafy vegetables because B6 reverses therapeutic effects of levodopa. ￭ Give INH (Isoniazid-Isonicotene acid hydrazide) - Peripheral neuritis
33
34
used with an implanted pacemaker-like device to deliver mild electrical stimulation to block the brain impulses that cause tremor, rigidity, stiffness, slowed movement, and problems with walking.
Activa TM Tremor Control therapy
35
neurosurgeon locates the affected areas of the globus pallidus and destroys the involved tissue.
Pallidotomy
36
(an x-ray is taken during neurosurgery to guide the insertion of a needle into a specific area of the brain) –destroys a small amount of tissue by creating a lesion in the ventrolateral nucleus of the thalamus, thus, decreasing tremors and rigidity in the contralateral extremity
Stereotaxic thalamotomy
37
brain cells from aborted fetuses are implanted into the brain in the hopes that the new cells will grow and produce enough dopamine to restore some lost mobility.
Fetal tissue transplantation
38
Surgeries for PD
Pallidotomy Stereotaxic thalamotomy Fetal tissue transplantation
39
Rehabilitation for PD
• Physical therapist • Occupational therapist • Speech therapist
40
A progressive, degenerative, inherited neurologic disease characterized by increasing dementia and chorea (jerky, rapid, involuntary movements).
Huntington’s disease (HD)
41
Possible cause of Huntington's disease
● a decrease in gammaaminobutyric acid (GABA) an inhibitory neurotransmitter in the basal ganglia. ●There is also a decrease in acetylcholine levels, suggesting that the manifestations are the result of an imbalance in dopamine and acetylcholine.
42
Early manifestations in motor effects of Huntington's disease
restlessness, “fidgety” feeling, minor gait changes – unsteady on feet, posture and positioning disturbances, inability to keep the tongue from protruding, slurred speech with poor articulation
43
Late motor effects of Huntington's diasease
● Chorea – severely altered gait with irregular uncontrollable movement, shoulders shrug arrhythmically; ●facial grimacing – raising of eyebrows,uncontrollable protrusion of tongue; ● dysphagia; unintelligible speech; ●impaired diaphragmatic movement
44
Psychosocial effects of huntington's disease
⚬ Early: irritability, outburst of rage alternating with euphoria, depression ⚬ Complication: Suicide ⚬ Late: decreasing memory, loss of cognitive skills, eventual dementia ⚬ Complications: total dependence
45
the only test available to diagnose a client who is suspected for Huntington's disease. Both blood and amniotic fluid may be tested for the presence of a gene mutation on chromosome 4 using DNA analysis. Can predict 95% accuracy which offspring have the disease.
Genetic testing
46
Pharmacolgic tx for Huntington's disease
●Antipsychotics (phenothiazines and butyrophenones)- block dopamine receptors in the brain. ●Antidepressants are prescribed in the early stage of the disease.
47
A rapidly progressive and fatal degenerative neurologic disease characterized by weakness and wasting of muscle under voluntary control, without any accompanying sensory or cognitive changes.
Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s disease
48
Possible cause for amyotropic lateral sclerosis
●Abnormal glutamate metabolism and hydrogen peroxide production. ●Environmental factors such as excess intracellular calcium, and antibodies to calcium channels.
49
Manifestations of ALS
Musculoskeletal System: weakness and fatigue, “heaviness” of legs, fasciculations (twitching), uncoordinated movements, loss of fine motor control in hands, spasticity, paresis, hyperreflexia, atrophy, problems with articulation • Complications: paralysis, loss of ability to perform ADLs, total immobility, aspiration, loss of verbal communication • Respiratory System: dyspnea, difficulty clearing airway • Complications: pneumonia, eventual respiratory failure • Nutritional Effects: difficulty chewing, dysphagia • Complication: Malnutrition • Emotional Effects: loss of control, lability • Complication: depression
50
Treats ALS
Riluzole (Rilutek), an antiglutamate, the first medication developed to treat ALS.
51
A chronic autoimmune neuromuscular disorder affecting the myoneural junction is characterized by fatigue and severe weakness of skeletal muscles.Women are affected more frequently than men.Mostly affects person between
Myasthenia gravis
52
Clinical manifestations of myasthenia gravis
Diplopia ⚬ Ptosis ⚬ Dysarthria ⚬ Dysphagia ⚬ Weakness of the muscles of the face and throat (Bulbar Symptoms) ￭ Bland facial expression ￭ Myasthenic smile/ snarl or grimace smile ￭ Dysphonia (voice impairment) ￭ Dysfunctional fine motor movement of hands like in writing ⚬ Generalized weakness
53
A sudden exacerbation of motor weakness putting the client at risk of respiratory failure and aspiration.
Myasthenic Crisis
54
Manifestations of myasthenic crisis
tachycardia, tachypnea, severe respiratory distress, dysphagia, restlessness, impaired speech, and anxiety
55
The result of overdosage with the anticholinesterase (cholinergic) medications used to treat MG.
Cholinergic Crisis
56
Manifestations of cholinergic crisis
gastrointestinal manifestations, severe muscle weakness, vertigo, and respiratory distress
57
single fiber electromyography to detect delayed or failed neuromuscular transmission is muscle fibers supplied by a single nerve fiber.
Nerve Stimulation studies
58
– can detect or fail neuromuscular transmission in muscle fibers supplied by a single nerve fiber
Single- fiber electromyography
59
Dx test for myasthenia gravis
Tensilon Test (Edrophonium chloride Test) ⚬ - Use of edrophonium chloride which is injected into the patient. ⚬ - Administered IV 2 – 10 mg slowly. ⚬ - Interpretation: (+) Tensilon Test – if there’s an immediate improvement in muscle strength 30-90 seconds after the administration. ⚬ Antidote: Atropine Sulfate
60
Pharmacolgic tx for Myasthenia gravis
Anticholinesterase ￭ E.g. Neostigmine (Prostigmin), Pyridostigmine (Mestinon, Regonol),
61
Management for myasthenia gravis ⚬ A technique used to treat exacerbations and performed before surgical intervention. ⚬ The goal is to remove the anti-Ach receptor antibodies, thus improving severe muscle weakness, fatigue. ⚬ 50ml/min is withdrawn to the centrifuge in the plasmapheresis machine then it is replaced with donor plasma or colloids and returned to the client.
PLASMAPHERESIS
62
Surgical management for myasthenia gravis
THYMECTOMY
63
• An acute inflammatory demyelinating disorder of the peripheral nervous system is characterized by an acute onset of motor paralysis (usually ascending). • Approximately 80% to 90% have a spontaneous recovery with little or no residual disabilities.
Guillain – Barre Syndrome (GBS)
64
Characterized by severe weakness, especially in the lower extremities, loss of muscle strength progressing to quadriplegia and respiratory failure; decreasing deep tendon reflexes; decreasing vital capacity; paresthesia, numbness; pain; facial muscle involvement. • ANS such as bradycardia, sweating, and fluctuating BP (notable hypotension) may last for 2 weeks.
ACUTE STAGE (GBS)
65
• Occurs 2 to 3 weeks after initial onset. • Marks the end of changes in condition; characterized by a “leveling off” of symptoms • Generally, labile autonomic functions stabilize
Stabilizing/Plateau Stage(GBS)
66
• May take from several months to 2 years • Marked by improvement in symptoms • Generally, muscle strength and function return in descending order.
Recovery Stage(GBS)
67
• Chronic irritation of the fifth cranial nerve is characterized by paroxysms of pain in the area innervated by any of the three branches, but most commonly the second and third branches of the trigeminal nerve. • Occurs most often before 35 years of age and is more common in women than men.
Trigeminal Neuralgia (Tic Douloureux)
68
3 divisions of CN V
Ophthalmic– supplies the forehead, eyes, nose, temples, meninges, paranasal sinuses, and part of the nasal mucosa. • Maxillary- supplies the upper jaw, teeth, lip, cheeks, hard palate, maxillary sinus, part of the nasal mucosa. • Mandibular- supplies the lower jaw, teeth, lip, buccal mucosa, tongue, part of the external ear, and meninges.
69
• A disorder of the seventh cranial (facial) nerve, characterized by unilateral paralysis of the facial muscles. • The facial nerve is primarily a motor nerve that supplies all the muscles associated with an expression on one side of the face. • The sensory component innervates the anterior two-thirds of one side of the tongue. • It occurs at any age but is seen most often in adults between 20 and 60.
Bell’s Palsy (facial paralysis)
70
Clinical manifestations of Bell's palsy
• Paralysis of the facial muscles on one side of the face. • Paralysis of the upper eyelid with loss of the corneal reflex on the affected side • Loss or impairment of taste over the anterior portion of the tongue on the affected side. • Increased tearing from the lacrimal gland on the affected side • Upward movement of the eyeball on closing the eye (Bells Phenomenon)
71
Affects multiple cortical functions, calculation, learning capacity, language, and judgment resulting from the death of neurons and/or the loss of communication. • A chronic and progressive deterioration of brain function marked by impairment of memory (all cases involve amnesia), confusion, and the ability to concentrate.
DEMENTIA
72
Factors that increase the risk of developing one or more kinds of Dementia
• Age-related cognitive decline • Family history • Mild cognitive impairment • Depression or other emotional problems • Delirium • Smoking and alcohol use • Huntington’s disease • Creutzfeldt-Jakob disease, also known as "mad cow disease," • Parkinson’s disease, associated with damage to a part of the brain involved with the movement.
73
Clinical Manifestations of dementia
• Amnesia • Aphasia • Apraxia • Agnosia • Disturbance in executive functioning • Decrease in intellectual functioning and judgment • Impairment in social and occupational functioning • Social blunders – sexually inappropriate behavior and language • Personality change
74
• A form of dementia characterized by progressive, irreversible deterioration of general intellectual functioning. • They live about 8 to 10 years following diagnosis, although some live as long as 20 years.
Alzheimer’s Disease (AD)
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Two types of AD
• Familial AD • Sporadic AD
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77
Why do we need to Instruct client- don’t take food Vitamin B6 (Pyridoxine) cereals, organ meats, green leafy vegetables when taking levodopa( anti-parkinsonian agent)
because B6 reverses therapeutic effects of levodopa.
78
What are the nursing considerations when client is taking anti-parkinsonian medications?
Nursing Considerations: ￭ Take with meals – to decrease GIT irritation ￭ Inform client – urine/ stool may be darkened ￭ Instruct client- don’t take food Vitamin B6 (
79
Nursing management for patients with huntington's disease
• Maintain in an upright position while the client eats; support the head to prevent aspiration during mealtime. • Provide food that is thick enough to manage, such as thick soups, mashed potatoes, stews, or casseroles. • Make sure food is swallowed before giving another spoonful of food. • Provide a calm, relaxing eating environment. • Provide ROM exercises on a regular schedule in the daytime. • Keep the skin clean and dry, • Pad side rails and headrests of special chairs. • Turn and inspect the skin at least every 2 hours, giving special considerations to the bony prominent area. • Choose alternative methods of communication while the client can participate. • Continue to incorporate therapeutic communication techniques, even the client is not responsive.

MEDICAL-SURGICAL(MIDTERM) (4 decks)

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