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Nursing IV > SCI&CNS Disorders (Gas#15&16) > Flashcards

SCI&CNS Disorders (Gas#15&16) Flashcards

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1
Q

upper motor neurons carry impulses to or from brain?

A

away (descending)

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2
Q

Damage to upper motor neurons results in

A

increased muscle tone, loss of voluntary control, decreased coordination, hyperactive/abnormal reflexes

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3
Q

Damage to lower motor neurons results in

A

decreased muscle tone, absent or decreased reflexes, muscle atrophy

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4
Q

Ascending paths

A

Sensory, carry pain, temp (Afferent)

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5
Q

Afferent

A

Ascending sensory paths

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6
Q

Descending pathways

A

Motor, voluntary purposeful movements (efferent)

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7
Q

Efferent

A

Descending motor pathways

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8
Q

Muscular Dystrophy

A

progressive muscle degeneration and wasting

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9
Q

Duchenne’s Muscular Dystrophy

A

loss of muscle tissue thats replaced with connective tissue; muscles deteriorate

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10
Q

Patients with Duchenne’s Muscular Dystrophy have an absense of what?

A

Dystrophin-protein

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11
Q

Duschenne’s Muscular Dystrophy s/s

A

weak pelvic & shoulder gait, waddling gait, toe walking, hypertrophy of calf muscles, fatigue, skeletal deformities, cardiomyopathy

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12
Q

What age does Duschenne’s Muscular Dystrophy occur

A

3-5 yrs old

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13
Q

Acute stage of Guillain-Barre Syndrome (GBS)?

A

Severe rapid weakness, loss of strength, resp failure, loss of facial movement, bradycardia, hypotension, sweating, SIAH (retaining H2O &NA)

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14
Q

what happens after 2-3 weeks after initial onset of Acute stage of Guillain-Barre Syndrome (GBS)

A

they go into a plateau stage, their symptoms level off

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15
Q

Is Guillain-Barre Syndrome (GBS) an emergency?

A

yes because they don’t know how fast

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16
Q

Guillain-Barre Syndrome (GBS)

A

Rapid muscle weakness & paralysis (disorder of the PNS), paralysis starts from the feet and goes up

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17
Q

what can cause Guillain-Barre Syndrome (GBS)

A

eating undercooked poultry, ebstein barr virus

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18
Q

what gets inflamed with Guillain-Barre Syndrome (GBS)

A

segmental demyelination of peripheral nerves causes inflammation & degeneration in sensory & motor nerve roots

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19
Q

s/s Guillain-Barre Syndrome (GBS)

A

Ascending paralysis, poor nerve conduction, facial nerve involvement, may have respiratory involvement

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20
Q

what system is not affected with Guillain-Barre Syndrome (GBS)

A

cognitive & LOC

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21
Q

Myasthenia Gravis

A

A chronic progressive neuromuscular disorder, it destroys, alters receptors for ACH

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22
Q

What do you need ACH for?

A

muscle contractions

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23
Q

Without ACH in Myasthenia Gravis what happens to muscles?

A

This results in voluntary muscle weakness that escalates with continued activity

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24
Q

Myasthenia Gravis s/s

A

Diplopia (double vision), Ptosis (drooping of eye lid), generalized muscle weakness (therefor at risk for aspiration), laryngeal involvement

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25
Q

Diplopia

A

double vision

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26
Q

Ptosis

A

drooping of eye lid

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27
Q

what system is not effect with Myasthenia Gravis

A

Sensory changes

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28
Q

Dianosis for Myasthenia Gravis

A

Edrophonium test

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29
Q

Edrophonium test

A

used for Myasthenia Gravis, IV Tensilon is used. It prevents the breakdon of ACH so youll see an improvement within 5 mins. If no improvement its not MG

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30
Q

IV Tensilon is used for?

A

Edrophonium Test, it prevents the breakdown of ACH in Myasthenia Gravis

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31
Q

Myasthenia Gravis medications

A

Pyridostigmine (mestinon, Regonol), Glucocorticoids (to reduce production of antibodies), Immunosuppressants (Imuran), plasma exchanges, IV immune globulin

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32
Q

Why are immunosuppressants (Imuran) used for Myasthenia Gravis used?

A

it inhibits T Lymphocytes & reduces ACH receptor antibody levels

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33
Q

Myasthenia Crisis

A

A sudden exacerbation of motor weakness

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34
Q

What is Myasthenia Crisis caused by

A

most often due to undermedication, missed doses or a developing infection

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35
Q

Myasthenia Crisis s/s

A

Tachycardia, Tachypnea, severe respiratory distress, dysphagia, restlessness, impaired speech, anxiety

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36
Q

What surgical operation can patient have with Myasthenia crisis

A

thymectomy

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37
Q

Myasthenia Gravis teaching

A

avoid extreme temperatures, avoid others who have respiratory infections

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38
Q

what things can cause an exacerbation of Myasthenia gravis

A

extreme temperatures, respiratory infection

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39
Q

Pyridostigmine (mestinon, Regonol) are used for & why?

A

used for Myasthenia gravis & used because they inhibit the breakdown of ACH

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40
Q

Amyotrophic Lateral Sclerosis (ALS) is also called

A

Lou Gehrig’s Disease

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41
Q

Amyotrophic Lateral Sclerosis (ALS)

A

a progressive degenerative neurological disease, loss of motor neurons in spinal cord & brain, muscles basically waste away.

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42
Q

what systems does Amyotrophic Lateral Sclerosis (ALS) not effect

A

no sensory or cognitive changes

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43
Q

what is destroyed with Amyotrophic Lateral Sclerosis (ALS)

A

Nerves are destroyed FIRST then Myelin Sheath is destroyed & replaced with scar tissue along spinal cord

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44
Q

Amyotrophic Lateral Sclerosis (ALS) s/s

A

Dyspnea, difficulty clearing airway, depression, difficulty chewing, dysphagia, malnutrion, visual changes

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45
Q

Disorders that mimic Amyotrophic Lateral Sclerosis (ALS)

A

Hyperthyrodism, hypoglycemia, compression of the spinal cord, infection, neoplasms, lymme disease,

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46
Q

Amyotrophic Lateral Sclerosis (ALS) medication

A

Riluzole (Rilutek) first med developed to prolong survival

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47
Q

Riluzole (Rilutek) is used for?

A

Amyotrophic Lateral Sclerosis (ALS); helps prolong survival

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48
Q

Amyotrophic Lateral Sclerosis (ALS) diagnostics

A

MRI, MRS, Nerve conduction

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49
Q

Primary vs secondary HA

A

Primary:no cause Secondary: due to tumor ex

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50
Q

Tension HA

A

pain is like a band squeezing head; most common, “stress HA”

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51
Q

Causes of Tension HA

A

stress, anxiety, depression, lack of sleep, abnormal posturing (bending over) 2ndary disorders of eye, ears, sinuses

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52
Q

Tension HA treatment

A

ibprofen, ASA, no real med specifically for it

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53
Q

Migraine HA

A

unilateral pain (can point to it), intense, throbbing or pounding pain located in foreheads, eye, back of head

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54
Q

Migraines last how long?

A

4-72 hrs

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55
Q

Stages of migraine HA

A

Prodrome, Aura (a sensation occurs just before), attack, postdrome (residual HA, difficulty concentrating)

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56
Q

Migraine Dietary Triggers

A

Caffeine, chocolate, nuts, yeast, MSG, marinated foods

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57
Q

Migraine Physical triggers

A

menses, ovulation, sleep, odors, high altitude, fasting,

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58
Q

@ least 4 symptoms that need to be present in order to be a Migraine

A

unilateral pain, pulsating or throbbing, produces moderate to severe pain, worsens with ADL’s, Accompanied by N/V or sensitivity to light or noise

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59
Q

2 kinds of Migraine treatments

A

Abortive & preventative

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60
Q

Abortive migraine treatment

A

used to treat the symptoms during an attack

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61
Q

Preventative migraine treatment

A

bb (inderal), anti-seizure (depakote, Topamax), antidepressants

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62
Q

Medications used for abortive migraine treatment

A

OTC analgesics & NSAIDS (take early), Triptans (Imitrex, Axert, Zomig), Narcotics, Combinations (treximet)

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63
Q

Triptans (Imitrex, Axert, Zomig) are used for ?

A

Migraine HA

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64
Q

What 3 triptans are used as abortive treatment with migraine HA

A

Imitrex, Axert and Zomig

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65
Q

Which antiseizure meds are used to prevent migraine HA

A

Valproate sodium (Depakote) & topiramate (Topamax)

66
Q

Cluster HA

A

Unilateral, excessive tearing, redness in eye, congestion on affected side, excruciating pain

67
Q

How long do cluster HA last?

A

1/2-3 hours

68
Q

Abortive treatment for cluster HA

A

100% O2 for 10-15 mins, imitrex

69
Q

Preventative treatment for cluster HA

A

Ccb (calan)

70
Q

What other things can a patient do to treat a cluster HA

A

Acupuncture, relaxation, massage, regular exercise, herbs

71
Q

Primary tumors

A

Cause unknown, originate from brain cells, meninges, nerves, or glands

72
Q

Gliomas

A

Most aggressive brain tumor, malignant, poor prognosis

73
Q

Astrocytomas

A

Less malignant brain tumor

74
Q

Meningiomas

A

Brain tumor 90% benign. More common in women. If found in kids don’t remove because it’ll cause more brain damage. Slow growing! Grows on the meninges

75
Q

Risk factors for primary tumor

A

Female, Caucasian, 70 yrs or older, family hx, chemical exposure

76
Q

Secondary tumors are usually due to

A

Metastasis

77
Q

Neurological s/s of a secondary brain tumor

A

HA, gait disturbances, visual impairment, personality changes, altered mental status, focal weakness, paralysis, Aphasia (inability to communicate )

78
Q

SIADH is what kind of disorder?

A

ADH disorder

79
Q

What happens with SIADH

A

Increased levels of ADH so you’ll have water retention, hyponatremia, aldosterone will be suppressed

80
Q

How is ADH affected with diabetes insipidus?

A

There is a deficit of ADH so you’ll have large amounts of dilute urine

81
Q

A deficit in ADH is related to what kind of problems?

A

Increased ICP, severe head injuries, glasgow coma scale 8 or lower diabetes insipidus

82
Q

ADH

A

Hormone that limits the amount of water excreted by the kidneys

83
Q

3 major risk factors for SCI

A

Age (16-30), gender (male), alcohol or drug abuse

84
Q

Why are head injuries associated with SCI

A

Because with a head injury, blood supply could be cut off or lowered to spinal cord

85
Q

Most common cause of abnormal spinal cord movements

A

Acceleration & deceleration

86
Q

SCI occur most often at which sites?

A

C1-2, C4-6, T11&12, L1&2

87
Q

Complete SCI

A

Total loss of sensation & voluntary muscle control below the level of injury. Loss of ability to perspire below level of injury

88
Q

A complete SCI can result in what?

A

Paraplegia ( paralysis of lower body) or tetraplegia ( paralysis of all 4 extremities)

89
Q

Incomplete SCI

A

Sensory or motor function or both are preserved below level of injury.

90
Q

What region is the injury located with a tetraplegia and what is a tetraplegia

A

Cervical region and they have paralysis of all four extremities

91
Q

What region is the injury located at with a paraplegia and what is a paraplegia

A

Injury at thoracic or lower levels of the spine. Paraplegia is the paralysis of just the lower body

92
Q

What injury to the spine do you have to have I order to have respiratory paralysis and be put on a ventilator?

A

Injury to C1-C4

93
Q

Brown-Sequard Syndrome

A

Loss of movement on same side as the cord damage; loss of pain, temp & sensation on opposite side of cord damage

94
Q

Central cord syndrome

A

More muscle weakness/paralysis in upper body than lower half of body

95
Q

Horners syndrome

A

Incomplete cord transection of the cervical sympathetic nerves, ptosis of eyelid, constricted pupil

96
Q

Anterior cord

A

Localized injury

97
Q

Spinal shock

A

Temporal sudden loss of reflex below the level of injury (areflexia)

98
Q

Areflexia

A

Absence of reflexes

99
Q

When does spinal shock appear? And how long does it last?

A

Can begin within an hour of injury and can last for a few minutes to months

100
Q

Spinal shock s/s(including vs)

A

Bradycardia, hypotension, loss of sensation of pain, temp, & pressure, bowel & bladder dysfunction, flaccid paralysis of skeletal muscles

101
Q

Why would you give an NG tube to a pt with spinal shock

A

To decompress the intestines if bowel distention & paralytic ileus occur

102
Q

Neurologic shock s/s (including vs)

A

Orthostatic hypotension, tachycardia, respiratory insufficiency, hypothermia, paralytic ileus, urinary retention, oliguria(<400 output), inability to perspire

103
Q

Autonomic dysreflexia (autonomic hyperflexia)

A

Serious complication of a SCI.blood pressure rises to dangerous levels Of=stroke &death

104
Q

Autonomic dysreflexia (autonomic hyperflexia) vs

A

Bradycardia, HTN

105
Q

Autonomic dysreflexia (autonomic hyperflexia) s/s

A

Severe HA, sweating above injury, nasal congestion, red blotches on skin, goose bumps & cold clammy skin below injury,

106
Q

What causes Autonomic dysreflexia (autonomic hyperflexia) besides a SCI?

A

Visceral contractions & pain, distended bladder, constipation, UTI, catheter bag too full

107
Q

What are pts who have Autonomic dysreflexia (autonomic hyperflexia) at risk for?

A

Stroke & death

108
Q

How to prevent Autonomic dysreflexia (autonomic hyperflexia)

A

Look for blocked catheter, check collection bag, irrigate catheter, remove kinks, dis impact stool, loosen clothing, check for pressure sores

109
Q

Triheminal neuralgia effects which cranial nerve

A

C5

110
Q

Bell’s palsy effects which cranial nerve

A

C7

111
Q

Glossopharyngeal neuralgia effects which cranial nerve & what is it

A

C9; it causes pain in back of throat, tonsils, & middle ear

112
Q

Third nerve palsy effects which cranial nerve disorder and what is it

A

C3; pupil dilation, ptosis, abduction of eye

113
Q

Trigeminal neuralgia what is it & what triggers it

A

Extreme sudden unilateral burning facial pain that is triggered by sneezing light touch, talking, washing face, change in temp, exposure to wind or eating. lasts seconds c intermittent episodes

114
Q

Trigeminal neuralgia is also called?

A

Tic douloureux

115
Q

Trigeminal neuralgia treatment

A

Anti-convulsants (1st line) (tegretol, Dilantin, neurontin, lioresal) tricyclic antidepressants & neurosurgical procedures

116
Q

Surgical treatments for trigeminal neuralgia

A

Microvascular decompression (pad is inserted under nerve), rhizotomy (nerves are cut)

117
Q

What’s a benefit of a rhizotomy?

A

Provides immediate nerve pain relief, pt can gradually be weaned off of meds

118
Q

What is a microvascular decompression used for and what is it

A

Nerve pain, a pad is inserted under nerve

119
Q

Bell’s palsy & what can cause it

A

C7; unilateral nerve inflammation; vascular ischemia, viral infections, autoimmune can cause it

120
Q

Bell’s palsy risk factors

A

Family members who have had it, pregnancy (bc of hormonal changes), cold or flu, diabetes, weakened immune system

121
Q

Bell’s palsy s/s

A

Facial weakness/paralysis, usually on one side, not able to smile, forehead is smooth, dropping corner of the mouth, drooling, inability to close eye, impaired taste, difficulty speaking, sound sensitivity in one ear, tearing

122
Q

Bell’s palsy treatment and why

A

Steroids (to decrease inflammation), antivirals, analgesics (to control pain), eye production, physical therapy, acupuncture

123
Q

What vitamins are used with Bell’s palsy and why

A

B12 because it helps nerve impulse/conduction

124
Q

What kinds of people does postpoliomyelitis syndrome effect and what is it and what gets inflamed

A

Affects polio survivors. It’s a new weakness with unaccustomed fatigue, muscle atrophy and pain-joint degeneration. Inflammation of gray matter of spinal cord

125
Q

Criteria for postpoliomyelitis diagnosis

A

Hx of polio, period of partial or complete recovery, gradual onset of progressive/persistent NEW muscle weakness, symptoms last over 1 year

126
Q

How long can a postpoliomyelitis syndrome diagnosis take?

A

It can take up to a yr to diagnose it

127
Q

Treatment of postpoliomyelitis and what if you have pain with activities

A

Whatever symptoms are: physical therapy, pulmonary rehab programs; if activity causes pain, stop activity

128
Q

Complications of postpoliomyelitis

A

Falls, malnutrition, dehydration, acute respiratory failure, osteoporosis

129
Q

Neurological disorders

A

Multiple sclerosis, Parkinson’s, huntingtons, ALS

130
Q

Infections

A

Postpoliomyelitis

131
Q

Multiple sclerosis

A

Autoimmune disease, myelin sheath is destroyed and replaced with scar tissue, axons are eventually destroyed causing permanent damage. It’s gradual, slow most of time

132
Q

Triggers of ms

A

Febrile states (hot bath, fever), pregnancy, extreme physical exertion, fatigue, stress

133
Q

What happens after a pt with ms gives birth

A

She’ll go into remission for 3 months after birth

134
Q

Risk factors of MS

A

Female, age 20-40, temperate climates

135
Q

MS vision s/s

A

Blindness in one eye, red/green color distortion, double/blurred vision

136
Q

MS muscle/GI s/s

A

Muscle weakness, ataxia (coordination & balance problems), spasticity (excess of muscle tone)/ loss of bowel/bladder function

137
Q

MS sensation/emotional s/s

A

Pins and needles sensation/ depression

138
Q

Specific test for MS

A

No specific test. MRI, spinal tap, neuro exam done to rule out other disorders

139
Q

MS disease modifying medications

A

Interferon beta 1 (rebif) and interferon beta 2 (betaseron) Sq, Avonex IM weekly, Copaxone SQ daily, methylprednisolone IV & novantrone IV q 3 months

140
Q

MS medication for Spasticity problems

A

Baclofen, klonopin

141
Q

MS medication given to pts with optic neuritis

A

Solumedrol

142
Q

MS medication given for fatigue

A

Antidepressant

143
Q

Because pts with MS have fatigue when should activities be done?

A

In the am when they have most of their energy

144
Q

Parkinson’s

A

Lack of dopamine resulting in abnormal nerve functioning which causes loss of ability to control movements

145
Q

1st symptoms of Parkinson’s

A

Muscle rigidity, tremors, bradycardia

146
Q

Later s/s of Parkinson’s

A

Hypokinesia (decreased motor rxn to stimulus), changes in speech/writing, loss of balance & increased falls, expressionless face, shuffling gait, heat intolerance, constipation

147
Q

What will a pt with Parkinson’s facial expression look like?

A

It’ll look frozen

148
Q

Total disability is seen how long after diagnosis of Parkinson’s?

A

10-20 years poor prognosis

149
Q

Parkinson’s diagnostic tests

A

H&P, PET scan, drug screens (to make sure it’s not a rxn of a med)

150
Q

How long do dopamine agonists take to work with Parkinson’s

A

Can take 6 months to work

151
Q

Sinemet, levodopa are what?

A

Dopamine agonists used for Parkinson’s

152
Q

Med category’s used for Parkinson’s

A

Dopamine agonists, anticholinergics, MAOIs

153
Q

Why are anticholinergics (Cogentin) used for Parkinson’s?

A

They help limit the breakdown of dopamine

154
Q

Sinemet and levodopa are what? What’s important about them

A

Dopamine agonists used for Parkinson’s. Pt can develop a Plato effect so pt increases dose & therefore has to get off it completely

155
Q

When do you give a dopamine agonist?

A

Before they get out of bed

156
Q

Surgery for Parkinson’s

A

Thalamotomy (destruction of portion of thalamus), pallidotomy (destruction of the globus pallidus)

157
Q

Huntingtons disease s/s

A

Increased dementia & chorea (jerky, rapid involuntary movements), intellectual decline, emotional disturbances

158
Q

Huntingtons disease symptoms occur between which age

A

30-40yrs old

159
Q

What happens to the brain with huntingtons disease

A

Premature death of brain cells-basal ganglia & Cortex. There is a relative excess of dopamine

160
Q

Chorea

A

Jerky rapid involuntary movements associated with huntingtons

161
Q

Why is it important to get genetic counseling with Huntingtons disease

A

It’s a dominant gene. Kids have 50% chance of getting it from parents

Nursing IV (20 decks)

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