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54/64 Final Content > Neuromuscular Disorders > Flashcards

Neuromuscular Disorders Flashcards

1
Q

Disease caused by an absence of hexosaminidase (Hex-A)

A

Tay Sach’s Disease

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2
Q

Enzyme needed to break down a particular lipid in the brain and CNS

A

Hexosaminidase (Hex-A)

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3
Q

Tay Sach’s is an autosomal _________ disease

A

Recessive

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4
Q

Tay Sach’s disease primarily impacts isolated and inbred groups/cultures such as

A

Amish, Cajun, Eastern European Jewish heritage

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5
Q

What is the chance of an offspring inheriting an autosomal recessive disease?

A

25% (1 in 4)

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6
Q

Tay Sach’s Disease behaviors

A

Progressive neurological deterioration, blindness, cherry red spot on macula

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7
Q

Tay Sach’s Disease onset

A

Most commonly early onset (infant) with death usually before age 4

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8
Q

progressive symptoms of the CNS related to Tay Sach’s Disease

A

Decreased muscle tone, visual difficulties, seizures

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9
Q

T or F: males and females are affected equally with an autosomal recessive disorder

A

True

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10
Q

Tay Sach’s disease diagnosis

A

Determine activity of Hex-A (serum, leukocytes, tears, body tissue), genetic testing

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11
Q

Tay Sach’s disease treatment

A

Supportive (PT, OT, neurology, anticonvulsants, palliative care)

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12
Q

T or F: there is a cure for Tay Sach’s Disease

A

False

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13
Q

A chronic and progressive autosomal dominant disease of the nervous system

A

Huntington’s Disease

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14
Q

Huntington’s Disease affects men and women ___-___ years old

A

35-45

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15
Q

Huntington’s Disease symptoms are caused by a deficiency of what two neurotransmitters?

A

Acetylcholine and GABA

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16
Q

The deficiency of acetylcholine and GABA in Huntington’s Disease causes premature death of cells in the

A

Basal ganglia, cortex, cerebellum

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17
Q

The basal ganglia play a role in

A

Movement

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18
Q

The cerebral cortex plays a role in

A

Thinking, memory, judgement, perception

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19
Q

The cerebellum plays a role in

A

Voluntary muscle activity

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20
Q

Huntington’s Disease (autosomal dominant) inheritance

A

50%

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21
Q

Huntington’s Disease behaviors

A

Chorea, athetosis, facial tics/grimaces, slurred speech, dementia, emotional instability

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22
Q

Huntington’s Disease diagnosis

A

Presence of behaviors, family hx, genetic testing

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23
Q

Management of Huntington’s Disease

A

Dopamine receptor blockers for chorea, antidepressants, supportive care

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24
Q

What is deutetrabenazine (Austedo) and what is it given for?

A

Dopamine receptor blocker given for chorea or involuntary movement associated with Huntington’s Disease

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25
Q

What medication can be given for dementia in the early stages of Huntington’s Disease?

A

Aricept

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26
Q

Huntington’s Disease supportive care

A

Speech, OT, PT, genetic counseling, psychiatric therapy

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27
Q

Lou Gerhig’s Disease is another name for

A

Amyotrophic Lateral Sclerosis (ALS)

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28
Q

Progressive deterioration of motor neurons in the spinal cord (anterior horn), some cranial nerves, and cerebral cortex (axon and muscular atrophy)

A

Amyotrophic Lateral Sclerosis (ALS)

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29
Q

What gender is most affected by ALS?

A

Males

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30
Q

General behaviors of ALS

A

Muscle atrophy and spasticity

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31
Q

ALS behaviors with lower motor neuron involvement

A

Muscle weakness and atrophy, fasciculations (twitching)

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32
Q

ALS behaviors with upper motor neuron involvement

A

Spasticity, hyperreflexia, (+) babinski

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33
Q

ALS behaviors with lower cranial nerve involvement

A

Drooling, speech problems

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34
Q

What is the ultimate cause of death in a patient with ALS?

A

Atrophy of respiratory muscles

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35
Q

ALS medical diagnosis

A

Electromyography (EMG), muscle biopsy

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36
Q

ALS medical treatment

A

PO Rilutek (Riluzoke; glutamate antagonist) and Radicava (edaravone) IV q14 days to slow progression

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37
Q

Cause of ALS

A

Unknown; multifactorial (neurological trauma, genetics, etc.)

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38
Q

An autoimmune disease characterized by a defect in transmission of impulses at the neuromuscular junction and loss of available receptors

A

Myasthenia Gravis

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39
Q

In Myasthenia Gravis, the body stops recognizing _________ receptors as part of self and attacks these receptors

A

Acetylcholine

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40
Q

Neurotransmitter responsible for carrying nerve impulses

A

Acetylcholine

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41
Q

Myasthenia Gravis Behaviors

A

Weakness and fatigue, Ptosis and double vision, mouth open, sagging jaw, expressionless face, “snarl-like” smile

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42
Q

Describe of Myasthenia Gravis progresses

A

Upper extremities affected before lower extremities; proximal (center) affected before distal (disease spreads outwardly)

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43
Q

What is the first sign of myasthenia gravis in 50% of affected individuals?

A

Ptosis/double vision

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44
Q

T or F: myasthenia gravis is characterized by flares and periods of remission

A

True

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45
Q

Myasthenia gravis main concern

A

Loss of respiratory function (mechanical ventilator may be needed)

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46
Q

Myasthenia Gravis medical diagnosis

A

Antibodies for Ach receptors

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47
Q

Myasthenia Gravis pharmacological management

A

Anticholinesterases, long-term corticosteroids (immunosuppressives)

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48
Q

Myasthenia Gravis can be managed by replacing plasma in the body that contains abnormal antibodies with other fluids. This is known as

A

Plasmapharesis

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49
Q

Plasmapharesis considerations

A

Indicated for MG crisis; not a long-term treatment or cure

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50
Q

Myasthenia Gravis surgical management that may remove the source of abnormal antibody production that causes the disease

A

Thymectomy

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51
Q

In patients with myasthenia gravis, ___% have complete remission of disease following a thymectomy, while ___% may have no effects

A

70; 30

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52
Q

Myasthenia Gravis complications

A

Cholinergic crisis, myasthenia crisis

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53
Q

In a patient with Myasthenia Gravis, a cholinergic crisis may be the result of

A

Over-medication (too much anticholinesterase)

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54
Q

Myasthenia Gravis cholinergic crisis treatment

A

Atropine, discontinue med, ventilate

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55
Q

Myasthenia crisis triggers

A

Under-medication, exacerbation of disease, illness/flu, change in meds, pregnancy

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56
Q

Myasthenia crisis interventions

A

Tensilon, ventilation, absolute quiet and bed rest

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57
Q

S/S of myasthenia crisis

A

Tachycardia, respiratory distress (cyanosis, absent cough/gag reflex, dysphasia)

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58
Q

Cholinergic crisis behaviors

A

SLUDGE: salivation, lacrimation, urination, diarrhea, GI upset, emesis; bradycardia

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59
Q

Degenerative disease of basal ganglia, part of the extrapyramidal system, causing an imbalance between acetylcholine and dopamine

A

Parkinson’s Disease

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60
Q

Hallmark feature of Parkinson’s Disese

A

Loss of dopaminergic neurons in substantia nigra (in basal ganglia) and other areas of brain

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61
Q

The extrapyramidal system (EPS) controls

A

Voluntary muscle movement

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62
Q

In Parkinson’s Disease, Acetylcholine is too ____ and Dopamine is too ____

A

High; low

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63
Q

Goal of treatment for Parkinson’s Disease

A

Increase supply of dopamine or block/lower acetylcholine levels

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64
Q

Myasthenia Gravis is 3x more common in

A

Females BUT if onset over age 50, then more common in males

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65
Q

Parkinson’s Disease is more common in _____ and incidence increased with ___

A

Men; Age

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66
Q

Most Parkinson’s Disease deaths are from

A

Falls and pneumonia

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67
Q

Parkinson’s Disease onset

A

50-70 years of age

68
Q

T or F: symptoms such as slowness, stiffness, and muscle pain usually begin on one side in patients with Parkinson’s Disease

A

True

69
Q

Parkinson’s Disease stimuli/causes

A

Multifactorial (genetics, environmental — agricultural chemicals, heavy metals)

70
Q

What are the four cardinal symptoms of Parkinson’s Disease?

A

Tremor (head-bob, pin roll), muscle rigidity, bradykinesia, postural instability

71
Q

Aside from the four cardinal symptoms, what are other symptoms of Parkinson’s Disease?

A

Shuffling gait, stooped posture, muscle rigidity, mask-like facial expression, akinesia (absence/poverty of normal movement) arms do not swing when walking, changes in handwriting (micrographia), drooling

72
Q

Parkinson’s Disease diagnosis

A

Based on symptoms, hx, and assessment; unified Parkinson’s disease rating scale (UPDRS), DaTscan

73
Q

Radioactive drug that determines how much dopamine is in the brain for diagnosis of Parkinson’s disease

A

DaTscan

74
Q

Parkinson’s disease management

A

Drug therapy (mainstay), self-help devices for ADLs, rehabilitation, warm baths and massages to relax muscles, raised toilet seat, long-handle comb and razor, ROM to loosen joints and prevent deformities

75
Q

Goal of Parkinson’s management

A

Maintain ADLs and independence as long as possible

76
Q

Surgical management of Parkinson’s Disease

A

Deep Brain Stimultion (DBS) and experimental measures such as adrenal cell transplant and fetal tissue transplant

77
Q

Group of permanent disorders of the development of movement and posture, causing activity limitations, that are attributed to nonprogressive damage that occurred in the developing fetal or infant brain

A

Cerebral palsy

78
Q

Most common clinical type of cerebral palsy (CP) that most often presents as hypotonia (developmental delay)

A

Spastic

79
Q

Type of cerebral palsy that involves all four extremities resulting in severe disability

A

Quadriparesis (tetraparesis)

80
Q

Behaviors of quadriparesis CP

A

Speech and swallowing difficulties, tongue protrusion (incomplete), labile emotions in some patients

81
Q

What is the single most important determinant of CP?

A

Preterm birth or ELBW/VLBW

82
Q

What is the most common cause of brain damage in CP cases?

A

Anoxia

83
Q

Prenatal risk factors for CP

A

Brain abnormalities, genetics, intrauterine infections, LBW infants, placental insufficiency (70%)

84
Q

Perinatal (at birth) risk factors for CP

A

Jaundice, infection acquired at birth, asphyxia (cord)

85
Q

Postnatal risk factors for CP

A

TBI, infections, stroke, skaken baby, near drowning

86
Q

Clinical S/S of CP

A

Increased OR decreased muscle tone, arching of back, poor head control, inability to sit up by 8 mo, seizures/epilepsy, random/uncontrolled body movements, balance/coordination problems, eating/swallowing impairment, learning difficulties, behavioral problems, visual/hearing problems, sleeping problems

87
Q

Spastic signs of CP

A

Increased muscle tone, tension, and resistance resulting in stiffness and unnatural positioning of limbs

88
Q

Non-spastic signs of CP

A

Floppy, inability to maintain posture, poor coordination

89
Q

Signs of CP in infants 2 months and older

A

Difficulties controlling head when picked up, stiff/shaking arms or legs, stiff legs that cross or “scissor” when picked up, problems with sucking and feeding

90
Q

Signs of CP in infants 6 months and older

A

Poor head control when picked up, reaching with one hand while the other is in a fist, problems eating and drinking, may not roll over w/o assistance

91
Q

Signs of CP in infants 10 months and older

A

Crawls by pushing off with one hand and leg while dragging opposite hand and leg, does not babble, unable to sit up on own, does not respond to own name

92
Q

Signs of CP in infants 12 months and older

A

Does not crawl or attempt to pull themselves up, unable to stand w/o support, does not search for things that they see you hide, does not say single words like “mama” or “dada”

93
Q

CP is characterized as a _________ _________ neuromuscular disorder

A

Severity spectrum

94
Q

CP diagnosis for high risk infants

A

Additional screening required for infants born preterm/LBW and/or low agar after 5 min

95
Q

CP diagnosis through physical exam

A

Assess muscle tone (stiff or floppy), primitive reflexes, milestones (sit, stand, walk)

96
Q

CP diagnosis MRI

A

Lesion found in movement center of brain

97
Q

CP management

A

Team approach, early intervention program and services, supportive therapy, promote socializtion

98
Q

T or F: CP is a progressive disease

A

False

99
Q

CP is more common in

A

Boys and African American children

100
Q

CP is related to prenatal, perinatal, and postnatal _____ damage

A

Brain

101
Q

CP is typically diagnosed by age

A

3

102
Q

Mobilizing devices for patients with CP

A

Braces, scooters, walkers, strollers

103
Q

Medications for CP

A

Antispasmodics, skeletal muscle relaxants, phenol nerve block, anticonvulsants, laxatives/stool softeners, anticholinergics

104
Q

Technical aids for CP

A

Voice synthesizers, computers for communication, picture boards

105
Q

CP surgery

A

If physical therapy is not adequate: Tendon release (decrease spasticity), spinal fusion/correction

106
Q

Therapeutic regimen for patients with CP

A

PT, OT, education (public school), recreation, speech therapy

107
Q

Gradual progressive degeneration of muscle fibers

A

Muscular Dystrophy (MD)

108
Q

Inherited X-linked recessive disease that primarily affects males

A

Muscular dystrophy

109
Q

General symptoms/behaviors of muscular dystrophy

A

Muscle weakness (primary), Gowers sign, pseudohypertrophy (enlarged calf), arched back, foot drop and tripping, toe walking, contractures, scoliosis

110
Q

Muscular dystrophy major cause of death

A

Respiratory and cardiac failure

111
Q

Types of muscular dystrophy

A

Duchenne’s (DMD), Becker’s, Myotonic (Steinert), Spinal muscular atrophy (SMA)

112
Q

Most common type of muscular dystrophy caused by absent dystrophin protein

A

Duchenne’s (DMD)

113
Q

Diagnosis of Duchenne’s typically occurs before age

A

10

114
Q

Less common and less severe type of muscular dystrophy caused by malformation of dystrophin protein

A

Becker’s

115
Q

Diagnosis of Becker’s muscular dystrophy is typically between ages

A

10-20

116
Q

Duchenne’s MD (pseudohypertrophy) timeline of symptoms

A

Usually begin to see S/S by age 3, wasting and weakness increase w/ calf muscle hypertrophy, loss of independent ambulation by age 10, wheel-chair bound by age 15, death r/t cardiac or respiratory arrest by age 25

117
Q

Attaining a standing posture by assuming a kneeling position, then gradually pushing torso upright (with knees straight) by “walking” hands up legs

A

Gower’s sign

118
Q

MD diagnosis

A

Clinical manifestations, hx of behaviors/symptoms, DNA test (mutations in dystrophin), EMG (how muscles respond to electric activity), muscle biopsy (increase serum creatine kinase reveals degeneration)

119
Q

MD complications

A

Contractures, disuse atrophy, weight gain (esp. after starting use of wheelchair), cardiac and pulmonary complications (late stage)

120
Q

1 goal of MD treatment

A

Maintained independence and function as long as possible and prevent complications

121
Q

MD treatment

A

Palliative, symptomatic, supportive

122
Q

Interventions to minimize deformity in patients with MD

A

ROM, PT, ortho procedures and surgery (for scoliosis; usually by age 13)

123
Q

Indications of corticosteroids such as prednisone for MD

A

Increase muscle bulk and strength, improve respiratory function, prolonged ambulation, decrease incidence of cardiomyopathy and scoliosis

124
Q

Recommendation for family of patient with MD

A

Genetic and family counseling

125
Q

Chronic, progressive, degenerative disorder of the CNS characterized by destruction and scarring of the myelin sheath which impedes nerve impulses

A

Multiple Sclerosis (MS)

126
Q

Disease of young to middle-aged adults (20-50) that affects women 2-3x more than men and is 5x more prevalent in temperate climates than tropical

A

Multiple Sclerosis

127
Q

What are the four types of MS?

A

Relapsing-remitting, primary-progressive, secondary-progressive, progressive-relapsing

128
Q

Most common type of MS characterized by acute attacks with full/partial recovery between attacks

A

Relapsing-remitting

129
Q

Type of MS characterized by progression of disability from onset WITHOUT plateaus/remissions or with occasional minor improvements

A

Primary-progressive

130
Q

Type of MS characterized by progression at a variable rate, occasional relapses, and minor remissions

A

Secondary-progressive

131
Q

Least common type of MS characterized by progression from onset with clear acute relapse with or without full recovery

A

Progressive-relapsing

132
Q

MS generally affects women between the age of

A

20 and 40

133
Q

Chronic inflammation, demyelination, and scarring of the CNS

A

MS

134
Q

MS results from an autoimmune response orchestrated by autoreactive _____

A

T-Cells

135
Q

MS is perpetuated by faulty

A

Immunoregulation

136
Q

In MS, _____ lesions are the initial inflammatory response by _____ lesions result in scarring and hard sclerotic plaque

A

Acute; chronic

137
Q

Characteristics of MS remissions

A

Typical occur after onset of symptoms and can be 1-3 months or maybe even years, recovery incomplete with successive attacks (exacerbations), results in more permanent damage after each one

138
Q

MS behaviors

A

Insidious onset, diverse presentation depending on location of plaque formation, frequent visits to Dr attempting to make sense of symptoms (difficult to diagnose)

139
Q

CNS symptoms of MS

A

Fatigue, cognitive impairment, depression, unstable mood

140
Q

Visual symptoms of MS

A

Nystagmus, optic neuritis, diplopia, faded color, loss of sight possible

141
Q

Speech symptoms of MS

A

Dysarthria

142
Q

Throat symptoms of MS

A

Dysphagia

143
Q

Musculoskeletal symptoms of MS

A

Weakness/one-sided weakness, muscle and joint spasms, ataxia, paralysis, heaviness of 1 leg, abnormal gait, foot dragging and poor control, fatigue

144
Q

Sensory symptoms of MS

A

Pain, paresthesias, numbness, tingling, impaired proprioception, decreased temperature sensation, crawling sensation

145
Q

GI symptoms of MS

A

Incontinence, diarrhea, constipation

146
Q

Urinary symptoms of MS

A

Incontinence, frequency or retention

147
Q

T or F: fatigue worsens as day goes on in patients with MS

A

True

148
Q

Sexual dysfunction related to MS in women and men

A

Women: decreased libido, decreased orgasmic sensation
Men: erectile and ejaculatory dysfunction

149
Q

_________ may cause some women to experience MS remission with improvement during ________ due to hormonal changes

A

Pregnancy; gestation

150
Q

Pregnant women are at increased risk of MS exacerbation _________

A

Postpartum

151
Q

Life expectancy is >___ years post MS diagnosis

A

25

152
Q

Death from MS usually results from

A

Infectious complications, immobility, or other dx

153
Q

MS diagnosis

A

Based primarily on hx, manifestations, and presence of multiple lesions over time; MRI, Lumbar puncture and CSF fluid exam, Basic Protein Assay (BPA)

154
Q

MS diagnosis that checks for plaque and random scarring and reveals lesions as small as 3-4 cm

A

MRI

155
Q

CSF fluid exam through lumbar puncture for MS diagnosis

A

Reveals increased levels of immunoglobulin G, lymphocytes, and monocytes

156
Q

MS diagnostic that checks for presence of active demyelination

A

BPA

157
Q

Primary pharmacological treatment for MS

A

Corticosteroids such as methyloprednisolone/ACTH/Prednisone/Decadron

158
Q

Corticosteroids for MS indications

A

Resolve edema, improve clinical symptoms of acute exacerbations, decrease inflammatory response

159
Q

Corticosteroids for MS consideration

A

Does NOT cure or alter course nor decrease # of future exacerbations

160
Q

Adjunctive medications for MS

A

Muscle relaxants, CNS stimulants, anticholinergics, cholinergics, TCAs, Anticonvulsants

161
Q

Muscle relaxants for MS

A

Baclofen, diazepam

162
Q

CNS stimulants for MS

A

Ritalin, cylert, provigil

163
Q

MS Interprofessional collaboration for symptom management

A

PT, OT, speech

164
Q

MS symptom management interventions

A

Balance exercise and rest, resistive/stretching exercises, psychotherapeutic drugs, hydrotherapy (warm mattress), nutrition, assistive devices

165
Q

Assistive devices for MS

A

Braces, splints, wheelchair

54/64 Final Content (4 decks)

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