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PHYSL 372 > Lecture 16 - Motor Disorders > Flashcards

Lecture 16 - Motor Disorders Flashcards

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1
Q

a disease where the immune system attacks the acetylcholine receptor by producing antibodies to this receptors

A

myasthenia gravis

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2
Q

what are some of the initial symptoms of myasthenia gravis?

A

ptosis (drooping eyelids), blurred vision, mouth hanging open, smile resembles a snarl

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3
Q

which muscles are typically affected first in myasthenia gravis?

A

facial muscles and external ocular muscles

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4
Q

what are some symptoms of myasthenia gravis as it begins to spread?

A

increased difficulty swallowing, dyspnea (shortness of breath) upon mild exercise, weakness of trunk and limb muscles

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5
Q

what is the average age for the onset of myasthenia gravis?

A

28 years in females and 42 years in males

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6
Q

what are the major treatments for myasthenia gravis?

A

removal of the thymus, immunosuppressants, anticholinesterase drugs

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7
Q

antibody binding to ACh receptors leads to:

A

increased rate of endocytosis

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8
Q

go review slide 443

A

how on earth does a woman turn all that text into flashcards

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9
Q

what is a key piece of evidence to suggest that myasthenia gravis is an autoimmune disease?

A

insertion of a fish ACh receptor that was close enough to the endogenous mouse receptors that the mouse antibodies attacked its own ACh receptors

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10
Q

do you remember the neuromuscular junction?

A

how could I not (but just incase its slide 445)

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11
Q

one treatment for myasthenia gravis is to give medicines that inhibit acetylcholinesterase inhibitors. that way, the ACh will _____ and it can _____

A

not be deactivated, stay around longer to keep muscles contracting

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12
Q

an anticholinesterase drug which reduces the symptoms of myasthenia gravis by inhibiting ACh-esterase, preventing the breakdown of ACh

A

neostigmine

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13
Q

neostigmine is _____, so you have to take it daily

A

reversible

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14
Q

a disease where the immune system attacks myelin and oligodendrocytes in the CNS (stage 1), and then those axons that lack myelin will eventually die (stage 2)

A

multiple sclerosis (MS)

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15
Q

what are the two major stages of symptoms of MS?

A

1) gradual decline in myelin and an increase in deficits
2) cycles of symptoms interspersed with remissions

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16
Q

what the major symptoms of MS?

A

blurred vision, numbness, incoordination, speech disturbances

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17
Q

what is the age of onset for MS?

A

20-40 years old

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18
Q

is MS more common in females or males?

A

there is a 3:1 ratio of females to males

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19
Q

where is MS the most prevelant?

A

the Northern hemisphere

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20
Q

what is the major treatment for MS?

A

corticosteroids or immunosuppressants

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21
Q

what does the animal model for MS look like?

A

inject myelin proteins or CNS tissue together with agents that stimulate the immune system

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22
Q

are immunosuppressents effective in halting MS?

A

no

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23
Q

a disease where the immune system attacks myelin and schwann cells in the PNS. typically follows infection and associated inflammation, and there is no known hereditary predisposition

A

Guillain-Barre syndrome

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24
Q

the symptoms of guillain-barre sydrome are dependent on:

A

severity

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25
can guillain-barre syndrome lead to paralysis?
yes
26
how is guillain-barre syndrome treated?
with immunosuppressants (if needed, breathing is supported with a respirator until the disease resolves)
27
in guillain-barre syndrome, the ____ surrounding peripheral axons is _____
myelin sheath, lost
28
loss of the myelin sheath in guillain-barre syndrome leads to:
impaired nerve impulse transmission
29
after guillain-barre syndrome resolves, myelin and nerve damage is:
spontaneously repaired (unlike in the CNS with MS)
30
a single motorneuron and all the the muscle fibers it innervates
motor unit
31
what is the muscle:nerve ratio for the eye muscles?
1:1 (every nerve innervates one muscle fiber)
32
what is the muscle:nerve ratio for the biceps?
750:1 (every nerve innervates 750 muscle fibers)
33
- motorneuron death - causes muscle weakness and paralysis - death occurs 3-5 years from onset (respiratory failure) - two forms: sporadic and familial - onset between ages 40-70 - more common in men than in women (2:1) - no proven treatments these are all characteristics of:
amyotropic lateral sclerosis (ALS)
34
go review slide 457
its got some fun facts about fruit bats
35
a genetic mutation that occurs in 10-15% of familial ALS, and is also linked to aporadic ALS
superoxide dismutase (SOD1) gene mutation
36
the SOD1 enzyme protects cells from:
reactive oxidative species
37
mutations in the SOD1 gene causes the SOD1 enzyme to be:
pro-apoptotic
38
do you need one or two copies of a mutated SOD1 gene to have ALS?
one (dominant)
39
in ALS, inadequate calcium buffering in large neurons leads to ____, which then leads to more ____ that damage neurons and glial cells (including glutamate transporters, depending on the ____
mitochondrial damage (excitotoxicity), reactive oxidative species, SOD1 enzymes
40
increased AMPA receptors in ALS leads to:
more Ca++ load
41
an autosomal recessive diesease caused by a genetic defect in the SMN1 gene, which encodes SMN, a protein widely used in all eukaryotic cells
spinal muscular atrophy (SMA)
42
SMN1 is apparently selective for:
development of motor neurons
43
a diminished abundance of the SMN protein results in:
the death of neuronal cells in the ventral horn of the spinal cord and subsequent system-wide muscle wasting (atrophy)
44
spinal muscular atrophy (SMA) manifests in various degrees of severity which all have in common:
general muscle wasting and mobility impairment
45
true or false: spinal muscular atrophy (SMA) is the most common genetic cause of infant death
true
46
the diagnosis of spinal muscular atrophy (SMA) is based on five physical symptoms:
- poor muscle tone in the limbs and trunk - feeble movements of the arms and legs - swallowing difficulties - a weak sucking reflex - impaired breathing
47
how many types of SMA are there?
four
48
- also known as Werdnig-Hofmann syndrome - the most severe form of SMA (lifespan 2-3 years) - symptoms present before six months old - children cannot crawl, walk, or breathe properly - affects 60% of all SMA patients these are all characteristics of:
type I SMA
49
- comes to medical attention before the age of 18 months - respiratory muscles and feeding problems - can sit, but not walk properly - can live into adulthood these are all characteristics of:
type II SMA
50
- known as Kugelberg-Welander disease or juvenile SMA - symptoms appear between 18 months and early adulthood - difficulty walking, muscle weakness, prone to respiratory infections - normal life expectancy these are all characteristics of:
type III SMA
51
- adult form of SMA (symptoms emerge after age 35) - uncommon - affects walking these are all characteristics of:
type IV SMA
52
SMA is less severe when a person has more copies of the:
backup SMN2 gene (but SMN2 often makes truncated ineffective SMN)
53
cures SMA by altering pre-mRNA splicing to make more full length copies of the SMN protein
antisense oligotide therapy (nusinersen)
54
what does nusinersen do?
improves the function of the SMN2 gene
55
other SMA treatments include using ____ to deliver a replacement _____ to increase production of SMN
viruses, SMN1
56
a muscle wasting disease caused by defects in the dystrophin gene
duschene muscular dystrophy
57
is the dystrophin gene sex linked or autosomal?
sex linked (extremely large gene on the X chromosome)
58
dystrophin has a critical role in the maintenence of stability by:
creating a link between the contractile machinery and the extracellular matrix
59
list the sequence of events in duschene muscular dystrophy that lead to muscle wasting
structrual defect --> membrane instability --> apoptosis necrosis --> inflammation --> fibrosis
60
what are some of the symptoms of duschene muscular dystrophy?
child doesn't run, weakness in the legs, pseudohypertrophy (!)
61
by what age do symptoms of duschene muscular dystrophy appear?
age 3
62
how long do people with duschene muscular dystrophy live?
often die within their third decade
63
duschene muscular dystrophy can be detected with ~95% accuracy by:
genetic studies performed during pregnancy
64
how is duschene muscular dystrophy treated?
there is no treatment right now, but genetic manipulations with viral vectors may help correct mutant gene in the future
65
an extracellular recording of action potentials travelling down muscle fibers during muscle contractions
electromyography (EMG)
66
go look at slide 471
dear god can i be done with this deck
67
what are the two types of strokes?
ischemic stroke (85%) and hemorrhagic stroke (15%)
68
what are the two types of hemorrhagic stroke?
- intracerebral hemorrhage - subarachnoid hemorrhage
69
the third leading cause of death in the US and the leading cause of disability
stroke
70
what is the most common problem for people who survive strokes?
hemiplegia (75-88%)
71
controls the movement of the left side of the body as well as analytical and perceptual tasks
the right hemisphere
72
controls the movement of the right side of the body as well as speech and language abilities
the left hemisphere
73
controls many of our reflexes and much of our balance and coordination
the cerebellum
74
the area of the brain that controls all of our involuntary "life-support" functions as well as abilities such as eye movements, hearing, speech, and swallowing
the brainstem
75
a chronic disability of the CNS characterized by aberrant control of movement of posture, appearing early in life and not the result of progressive neurological disease
cerebral palsy
76
list six cerebral palsy associated disabilities
- motor disorders, hypertonia, spasms - epilepsy (20-50%) - speech disorders (50%) - vision and hearing (25%) - behaviour abnormalities - learning difficulties
77
list six type of brain damage associated with cerebral palsy
- bleeding or clot (in utero stroke) - brain or ventricle malformation - trauma to the brain - lack of oxygen - infection - toxins

PHYSL 372 (18 decks)

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