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Pathophysiology > Lecture 21/22: Skeletal Muscle Disorders > Flashcards

Lecture 21/22: Skeletal Muscle Disorders Flashcards

1
Q

Which of the following conditions is an autoimmune condition associated with anti-Ach receptor antibodies?

A

Myasthenia gravis

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2
Q

A patient comes into clinic with complains of weakness in eye, face, neck, and limb muscles. They have noticed eyelids are droopy and difficulty holding their head up. What condition do they most likely have?

A

Myasthenia gravis

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3
Q

A patient with Myasthenia gravis is most likely to have:
A. T cell hyperplasia
B. Thymic B cell hyperplasia

A

B. Thymic B cell hyperplasia

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4
Q

True or False: Repetitive EP stimulation (exercise) can worsen Myasthenia gravis

A

True - worsens muscle weakness

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5
Q

What are three ways to treat Myasthenia gravis?

A
  1. Acetylcholinesterase Inhibitor
  2. Immunosuppression
  3. Plasmapheresis
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6
Q

_____ is an auto-immune disorder that can be transferred by serum and is characterized by the presence of antibodies that inhibit function of pre-synaptic VG Ca channels

A

Lambert-Eaton Syndrome

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7
Q

Which drug can be used to treat Lambert-Eaton syndrome? How does it work?

A

3,4 DAP
- Prolongs AP
- Decreased amount of K reflux
- More Ca entry

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8
Q

True or False: Unlike myasthenia gravis, weakness may temporarily improve with exercise (exertion) in Lambert-Eaton Syndrome

A

True

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9
Q

Autonomic nervous system dysfunction may occur in Lambert-Eaton Syndrome. What is the most common symptom?

A

Dry mouth

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10
Q

Which of the following condition is usually associated with small cell lung carcinoma?
A. Lambert-Eaton Syndrome
B. Myasthenia Gravis

A

A. Lambert-Eaton Syndrome

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11
Q

True or False: Acetylcholinesterase inhibitors can be used to treat Myasthenia Gravis and Lambert-Eaton Syndrome

A

False - does not help in case of Lambert Eaton

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12
Q

Why is the prognosis for Lambert-Eaton Syndrome worse than myasthenia gravis?

A

Small cell lung cancer association

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13
Q

___ ____ ____: Rare autosomal recessive mutations that disrupt function of NMJ proteins

A

Congenital Myasthenic Syndromes

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14
Q

What is the most common CMS mutation?

A

LOF mutations in gene encoding episolon-subunit of Ach receptor

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15
Q

True or False: CMS is characterized by weakness and fatigue, results from problems at NMJ

A

True

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16
Q

Tetrodotoxin and Saxitoxin act on the NM to inhibit
A. K channel/Neuronal Na channel
B. Neuronal Ca/Na channel
C. Neuronal Na/Muscle Na Channel

A

C. Neuronal Na/Muscle Na Channel

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17
Q

True or False: Lambert Eaton Syndrome inhibits neuronal calcium channels

A

True

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18
Q

True or False: Ach and Nicotine positively act on Ach receptor, while Myasthenia gravis has an inhibitor effect

A

True

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19
Q

Tetanus and Botulinum toxin inhibit Ach release while _____ increases release

A

Black widow spider venom

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20
Q

True or False: Dendrotoxin inhibits K+ channel

A

True

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21
Q

Which of the following prevents INACTIVATION of Ach?
A. Black Widow Spider Venom
B. Botulinum toxin
C. Lambert-Eaton Syndrome
D. OP’s

A

D. OP’s

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22
Q

Which two conditions involves BLOCKING of Ach-R sites?

A

Curare and Myasthenia Gravis

23
Q

True or False: Botulinum, LE Syndrome, and black widow spider venom alters release of Ach

24
Q

True or False: Botulinum blocks Ach release while black widow spider venom causes explosive release of Ach

25
Which condition is characterized by self-produced antibodies to Cal channels, which diminish calcium influx, thereby reducing Ach release?
Lambert Eaton
26
In myasthenia gravis, self produced antibodise inactivate N1 receptors while in Lambert-Eaton syndrome, autoantibodies inactivate VG Ca channels in synaptic terminals . Which of the following phenomena will be found in both diseases?
Reduced PS potential
27
Which of the following fibers have low oxidative capacity and high fatigue, but is good for short periods of high intensity? A. Slow Oxidative Fibers B. Fast Ox-Glycolytic Fibers C. Fast Glycolytic Fibers
C. Fast Glycolytic Fibers (IIb)
28
True or False: Slow oxidative fibers (Type 1) have a high oxidative capacity (many mitochondria!) and therefore can maintain low-intensity contractions for long periods, without fatigue
True
29
True or False: A single motor unit consists of one motor neuron and the muscle fibers it innervates, while TWO motor units have intermingled fibers
True
30
Motor units size = ____ / ____
of myocytes / motor neuron note: the more myocytes there are, the stronger the muscle force and the less control
31
Motor units with the lowest thresholds are the first to be activated. Given this, which is activated first? A. Slow Twitch (Type I) Fibers B. Fast Twitch (Type II) Fibers
A. Slow Twitch (Type I) Fibers - low threshold
32
True or False: Neurogenic muscle fiber atrophy is due to destruction of a motor neuron, leads to denervation atrophy
True
33
True or False: Prolonged disuse (i.e. immobilization) causes focal or generalized atrophy
True
34
Which fiber exhibits more atrophy: Type II or Type I? A. Type II B. Type I
A. Type II
35
What do Duchenne Muscular Dystrophy (DMD) and Becker Muscular Dystrophy have in common, as far as how they are inherited genetically?
X-linked - Also, they're both due to mutations in Dystrophin
36
What is the function of the DGC (dystrophin-glycoprotein complex)?
Structural stability to muscle cell membrane during contraction/relaxation Important for cardiac and skeletal muscle function
37
a2 laminin’s mutations causes: A. Duchenne/Becker Muscular Dystrophy B. Congenital Muscular Dystrophy C. Limb Girdle Muscle Atrophy
B. Congenital Muscular Dystrophy
38
Which drug class causes atrophy due to increased proteolysis for gluconeogenesis? A. NSAID's B. Glucocorticoids C. Anti-virals
B. Glucocorticoids - atrophy primarily in Type II fibers and proximal muscles
39
Dystrophin mutation causes: A. Duchenne/Becker Muscular Dystrophy B. Congenital Muscular Dystrophy C. Limb Girdle Muscle Atrophy
A. Duchenne/Becker Muscular Dystrophy
40
Mutation in sarcoglycans causes: A. Duchenne/Becker Muscular Dystrophy B. Congenital Muscular Dystrophy C. Limb Girdle Muscle Atrophy
C. Limb Girdle Muscle Atrophy
41
True or False: In DMD (Duchenne Muscular Dystrophy) dystrophin is ABSENT - however, in Becker's there is partial function of dystrophin, making it a milder form of DMD
True
42
____ is an X-linked recessive condition that is characterized by progressive, severe muscle weakness. It ultimately causes death in late teens due to respiratory or cardiac muscle failure.
Duchenne Muscular Dystrophy
43
True or False: DMD results in loss of muscle fibers, increased fibrosis and adipose tissue
True
44
Muscular Dystrophy treatment?
1) Corticosteroids 2) ACE Inhibitors or B-blockers if there are cardiac effects
45
"Anticipation" --the idea that there are increasing repeats of a particular genetic abnormality with each passing generation--is found in DM1/DM2, also known as ____
Myotonic Dystrophy or Dystrophia Myotonica
46
True or False: Myotonic Dystrophy or Dystrophia Myotonia are characterized by sustained involuntary contractions and trinucleotide CTG expansions on chrom 19
True
47
Mutation in Na channel can lead it to FAIL to INACTIVATE. Which of the following conditions may arise? A. Ion Channel Myopathy B. Hyperkalemic Periodic Paralysis
B. Hyperkalemic Periodic Paralysis
48
Which condition results due to mutations in Ryanodine receptor, a Ca release channel protein, and is trigged by halogenated anesthetics? A. Malignant Hyperthermia B. Hyperkalemic Periodic Paralysis
A. Malignant Hyperthermia
49
True or False: Ca is stored and released via SR cisterna
True
50
True or False: In skeletal muscle, the DHPR and RyR are physically associated; therefore: polarization induced DHPR activation results in opening of RyR
True
51
In malignant hyperthermia, there is reduced affinity for Mg to calcium binding site. Therefore: Mg does not block activation
True
52
True or False: Malignant Hyperthermia PROMOTES Ca release - channel becomes more active and does not inactivate
True
53
True or False: There's reduced threshold for luminal calcium activation of RyR1 in malignant hyperthermia
True
54
True or False: Myofilament contraction and activation of Ca2/ATPase leads to excess heat, therefore: malginant hyperthermia
True

Pathophysiology (26 decks)

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