Skeletal Muscle Disease Flashcards

(31 cards)

1
Q

T/F Sprinters have predominantly fast twitch fibres

A

True, the muscles are large, but more prone to fatigue

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2
Q

How to we intervene with muscle wasting

A

attenuate the atrophy and promote muscle strength and fatigue resistance

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3
Q

Why isn’t steroid an ideal drug for muscle wasting

A

Because the increase in muscle size will just increase muscle fatigue

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4
Q

How does myostatin affect muscle growth?

A

it’s a negative regulator. Muscle wasting corresponds to increase in myostatin

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5
Q

What are some causes of muscle atrophy?

A

inactivity
denervation
cachexia
ageing

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6
Q

How much muscle can we lose before it becomes fatal

A

40%, especially when affecting respiratory or endocrine muscles

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7
Q

T/F Electrical stimulation can be used to treat muscle wasting in ICU

A

True, it turns on the physiological properties

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8
Q

What is sarcopenia?

A

age-related muscle wasting and weakness

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9
Q

What does an X ray image of sarcopenia patient look like?

A

the muscles are replaced by non-contractile tissue like fat and connective tissue

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10
Q

How do we consider someone to have sarcopenia?

A

When patients are bedridden and cannot independently rise from a chair. Measured gait speed <1 m/s

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11
Q

T/F We can prevent age-related muscle wasting

A

False, decline will still occur with best condition

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12
Q

T/F Fast twitch fibres deteriorate quicker than slow twitch fibres

A

True

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13
Q

What is the technical definition of “weakness”

A

inability to develop an initial force appropriate for the circumstance

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14
Q

When does loss of muscle strength develop more severely

A

beyond the age of 50

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15
Q

What is the neural mechanism of age related muscle remodelling

A

muscle is normally innervated by both type I and type II motor units, and with age, type II denervates first. Here, we re-innervate the loss type II units with type I units, hence remodel the muscle

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16
Q

T/F Biochemical changes in muscles occur before muscle wasting

A

True, there are changes in Ca level that affect speed of contraction

17
Q

What’s the goal of treatment for patients with Duchenne Muscular Dystrophy

A

turning it into Becker Muscular Dystrophy

18
Q

T/F DMD has a late-onset

A

False, it’s early at around 2 to 6 years

19
Q

What are the symptoms of DMD?

A

generalised weakness and muscle wasting affecting limb and trunk muscles first.

Enlarged calves

20
Q

T/F DMD is a X-linked disease

A

True, X-linked recessive

21
Q

T/F DMD patients have strengthened and enlarged calves

A

False, they are hypertrophic, but it’s not muscle. It’s fats and connective tissue

22
Q

What is the Gower’s sign?

A

sign indicating weakness of proximal muscle. Patient needs to use hands to aid standing

23
Q

Which muscle is sparred in DMD?

A

extraocular muscles due to small diameter and low mechanical stress per surface area

24
Q

What’s the protein deficiency in DMD?

A

dystrophin deficiency

25
What is dystrophin?
it's a cytoskeletal protein that maintain the structure of muscles actin, for example, is connected to the membrane via dystrophin
26
What roles does dystrophin play aside from anchoring muscular proteins
signalling of muscles - anabolic signals, signal of blood flow
27
how does the absence of dystrophin affect cell membrane
cell membrane becomes very fragile
28
How is BMD different to DMD
BMD has later onset, slower time course, some abnormal, smaller dystrophin present. Hence, BMD is not as severe
29
How does lack of dystrophin contribute to muscle wasting?
due to membrane instability, there may be 1) enhanced membrane leak, increased oedema and Ca 2) increased susceptibility of rupture and injury with stretch 3) inappropriate repair
30
how does dystrophin affect intracellular calcium level?
Aside from intracellular release of Ca, there will also be Ca entry due to stretched membrane. Muscles cannot buffer the Ca, and there is increased secondary messenger activity
31
What is the current treatment of muscular dystrophy
corticosteroids to extend the life of patients