Skeletal Muscle Disease Flashcards

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
Q

What is dystrophin?

A

it’s a cytoskeletal protein that maintain the structure of muscles

actin, for example, is connected to the membrane via dystrophin

26
Q

What roles does dystrophin play aside from anchoring muscular proteins

A

signalling of muscles - anabolic signals, signal of blood flow

27
Q

how does the absence of dystrophin affect cell membrane

A

cell membrane becomes very fragile

28
Q

How is BMD different to DMD

A

BMD has later onset, slower time course, some abnormal, smaller dystrophin present. Hence, BMD is not as severe

29
Q

How does lack of dystrophin contribute to muscle wasting?

A

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
Q

how does dystrophin affect intracellular calcium level?

A

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
Q

What is the current treatment of muscular dystrophy

A

corticosteroids to extend the life of patients