Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ESA1 > ToB 15 Alterations in Skeletal Muscle Function > Flashcards

ToB 15 Alterations in Skeletal Muscle Function Flashcards

1
Q

What are the 4 main functions of skeletal muscle?

A

1) Stability of joints
2) Movement
3) Posture
4) Heat generation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How often are the actin and myosin filaments within skeletal muscle replaced?

A

Every 2 weeks, on average

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can the number of fibers within a muscle be changed?

A

Cannot increase or decrease number of fibres present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can you change the size of a muscle, as the number of fibres present cannot change?

A

Number of proteins present in the fiber (actin and myosin) can increase or decrease, changing the size of the muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the name given to muscle wasting?

A

Muscle atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the name given to describe an increase in muscle size?

A

Muscle hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does regular exercise affect the ATPase activity in skeletal muscle?

A

It increases the amount of ATPase activity present on the myosin II molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does regular exercise affect the t tubules present in skeletal muscle?

A

It increases the density of t tubules systems throughout the muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does regular exercise affect the number of contractile proteins present in skeletal muscle?

A

It increases the number of contractile proteins (actin and myosin) present within muscle fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why does an increase in protein in skeletal muscle lead to increase in muscle strength?

A

Strength is determined by the amount of cross-bridges that can occur between the actin and myosin in a muscle fiber. If increased protein, then increased actin and myosin = increased number of cross-bridges.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why does high resistance exercise cause muscle growth?

A

It stimulates protein synthesis to increase the strength of the muscle. More actin/myosin = fatter muscle fibres = larger muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why does endurance exercise have more health benefits compared to high resistance training?

A

Over time it causes the muscle to shift to an oxidative metabolism, which causes the muscles to use lipids rather than glucose from the blood, so reduces amount of lipid in blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does bed rest and limb immobilisation affect skeletal muscle?

A

It causes disuse atrophy, which results in loss of protein and power of muscles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Define sarcopenia:

A

The loss of skeletal muscle mass and strength, as a result of ageing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

After what age does muscle atrophy begin as a natural process?

A

After 30 years old.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does sarcopenia affect temperature regulation?

A

Not enough muscle mass to generate enough heat via shivering.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of motor neurones innervate skeletal muscle?

A

Lower motor neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the 2 main signs of a lower motor neuron lesion?

A

1) Muscle weakness

2) Muscle atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Define lower motor neuron lesion:

A

Lesion affecting any motor neuron which runs from the anterior horn to a skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Re innervation of a muscle after a lower motor neuron lesion within what time frame is likely to save the muscle and allow regain of control?

A

3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Explain neurogenic muscular atrophy:

A

Muscle death after a lesion to the innervating nerve (lower motor neuron lesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can you distinguish between unaffected muscle and atrophic muscle in a histology slide?

A

Atrophic fibers will be much smaller and more angulated, with an increase in nuclei.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How can the length of the sarcomere of a muscle fiber be increased?

A

Via sustained stretching, such as yoga/pilates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What causes the decrease in length of a sarcomere within a muscle fiber?

A

Limb immobilisation, ie in plaster.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why are muscle end plates slightly invaginated?

A

To increase the surface area, to increase the maximum number of neurotransmitter receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Each muscle is innervated by how many motor neurons?

A

1 motor neuron innervates each muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How can 1 motor neuron innervate multiple fibers within 1 muscle?

A

A motor neuron commonly has multiple end plates, each innervating different fibers within the same muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What neurotransmitter is released into neuromuscular junctions?

A

Acetylcholine

29
Q

What receptor does acetylcholine bind to on the post-synaptic membrane of a neuromuscular junction?

A

Nicotinic Ach Receptor (NAchR)

30
Q

Opening of what pre-synaptic channels causes the release of Ach into a neuromuscular synaptic cleft?

A

Voltage-gated Ca2+ channels

31
Q

What happens to Acetylcholine in the post-synaptic membrane of a neuromuscular junction?

A

It is terminated by Acetylcholinesterase, and the products diffuse back across the synaptic cleft, taken up by thepre-synaptic membrane (re-used)

32
Q

What proportion of NAchR need to be occupied to achieve a full sustained muscle contraction?

A

~25%

33
Q

What is Myasthenia Gravis?

A

Rare autoimmune disease causing muscle weakness without atrophy. Caused by destruction of NAchR by IgG antibodies.

34
Q

How do IgG antibodies affect the motor end plate in myasthenia gravis?

A
  • Destroys NAchR’s

- Reduces invaginations of the sarcolemma, reducing surface area

35
Q

What causes the sudden falling without fatigue of the muscles, in Myasthenia Gravis?

A

Due to the decreased number of NAchR’s, when the amount of Ach released from motor neuron drops, not enough NAchR’s are occupied to achieve a full sustained muscle contraction.

36
Q

What happens to the amount of Ach released from the motor neuron over time?

A

Large initial peak, then drops quickly

37
Q

What are the 3 primary signs of Myasthenia Gravis?

A

1) Drooping of upper eyelids
2) Double vision
3) Sudden falling without fatigue of muscles

38
Q

What can cause symptoms of Myasthenia Gravis to worsen (short-term)?

A
  • Poor general health
  • Emotions
  • Fatigue
39
Q

What are the 4 treatments given to relieve Myasthenia Gravis symptoms?

A

1) Acetylcholinesterase inhibitors
2) Immune suppressants
3) Plasmapheresis
4) Thymectomy

40
Q

Why does plasmapheresis relieve the symptoms of Myasthenia Gravis?

A
  • Myasthenia Gravis is caused by autoimmune antibodies,
  • Antibodies are carried in the blood plasma,
  • Removal of plasma containing autoimmune antibodies
  • Replaced with ‘good’ plasma, or plasma substitute
41
Q

Why does a thymectomy often relieve the symptoms of Myasthenia Gravis?

A
  • The Thymus gland helps protect the body against autoimmunity
  • Patients suffering from MG often have a benign tumour of the thymus gland
  • When removed, can alleviate symptoms
42
Q

Name the 6 main types of Muscular Dystrophy:

A

1) Duchenne (and Becker)
2) Emery-Dreifuss
3) limb girdle
4) facioscapulohumeral
5) distal
6) occulopharyngeal

43
Q

What muscles does Duchenne and Becker muscular dystrophy affect?

A

At first - upper arms/legs and pelvis

Later - All voluntary muscles

44
Q

What muscles does Emery-Dreifuss muscular dystrophy affect?

A

Upper arms and shin muscles

45
Q

What muscles does limb girdle muscular dystrophy affect?

A

Shoulder girdle and pelvic girdle muscles

46
Q

What muscles does facioscapulohumeral muscular dystrophy affect?

A

Facial, shoulder and upper arm muscles

47
Q

What muscles does distal muscular dystrophy affect?

A

Lower arm/leg muscles

48
Q

What muscles does occulopharyngeal muscular dystrophy affect?

A

Eyelids and throat muscles

49
Q

What is the difference between Duchenne- and Becker-type muscular dystrophies?

A

Duchenne-type has earlier onset and quickly progesses compared to Becker-type

50
Q

Why does the lack of dystrophin cause the symptoms of Duchenne muscular dystrophy?

A
  • Dystrophin links the sarcolemma and the actin/myosin fibres
  • When lost, the muscle fibres tear apart on contraction
  • Progressive atrophy of muscles
51
Q

Why is Duchenne muscular dystrophy progressive?

A

It causes the muscles to tear themselves apart on contraction, so the more the muscles are contracted, the worse the symptoms and muscle atrophy

52
Q

Why can elevated serum creatine kinase levels be indicative of muscular dystrophy?

A
  • Muscular dystrophy is characterised by muscle destruction and atrophy,
  • This causes muscle cell contents to leak out into blood
  • Creatine kinase is released into serum, and easily tested for
53
Q

What happens to the muscle after it has been destroyed in a patient with a type of muscular dystrophy?

A

The muscle fibres are replaced with fat and connective tissue

54
Q

What is the typical presentation which leads to a diagnosis of Duchenne muscular dystrophy?

A
  • Young male
  • Aged below 6 yrs
  • Late motor milestones
  • Inability to run
  • Fatigue
  • Climbing up legs to stand up (Gower’s sign)
55
Q

What is the initial investigation when Duchenne muscular dystrophy is suspected?

A

Serum creatine kinase levels, if elevated, supports possible diagnosis of DMD.

56
Q

Why is swelling/hypertrophy a common symptom in patients with a muscular dystrophy?

A

This is pseudohypertrophy, in which the muscle fibres are being replaced with fat and connective tissue

57
Q

What is the common management given to prolong independent mobility in Duchenne muscular dystrophy sufferers?

A

Corticosteroid therapy (Prednisolone), tends to slow rate of muscle damage.

58
Q

Why is it unnecessary to give corticosteroids to a Duchenne muscular dystrophy sufferer when they are dependant on a wheelchair?

A

Corticosteroids are only given to DMD sufferers to prolong independent mobility. When this is lost, it is unnecessary to take corticosteroids.

59
Q

What is the difference between myopathies and denervation?

A

Myopathies are caused by disease of the muscle, whereas denervation is caused by a disease of the nerves innervating the muscles.

60
Q

What is the main risk factor for Duchenne muscular dystrophy, and why?

A

Family history of DMD, as it is an inherited disorder

61
Q

What pattern of inheritance does Duchenne muscular dystrophy follow?

A

X-linked recessive

62
Q

Which gender is most at risk of inheriting Duchenne muscular dystrophy, and why?

A

Male, as DMD is X-linked recessive, and males only have one X chromosome so only require 1 mutant copy to be affected, whereas females require 2 copies to be affected.

63
Q

Give an example of an X-linked recessive myopathy:

A

Duchenne muscular dystrophy

64
Q

What causes Duchenne muscular dystrophy?

A

It is an inherited disorder

65
Q

What causes malignant hyperthermia susceptibility?

A

It is an inherited disorder

66
Q

What (usually) triggers malignant hyperthermia episodes?

A

Anaesthetic agents

67
Q

Why may some people with malignant hyperthermia susceptibility never know they have the condition?

A

Malignant hyperthermia episodes are only usually triggered by anaesthetic agents, so diagnosis cannot be made until person is exposed to anaesthesia.

68
Q

What is the pathophysiology of a malignant hyperthermia episode?

A
  • Increased CO2 production = metabolic and respiratory acidosis
  • Activation of sympathetic nervous system
  • Hyperkalemia
  • Oedema
  • Total skeletal muscle contraction = excessive heat production
    = multiple organ failure, death
69
Q

What process does anaesthetic agents trigger in a person susceptible to malignant hyperthermia?

A

Release of all Ca2+ from sarcoplasm of skeletal muscle

ESA1 (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions