Brainscape's Knowledge GenomeTM

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


See full index

Musculo-Skeletal > Muscle Contraction and Dysfunction > Flashcards

Muscle Contraction and Dysfunction Flashcards

1
Q

What are the three types of muscle?

A

→ Skeletal
→ Smooth

→ Cardiac

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

How many muscle fibres are there in bundles and what are they called?

A

→ fasciculi

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

What is the muscle fibre membrane called?

A

→ Sarcolemma

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

What is a muscle fibre made from?

A

→ 100s-1000s of myofibrils

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

What does the sarcoplasm contain?

A

→ glycogen
→ fat

→ mitochondria
→ enzymes

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

What does the sarcoplasmic reticulum do?

A

→ Release Ca2+

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

What is a sarcomere?

A

→ a contractile unit

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

What is the anisotropic band?

A

→ high density band

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

What is the isotropic band?

A

→ actin filaments

→ titin

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

Describe how the actin myosin binding sites are exposed

A

→ Troponin forms a complex with tropomyosin
→ When Ca2+ binds to troponin it causes a conformational change to the troponin

→ This causes the tropomyosin to move
→ It exposes the actin-myosin binding sites
→ Allows the myosin head to bind to the actin

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

Describe the sliding filament theory?

A

Motor neuron stimulates a muscle to contract
→ Release of Ca2+ into the muscle cell

→ myosin has a globular head that ATP binds to
→ ATP is hydrolysed
→ Phosphate bond breaking provides energy for the power stroke
→ releases ADP and an inorganic phosphate
→myosin head is cocked

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

What does the somatic nervous system do?

A

→ Provides voluntary control over skeletal muscle

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

What are motor neurons?

A

→ Efferent neurons that innervate muscle

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

What does one motor unit include?

A

→ A single motor neuron and all the muscle fibres it controls

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

How do motor units regulate the strength of contraction?

A

Varying how many activated motor units are recruited

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

Describe what happens at a neuromuscular junction when a stimulus is applied?

A

→ A stimulus from the brain causes an action potential
→ ACh is released

→ ACh binds to receptors and causes depolarisation of the membrane
→ depolarisation moves along the membrane and through T tubules
→ T tubules enter the muscle and cause depolarisation of the SR
→ SR releases Ca2+
→It is released into the cytosol and causes contraction of muscle fibres

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

What are the 2 types of cholinergic receptor?

A

→ Muscarinic

→ Nicotinic

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

How many molecules of ACh bind to a nicotinic receptor?

A

→ 2

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

What does a single action potential produce?

A

→ a single twitch

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

How do you get greater tension within a muscle?

A

→ if an additional action potential arrives before the muscle relaxes from the first action potential
→ There is summation of the two and greater contraction

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

What is tetanus?

A

→ When the rate of action potentials is so high that the muscle doesn’t relax between stimuli

22
Q

What is the mutated gene in DMD? (duchenne muscular dystrophy)

A

→ dystrophin

→allows for cell membrane to be stabilised as contraction happens

23
Q

What is the function of dystrophin?

A

→ Connects the sarcomere to the plasma membrane

24
Q

Where is the dystrophin gene located?

A

short arm of the X chromosome

25
Q

What is the difference between Duchenne and Becker disease?

A

→Duchenne=total loss of dystrophin

→Becker= reduced or dysfunctional dystrophin

26
Q

What are the effects of dystrophic myopathy diseases?

A

→increased permeability to macromolecules
→abnormal permeability is made worse by mechanical stress
→Muscle fibre necrosis, fibrosis and fat inflitration

27
Q

What happens to people with DMD?

A

→ unable to walk by 10-12 years

→ death by early to mid 20s

28
Q

What are the effects of a lack of dystrophin?

A

→ Dysfunction of the sarcolemma stretch
→ ion pores open and there is increased intracellular Ca2+

→ membrane gets torn

29
Q

What is an indication of muscle damage in DMD?

A

→ CK (creatine kinase) is lost from the cell and goes into the blood
→ degradation of structural proteins

30
Q

what is creatine kinase needed for?

A

→ recycling of ATP

31
Q

What enables patients with DMD to walk for longer?

A

→ corticosteroids like prednisone

32
Q

What is myasthenia gravis?

A

→chronic autoimmune motor neuron disease
→ Body makes antibodies against AChRs at neuromuscular junctions
→ targets alpha-1 subunit

33
Q

How do you treat myasthenia gravis?

A

→ AChesterases inhibitors

34
Q

What toxin does myasthenia gravis mimic?

A

botulinum toxin

35
Q

What is multiple sclerosis?

A

→Immune attack of myelin
→Leaky blood brain barrier
→Sclerotic lesions

36
Q

What are the manifestations of MS?

A 
→Numbness
→Tingling
→Speech problems
→Visual problems
→Debilitating muscle weakness
37
Q

What cells produce myelin?

A

→glial

→non-neuronal

38
Q

What are glial cells called in the CNS and PNS?

A

CNS=form the myelin sheath are called oligodendrocytes

PNS=called Schwann cells

39
Q

What is the AIS?

A

Axon initial segment

40
Q

What is the function of AIS?

A

→Sodium entry through channels at the AIS

→serves as the site of action potential firing and helps to maintain neuron polarity.

41
Q

What is the role of nodes of Ranvier?

A

Rejuvenation of excitation

→Concentration of voltage gated sodium channels

42
Q

What is the purpose of myelin sheath?

A

→Prevents charge leakage and dissipation of excitation

43
Q

What are the features of non-dystrophic myotonias?

A

→Delayed relaxation of the muscle after voluntary contraction or mechanical stimulation.
→highly organized repetitive electrical activity of the muscle fibres

44
Q

What mutations characterise NDM?

A

SCN4A gene(codes for a VGSC)

45
Q

Give examples of NDMs?

A

Potassium-aggravated myotonia (PAM),
→Paramyotonia congenita (PMC)
→Hyperkalemic periodic paralysis (HyperPP),
→Hypokalemic periodic paralysis (HypoPP),
→A form of congenital myasthenic syndrome (CMS)

46
Q

What do mutations in NDM cause?

A

→decreased rate of channel inactivation
→increased rate of recovery from inactivation
→slower channel deactivation

47
Q

What are some NDMs due to?

A

loss of Cl channel (CLC-1)
→Less Cl channel activity
→Prolonged contraction

48
Q

What does NDM result in?

A

→ paralysis

49
Q

Describe the activation of VGSC?

A

→When the membrane potential depolarises the voltage sensor domains move out of the plain of the membrane
→allows sodium ions to pass through the pore
→sodium flow is brief because a few ms later the so called inactivation ‘lid’ part of the channel then moves to and blocks the channel pore
→no flow of sodium but the voltage sensors are still poking up so the channel is not closed but is INACTIVATED

50
Q

Describe VGSCs

A

→formed from one large protein comprised of 4 repeated regions and each has 6 transmembrane domains
→4th transmembrane domain of each region is packed with positively charged amino acids and is known as the voltage sensor.

51
Q

How are VGSCs implicated in NDMs?

A

mutations to the gene that affects the property of inactivation will allow for longer / more persistent sodium influx.

Musculo-Skeletal (6 decks)

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