Skeletal Muscle Contraction & Dysfunction Flashcards

1
Q

What structures conduct the nerve message?

A

Voltage gated sodium channels

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

Which chemicals are released into the synapse?

A

Acetylcholine

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

What is the effect of this chemical?
Can the chemical work by itself?

A
  • Doesn’t work by itself
  • Uses a nicotinic receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What structure does the chemical then enter into?
What’s the next structure the chemical travels into?

A
  • Into T tubules
  • Then into the Sarcolemma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What goes on at the thin and thick filaments interactions?

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

What are the key features of this smooth muscle?

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

How does cellular excitation lead to shortening?

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

Name the different parts of a neurone

A
  • Dendrites
  • Nerve cell body
  • Axon
  • Myelin sheath
  • Schwann cells
  • Nodes of Ranvier
  • Axon branch
  • Axon terminal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the axon contain?

A

Concentration of ion channels
- Na V
- K V
- Ankyrin

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

State the different stages of a neuronal action potential graph

A
  • Threshold region: at -55mV
  • Depolarisation: From -55mV to 30mV (Sodium conc increases causing influx)
  • Repolarisation: From 30mV to -70mV (3Na+ leave &2K+ enter the cell)
  • Hyperpolarisation: Goes below the normal region but shoots back up again
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the Voltage gated sodium channels

A
  • A family of 9 genes termed SCNA1-9
  • Rapid opening upon depolarisation
  • Exhibit distinctive inactivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does contraction involve?

A

Contraction involves the interaction of actin & myosin

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

What is contraction fuelled by?

A

Fuelled by ATP

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

What is contraction driven by?

A

Driven by a rise in [Ca2+]

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

What events occur during contraction?

A

Membrane events -> Rise in Calcium -> Binding to sensor ->
Contractile Mechanism (at the same time, ATP is hydrolysed by myosin) -> Myosin interaction -> Cell shortens

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

Describe the contractile cycle

A
  1. Cross bridge formation; release of Pi
  2. Power stroke: ADP is released, myosin undergoes a conformational change
  3. ATP binds myosin, causing detachment of myosin from actin; cross bridge dissociates
  4. ATP hydrolysis occurs, cocking myosin heads
17
Q

List some factors that could go wrong during the contractile cycle?

A
  • Multiple Sclerosis
  • Myaesthesia gravis
  • Non-dystrophic myotonias
  • Mascular dystrophy
18
Q

How does the myelin sheath insulate the axon?

A
  • Myelin formation occurs in the peripheral nervous system
  • Schwann cells wrap around the axon many times
  • Each Schwann cell forms myelin around a small segment of one axon
  • The Nodes of ranvier is a section of unmyelinated axon membrane between two Schwann cells
19
Q

How long is each section of the myelin sheath?

A

1-1.5 mm

20
Q

What does the CNS neurones contain in comparison to the PNS neurones?

A
  • CNS = Oligodendrocytes
  • PNS = Schwann cells
21
Q

What is the issue with the myelin sheath?

A
  • Myelin does not allow movement of ions
  • Nodes of ranvier contain NaV and Kv channels
  • Minimize number of Na/K ATPase required
22
Q

What happens during Multiple Sclerosis?

A
  • Immune attack of myelin
  • Leaky blood brain barrier
  • Sclerotic lesions such as:
  • Numbness, Tingling, Speech problems, Visual problems
23
Q

What happens during Myaesthesia Gravis?

A
  • Muscle nicotinic AChRs become degraded
  • Is a type of autoimmune disease
  • Targets the ã1 subunit
  • Neuronal nicotinic AChR’s unaffected
24
Q

What are some symptoms of Myaesthesia Gravis?

A
  • Muscle weakness
  • Drooping eyelids
  • Fatigue
  • Difficulty swallowing or talking
  • Exertion is difficult
25
Q

What are the features of non dystrophic myotonias?

A
  • Delayed relaxation of the muscle after voluntary contraction or mechanical stimulation
  • Electrophysiologically characterised by highly organised repetitive electrical activity of the muscle fibres
26
Q

What happens during Non dystrophic myotonias?

A

Five different skeletal muscle disorders are caused by mutations to the SCN4A gene that encodes for a voltage gated sodium channel expressed in the skeletal muscle

27
Q

What do these mutations result in?

A
  • Decreased rate of channel inactivation
  • Increased rate of recovery from inactivation
    Or
  • slower channel deactivation
28
Q

What do these mutations further lead to?

A
  • Less Cl channel activity
  • Prolonged contraction
29
Q

What is Dystrophic myopathy?

A
  • The dystrophin gene contains 79 exons
  • Spans >2,200 kb = 0.1% of the genome
  • Located in the short arm of the X chromosome
30
Q

What are the different types of Dystrophic myopathy?

A
  • Duchenne = Total loss of Dystrophin
  • Becker = Reduced or dysfunctional dystrophin
31
Q

What does Dystrophic myopathy lead to?

A
  • Increased permeability to macromolecules
  • Abnormal permeability is made worse by mechanical stress
  • Muscle fibre necrosis, fibrosis and fat infiltration