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Block 4 > Muscle Structure and Pathologies > Flashcards

Muscle Structure and Pathologies Flashcards

1
Q

How are skeletal muscles organised?

A

Skeletal muscles are wrapped in dense connective tissue called epimysium

Muscle fascicles within skeletal muscle are wrapped in perimysium

Muscle fibres (cells) within fascicles are wrapped in endomysium and sarcolemma

Actin and myosin filaments (myofibrils) are within the muscle fibres.

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2
Q

What are the features of skeletal muscle cells?

A
  • Cylindrical cells
  • Striated
  • Multinucleate
  • Limited regeneration (satellite cells)
  • Voluntary control
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3
Q

What are the features of cardiac muscle cells?

A
  • Branched cells
  • Intercalated discs
  • Striated
  • Mono/binucleate
  • No regeneration
  • Spontaneous contraction (involuntary)
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4
Q

What are the features of smooth muscle cells?

A
  • Spindle shaped
  • Central nucleus
  • Capable of regeneration
  • ANS and endocrine regulation
  • Found in hollow organs, vessels, glands
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5
Q

What are the different types of muscle fibres?

A

Type 1 (slow twitch):

  • Aerobic- slow oxidative
  • Many mitochondria
  • Slow contraction, fatigue resistant

Type 2A:

  • Aerobic and anaerobic- fast oxidative
  • Many mitochondria
  • Intermediate contraction speed

Type 2B (fast twitch):

  • Anaerobic
  • Few mitochondria
  • Fast, powerful, rapidly fatiguable
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6
Q

What are the stages of transmission of an action potential at the neuromuscular junction?

A
  1. Action potential arrives and depolarises the presynaptic membrane of the motor neurone
  2. Calcium channels open: calcium slows into the pre-synaptic terminal down its concentration gradient
  3. Vesicles containing Ach move into the presynaptic membrane, fuse and release Ach into the synaptic cleft by exocytosis.
  4. Ach diffuses across the synaptic cleft and binds to nicotinic Ach receptors on the post-synaptic terminal
  5. Ach causes conformational change in the receptor which opens its ion channel, Na+ enters the motor end plate and K+ leaves. Motor end plate depolarises to meet end plate potential.
  6. End plate potential causes opening of voltage gated Na+ channels in the adjacent membrane which initiates an action potential which propagates down the muscle fibre
  7. Ach (only binds to nicotinic receptors briefly then dissociates) is broken down by acetylcholinesterase in the synaptic cleft into acetate and choline. This is taken back up into the presynaptic terminal.
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7
Q

What is a motor unit?

A

Motor neuron and the muscle fibres it innervates.

(Each motor unit only innervated by 1 motor neuron)

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8
Q

Where are nicotinic Ach receptors found?

What are they?

A

NMJ on skeletal muscle cells

Ligand gated ion channels

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9
Q

What causes myasthenia gravis?

How is it treated?

A

Autoantibodies against nicotinic Ach receptors on post-synaptic membrane block receptors preventing Ach bindng.

This causes muscle weakness.

Often affects extraocular muscles

Treated with acetylcholinesterase inhibitors (neostigmine)

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10
Q

What is botulinum toxin?

A
  • Produced by clostridium botulinum
  • Degrades the SNARE protein complex
  • Blocks Ach release from presynaptic terminals causing a total blockade at the NJM
  • Causes flaccid paralysis, can cause paralysis of resp muscles.
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11
Q

What are T-tubules?

A

Invaginations of the sarcolemma.

When the sarcolemma depolarises, the wave of depolarisation extends down the T-tubules which stimulates the release of calcium from the adjacent sarcoplasmic reticulum.

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12
Q

Describe the structure of the sarcomere

A

A band: located in the centre of the sarcomere

  • Mainly thick filaments, some overlapping thin

I bands: Located either side of the A band.

  • Only thin filaments

Z discs: the point where thin filaments from adjacent sarcomeres join

H zone: area in the centre of the A band

  • Thick filaments only

M line: point at which thick filaments meet and connect with the cell membrane

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13
Q

What is the structure of thick filaments

A

Composed of myosin containing light and heavy chains.

Heads of the myosin molecule contain actin binding site for cross bridge formation with actin.

Also contains an ATPase site.

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14
Q

What is the structure of thin filaments

A

Composed of actin, tropomyosin and troponin.

Tropomyosin runs along the groove of each twisted actin filament. Covers the actin binding site.

Troponin:

  • T component is bound to tropomyosin
  • I component helps to block actin binding site
  • C component is for calcium binding on contraction.
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15
Q

Describe the process of excitation-contraction coupling

A
  1. Depolarisation of muscle fibre membrane→ action potential propagation down T-tubules
  2. Conformational change in dihydropyridine receptors on T-tubules→ conformational change in ryanodine receptors on SR
  3. Ca2+ released from SR→ increased intracellular Ca2+ concentration
  4. Ca2+ binds to troponin C→ binding sites exposed
  5. Actin binds to myosin = contraction
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16
Q

Describe the process of cross-bridge cycling (sliding filament theory)

A
  1. Calcium binds to troponin C displacing tropomyosin and exposing binding site- myosin heads bind to actin forming cross bridges.
  2. ATP binds to myosin head causing conformational change→ reduces affinity of myosin for actin. Myosin head releases actin.
  3. ATPase hydrolysis ATP to ADP and inorganic phopshate, initially remain bound to myosin head. Release of energy from hydrolysis of ATP causes conformational change in myosin head into a high energy position→ binds to a site on actin further down from its original binding site.
  4. Phosphate released from actin molecule and myosin head returns to its original position, propelling the actin molecule towards M line. Thick and thin filaments slide over eachother, shortening the sarcomere.
  5. ADP is released and myosin head binds to actin again in the rigor position. Cycle continues as long as ATP is available.
17
Q

Describe the process of termination of muscle contraction

A
  1. Fall in intracellular Ca2+
  2. Troponin releases Ca2+
  3. Tropomyosin covers myosin head and binding site
  4. Calcium is taken up into the SR by SRcalcium ATPase (SERCA)
18
Q

What is Becker’s Muscular Dystrophy?

A
  • X-linked genetic disorder
  • Reduction in dystrophin (not a total absence)
  • Later onset (teens-early adulthood)
  • Milder symptoms than Duchenne’s, slower progression
19
Q

What is Duchenne Muscular Dystrophy?

A
  • Absence of dystrophin, protein that anchors cytoskeleton to the ECM.
  • Causes necrosis and destruction of muscle fibres which are replaced with adipose tissue→pseudohypertrophy
  • Early onset, 3-4 years.

Symptoms:

  • Gower’s sign (pushing hands on legs to stand)
    *
20
Q

What is polymyositis?

Symptoms

Treatment

A
  • Autoimmune inflammatory disorder.
  • Causes inflammatory cell infiltration of skeletal muscle and muscle cell necrosis.

Symptoms:

  • Proximal symmetrical muscle wasting and weakness
  • Dysphagia
  • Dystonia
  • Respiratory muscle weakness
  • Cardiac involvement
  • Malaise
  • Weight loss
  • Fever in acute phase

Treatment:

  • Steroids
  • Immunosuppression
21
Q

What is dermatomyositis?

Symptoms

Treatment

A

Features of polymyositis plus skin change

Typically affects muscle and skin

Can also affect heart, lungs, oesophagus and joints

Symptoms:

  • Heliotrope rash (around eyes)
  • Gottron’s papules

Block 4 (20 decks)

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