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muscle Flashcards

0
Q

What is myasthenia?

A

-Weakness of the muscles

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1
Q

What is myalgia?

A

-Muscle pain

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2
Q

What is myocardium?

A

-The muscle component of the heart

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3
Q

What is myopathy?

A

-Any disease of the muscles

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4
Q

What is myoclonus?

A

-Any sudden spasm of the muscles

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5
Q

What is sarcolemma?

A

-The outer membrane of a muscle cell

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6
Q

What is sarcoplasm?

A

-Cytoplasm of muscle cells

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7
Q

What is sarcoplasmic reticulum?

A

-The smooth endoplasmic reticulum of muscle

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8
Q

What are two characteristics of all types of muscle?

A
  • Contractility

- Conductivity

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9
Q

What are the three types of muscle?

A
  • Skeletal muscle
  • Smooth muscle
  • Cardiac muscle
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10
Q

Which types of muscle are striated?

A
  • Skeletal muscle

- Cardiac muscle

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11
Q

Which type of muscle is non-striated?

A

-Smooth muscle

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12
Q

Where are skeletal muscle cells derived from?

A

-Mesodermally-derived multipotent myogenic stem cells

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13
Q

How do multinucleated skeletal muscle cells develop?

A

-Myogenic stem cells-> myoblasts which fuse together to form primary myotube with a chain of multiple central nuclei

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14
Q

Why are skeletal muscle nuclei displaced to the periphery?

A

-The synthesis of actin and myosin filaments displace the nuclei

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15
Q

What are the three types of muscle fibre?

A
  • Narrow red
  • Intermediate
  • Wide white
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16
Q

Which muscle fibre is small in diameter?

A

-Red

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17
Q

Which muscle fibre has poor vasculature?

A

-White

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18
Q

Which muscle cell has a poor store of myoglobin?

A

-White

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19
Q

Which muscle fibre has the most mitochondria?

A

-Red

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20
Q

What are the contractions like in red skeletal muscle fibres?

A

-Slow, repetitive, weak

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21
Q

What are the contractions like in white skeletal muscle fibres?

A

-Fast and strong

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22
Q

How do the red and white skeletal muscle fibres fatigue?

A
  • Red-> slowly

- White-> radiply

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23
Q

Which skeletal muscle fiber has the most neuromuscular junctions?

A

-White

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24
Q

Give an example of where red and white skeletal muscle fibres are found

A
  • Red-> postural muscles of the back

- White-> extraocular muscles and the fingers

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25
Q

Describe the structural organisation of muscle units from bone to myofilaments

A
  • Bone
  • Tendon
  • Muscle
  • Fasicle
  • Muscle fibre
  • Myofibrils
  • Myofilaments (actin and myosin)
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26
Q

How can you tell a fascicle from a muscle fibre?

A

-The fibre will have multiple nuclei on its sarcolemma

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27
Q

What is epimysium?

A

-Connective tissue sheath which surrounds the entire muscle

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28
Q

What is perimysium?

A

-Connective tissue sheath which surrounds fascicles

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29
Q

What is endomysium?

A

-Connective tissue sheath which surrounds muscle fibres

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30
Q

What is another name for a muscle fibre?

A

-Muscle cell

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31
Q

What are the different anatomical arrangements of muscles?

A
  • Circular
  • Convergent
  • Multipennate
  • bipennate
  • Unipennate
  • Parallel
  • Fusiform
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32
Q

What is a myotendinous junction?

A

-Where the muscle and tendon meet

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33
Q

How is skeletal muscle arranged at a myotendinous junction?

A

-The fibres interdigitate with tendon collagen bundles

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34
Q

What two types of skeletal muscle are found in the tongue?

A

-Extrinsic and intrinsic muscles

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35
Q

What are the extrinsic muscles of the tongue attached to?

A

-The have insertions into bone and cartilage

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36
Q

What are the functions of the extrinsic tongue muscles?

A

-To protrude, retract and move the tongue from side to side

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37
Q

What is the function of the intrinsic muscles of the tongue?

A

-Allow the tongue to change shape but not position

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38
Q

How are nuclei arranged in muscle fibres?

A

-In rows at the periphery of the cell

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39
Q

What structures does the perimysium contain?

A
  • Nerves

- Blood vessels

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40
Q

What structures do endomysium contain?

A
  • Capillaries

- Nerves

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41
Q

What are myofibrils made up of?

A

-Myofilaments (thin actin and thick myosin)

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42
Q

How are myofilaments arranged?

A

-In a strict banding pattern of A and I bands

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43
Q

What shade is the A band of a myofibril?

A

-Dark

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44
Q

What shade is an I band of a myofibril?

A

-Light

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45
Q

Where is the Z line located?

A

-In the centre of an I band

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46
Q

What is a sarcomere?

A

-A contractional unit from Z line to Z line

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47
Q

What myofilament(s) do the A binds contain?

A

-Both actin and myosin as they overlap

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48
Q

What myofilament(s) do the I bands contain?

A

-Actin only

49
Q

What is the H zone?

A

-The segment within an A band which only contains myosin

50
Q

Where is the M line?

A

-In the centre of an H zone

51
Q

What is a pneumonic for remembering these bands?

A

-MHAZI (M is in H in A, Z is in I)

52
Q

Which bands decrease in size during contraction and which stay the same length?

A
  • I and H zones get smaller

- A remains the same

53
Q

What happens to the size of the sarcomere during contraction?

A

-It decreases

54
Q

What is the structure of an actin myofilament?

A

-Contains actin, troponin and tropomyosin which form a helix by troponin attaching to tropomyosin which then wraps around actin

55
Q

What can troponin be used as a marker for?

A

-Cardiac ischaemia

56
Q

Describe the structure of myosin

A
  • An individual myosin molecule has a rod-like structure from which two heads protrude
  • Each thick filament is made up many myosin molecules in such a way that the ‘heads’ protrude in a multidirectional way
  • The filaments are devoid of myosin heads in the centre of the filament (where there is no overlap)
  • The heads extend towards the actin filaments
57
Q

What is the role of calcium in muscle contraction?

A
  • Influx of calcium into the the muscle fibril
  • Binds to troponin causing a conformational change leading to dissociation from the tropomyosin, and causing tropomyosin to change position, exposing the active site of actin
  • This allows the myosin head to bind to actin and contraction to begin
58
Q

Describe the sequence of events in the sliding filament model

A
  • Myosin head attaches to actin filament as ATP is hydrolysed
  • Working stroke-> myosin head pivots and bends as it pulls on the actin filment, sliding it towards the M line
  • Release of ADP and Pi
  • A new ATP molecule binds to myosin causing the myosin cross-bridge to detach
  • ATP hydrolysis causes the cycle to repeat
59
Q

What is the cause of rigor mortis?

A

-Lack of ATP results in myosin heads staying bound to actin

60
Q

What is a neuromuscular junction?

A

-The point at which an axon meets muscle containinf a small terminal swelling of the axon and a synaptic cleft

61
Q

Describe the mechanism of innervation of muscle and excitation contraction coupling

A
  • Nerve impulse along motor neurone arrives at neuromuscular junction
  • Influx of calcium at the synaptic bulb causes the release of acetylcholine
  • Acetylcholine diffuses across the synaptic cleft and fuses with nicotinic receptors located on the sarcolemma of the muscle causing depolarisation
  • This cause voltage-gated Na+ to open, causing the action potential to enter
  • Action potential (depolarisation) spreads along sarcolemma down T tubules and to two sarcoplasmic reticulum
  • This causes the opening of voltage gated calcium channels at the terminal cisternae of the two adjacent sarcolasmic reticulum; calcium is released into the sarcoplasm
  • Resulting in the sliding filament model
62
Q

What happens to the calcium after the action poteltial is complete?

A

-Returned to the sarcoplasmic reticulum by active transport

63
Q

What is the triad in skeletal muscle contraction?

A

-One T tubule causes calcium release from two sarcoplasmic reticulum

64
Q

Describe the histology of cardiac muscle in longitudial section

A
  • Striations
  • Centrally positioned nuclei(one or two per cell)
  • Intercalated discs
  • Branching
65
Q

Why does cardiac muscle contain intercalated discs?

A

-For electrical and mechanical coupling with adjacent cells

66
Q

Describe cardiac muscle in transverse section

A
  • Centrally positioned nuclei
  • Endomysium bearing rich supply of capillaries
  • Some lobular profiles which represent branching
67
Q

Are myofibrils arranged in bands in cardiac muscle?

A

-Yes however myofilaments of actin and myosin form continuous masses in cytoplasm

68
Q

What other structures are present in the cytoplasm of cardiac muscle?

A
  • Mitochondria

- Sarcoplasmic reticulum

69
Q

How are intercalated discs associated with Z lines?

A

-Intercalated discs lay over the Z lines (Z lines become obscured in LM)

70
Q

Why does cardiac muscle contain many gap junctions?

A

-For electrical coupling

71
Q

What is the function of adherens-type junctions in cardiac muscle?

A

-To anchor the cells and provide anchorage for actin filaments

72
Q

Where in skeletal muscle are the T tubules located?

A

-At the A I band junction

73
Q

Where do T tubules lie within cardiac muscle?

A

-At the points of intercalated discs and Z lines

74
Q

What is meant by cardiac muscle having a diad not a triad?

A

-One T tubule serves on sarcoplasmic reticulum

75
Q

How does muscle contraction occur in cardiac muscle?

A

-Same as skeletal muscle except electrical impulse is generated from the heart itself

76
Q

Where are purkinje fibre located?

A

-Ventricle walls

77
Q

-What generates the action potential in the heart and how does this travel to the ventricles?

A
  • SAN generates

- Passes to AVN into ventricles

78
Q

What is the function of the purkinje fibres?

A

-Transmit the action potential from the AVN to the ventricles to allow rapid conduction enabling ventricles to contract in a synchronous manner

79
Q

Describe the characteristics of the purkinje fibres

A
  • Large cells
  • Abundant glycogen
  • Sparse myofilaments
  • Extensive gap junctions
80
Q

Describe the histology of smooth muscles

A
  • Spindle-shaped (fusiform)
  • Have a central nucleus
  • Non striated, no sarcomeres, no T tubules
81
Q

What is the mechanism of contraction of smooth muscle? (simply)

A

-Actin-myosin interactions

82
Q

How do contractions of smooth muscle differ from cardiac and skeletal contractions?

A
  • Slower
  • More sustained
  • Require less ATP
83
Q

Which of the muscle types is capable of being stretched?

A

-Smooth

84
Q

What generic stimuli cause smooth muscle to contract?

A
  • Nerves (ach)
  • Hormones
  • Drugs
85
Q

What conformation do lots of smooth muscle cells make?

A
  • Sheets
  • Bundles
  • Layers
86
Q

-Where is smooth muscle most frequently located?

A

-The contractile walls of passageways or cavities

eg vascular structures, the GI, respiratory and genitourinary tract

87
Q

When can smooth muscle become clinically significant?

A
  • High bp
  • Dysmenorrhoea
  • Asthma
  • Atherosclerosis
  • Abnormal gut mobility
88
Q

What are myofibroblast cells?

A

-Specialised smooth muscle cells involved in wound healing which produce a collagenous matrix but also contract the wound

89
Q

What are myoepithelia?

A

-Specialised smooth muscle cells known as satellite cells which form a basketwork around the secretory units of some exocrine glands to help secretion via contraction eg sweat, salivary, mammory and iris

90
Q

Outline the contraction of smooth muscle

A
  • Thick and thin myofilaments are arrananged diagonally within a cell, spiralling down the long axis
  • Smooth muscle contracts in a twisting way
  • Requires Ca2+ (binds to CaM, binds to MLCK, phosphorylates myosin-> sliding filament model)
  • Intermediate filaments attach to dense bodies in the sarcoplasm
91
Q

Describe the nature of repair of skeletal muscle

A
  • Cannot divide
  • Can regenerate-> mitotic activity of satellite cells result in hyperplasia after muscle injury
  • Satellite cells fuse with existing muscle to increase muscle mass
92
Q

Describe the nature of repair of cardiac muscle

A
  • Not capable of regeneration

- Following damage fibroblasts invade, divide and lay down scar tissue

93
Q

Describe the nature of smooth muscle repair

A
  • Retain mitotic activity and form new smooth muscle cells

- Evident in pregnant uterus which undergoes hypertrophy and hyperplasia

94
Q

Describe the process of skeletal muscle remodelling

A
  • The contractile proteins actin and myosin can increase/decrease in number
  • This is known as remodelling and is a continual process
  • All the myofilaments can be replaced within two weeks
95
Q

How does atrophy of skeletal muscle occur?

A

-Destruction of the myofilaments during remodelling is greater than replacement

96
Q

How does hypertrophy of skeletal muscle occur?

A

-Replacement of the myofilaments during remodelling is greater than destruction

97
Q

What is the cause of hypertrophy in skeletal muscle?

A

-Increased demand, ie exercise

98
Q

What happens to skeletal muscle cells when they undergo hypertrophy?

A
  • Increase metabolic demand
  • Sarcoplasmic reticulum swelling
  • Increased mitochondria
  • Increased Z line width
  • Increased ATPase
  • Increased density of T tubules
  • Increased contractile proteins
99
Q

What are the main causes of atrophy?

A

-Immobility, age, denervation

100
Q

How long after denervation does re-innervation need to occur for full use?

A

-3 months

101
Q

What increases uptake of acetylcholine at the neuromuscular junction?

A

-Motor neurone is embedded into the muscle with the muscle having a highly-folded endplate to increase surface area

102
Q

What terminates acetylcholine in the synaptic cleft?

A

-Acetylcholine esterase

103
Q

What causes myasthenia gravis?

A

-Autoimmune destruction of the endplate ach receptors, specifically by IgG

104
Q

What does autoimmune destruction of the achR in myasthenia gravis do to the endplate?

A

-Causes the loss of junctional fold resulting in widening of the synaptic cleft

105
Q

What are the signs and symptoms of myasthenia gravis?

A
  • Fatiguability and sudden falling
  • Drooping upper eyelids (ptosis)
  • Blurred vision
106
Q

Why does sudden falling occur in myasthenia gravis?

A

-Muscles fail die to lack of excitation caused by the lack of AchR

107
Q

Why are the eyes one of the first structures to be effected in myasthenia gravis?

A

-Have a low amount of muscle and therefore are effected easier

108
Q

Why do the symptoms in myasthenia gravis fluctuate?

A

-Based on general state of health

109
Q

What are the treatment options for myasthenia gravis?

A
  • Acetylcholinesterase inhibitors (pyridostigmine)
  • Immune suppressants
  • Plasmapheresis
  • Thymectomy
110
Q

How can acetylcholinesterase inhibitors treat myasthenia gravis?

A

-Ach not as quickly broken down so it can stimulate muscles for longer

111
Q

How can plasmapheresis treat myasthenia gravis?

A

-Removal of specific IgG from serum

112
Q

How can a thymectomy treat myasthenia gravis?

A

-Thymus is producing abnormal lymphocytes, removal will stop production

113
Q

How does botulism disrupt the neuromuscular junctions?

A

-Reduces acetylcholine release and thus decreases excitation of muscles

114
Q

How does organophosphate poisoning disrupt neuromuscular junctions?

A

-Decreased production of acetylcholinesterases; ach stays active for longer; overexcitation of muscles

115
Q

What type of disorder is muscular dystrophy?

A

-Genetic

116
Q

How is muscular dystrophy characterised?

A

-By progressive muscle weakness and wasting

117
Q

What is the cause of muscular dystrophy?

A

-Complete absence of the protein dystrophin (protein for stength) causing the muscles to tear apart upon contraction

118
Q

What is the consequences of muscle fibres tearing?

A
  • Muscle wastage
  • The enzyme creatine phosphokinase is liberated into the serum causing calcium to enter the cell resulting in necrosis
  • Pseudohypertrophy (swelling) occurs before fat and connective tissue replace muscle fibres
119
Q

Outline the pathophysiology of malignant hyperthermia

A
  • Large quantities of calcium released from sarcoplasmic reticulum of skeletal muscle due to altered calcium channel gated kinetics so ca2+ is not taken back up into SR
  • Causes hypermetabolic state
  • Sustained Ca2+ elevation allows excessive stimulation of glycolytic metabolism
  • Causes respiratory and metabolic acidosis
  • Causes rigidity due to all muscles contracting at once
  • High heat generation due to hypermetabolic state
120
Q

What type of disease and what are triggering agents of malignant hyperthermia?

A
  • Inherited disease

- Anaesthetic gases

121
Q

How can some people have malignant hyperthermia and never know?

A

-Never exposed to a trigger

Tissues of the body (17 decks)

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