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Medicine Year 1 Semester 1 > MB Quiz 3 > Flashcards

MB Quiz 3 Flashcards

1
Q

What are the three types of muscle

A

Skeletal
Cardiac
Smooth

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2
Q

Perimysium

A

Connective tissue that surrounds fascicles of muscle fibers

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3
Q

Endomysium

A

Connective tissue that surrounds skeletal muscle cells

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4
Q

How are skeletal muscle cells grouped within the perimysium?

A

In Fascicles

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5
Q

Epimysium

A

Connective tissue where all Fascicles are grouped together forming the muscle

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6
Q

Describe the gross structure of a skeletal muscle in terms of connective tissue.

A

Skeletal muscle cells are surrounded by a connective tissue sheath called the Endomysium

Cells are grouped in fascicles surrounded by Perimysium

Fascicles are grouped together to form the muscle which is surrounded by Epimysium

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7
Q

What are tendons

A

Tendons are tissues that connect muscle to bone

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8
Q

List the connective components of the skeletal muscle organ from the single muscle cell until the organ

A

Muscle fiber/cell -> Endomysium -> Fascicle-> Perimysium -> Group of Fascicles -> Epimysium

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9
Q

Are Skeletal muscle cells mono-nucleated or multinucleated?

A

Multinucleated

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10
Q

Sarcomere

A

Unit of a myofibril contained between two Z lines

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11
Q

Describe the structure of a sarcomere

A

A sarcomere is the unit of a myofibril contained between two z lines

The Z line/disk separates two sarcomeres
The I band is the area where there are only thin filaments
The H zone is the area where are only thick filaments
The M line is in the center where thick filaments are linked with accessory proteins
The A band goes along the length of the thick filaments.

The Z line bisects the I band
The H zone bisects the A band
The M line bisects the H zone

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12
Q 
The outer edge of the A band has 
A) Thick filaments only
B) Thin Filaments only
C) No Filaments
D) Thick and Thin Filaments
E) Connective Tissue
F) Filaments linked with accessory proteins
A

D

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13
Q

What is the main function of accessory proteins in the sarcomere?

A

Maintenance of structure

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14
Q

What is the function of alpha actinin?

A

Maintains the actin lattice

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15
Q

What is the function of dystrophin

A

Anchors actin filaments to the Sarcolemma

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16
Q

Sarcolemma

A

Specialized membrane which surrounds striated muscle fiber cells

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17
Q

Give two accessory proteins in the sarcomere along with their functions

A

Alpha actinin Maintains actin lattice

Dystrophin anchors actin filaments to the Sarcolemma

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18
Q

What is the sarcoplasmic reticulum

A

Modified smooth ER

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19
Q

What are T-tubules

A

Inwards extensions of the Sarcolemma.

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20
Q

What are myofibrils composed of?

A

Myofibril is composed of overlapping myosin (thick), actin (thin), and accessory proteins.

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21
Q

Muscle fibers contain a large amount of which organelle?

A

Mitochondria

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22
Q

Where are triads located?

how many are found per sarcomere?

A

Junction of the A and I bands

Two

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23
Q

What are the components of each filament and how are the filaments associated with each other.

A

The myosin (thick filament) consists of a large number of individual myosin molecules. It is made up of a myosin tail which makes up the filament itself, a hinge region which allows the molecule to move and swivel and a myosin head which forms the cross bridge where it binds to the thin filaments (actin)

The thin filament consists of actin (G-actin molecules) aggregated together forming the fiber. Tropomyosin is a protein that goes along the length of the thin filament forming a complex with Troponin which attaches to the myosin head

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24
Q

What are the two globular sites of the Myosin Head and how does it bind to Troponin?

A

The myosin head contains two globular sites:

  1. Myosin ATPase Site (energy)
  2. Actin binding site (To bind with Troponin)

Troponin binds to Ca2+ causing conformational changes which move tropomyosin relative to actin exposing sites on actin allowing myosin heads to bind

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25
Q

Describe the interactions between actin and myosin in muscle contraction

A
  1. Action potential in T tubule activates voltage-sensitive receptors which trigger Ca2+ release into cytosol
  2. Calcium ions bind to Troponin changing its shape, exposing actin active sites
  3. Myosin head attaches to the actin myofilament, forming a cross bridge
  4. Myosin Head executes power stroke
  5. Removal of Ca2+ by active transport into the sarcoplasmic reticulum (SR) after action potential ends
  6. Tropomyosin blockage restored blocking myosin binding sites on actin relaxing the muscle by breaking the cross-bridge link
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26
Q

Describe how a power stroke is generated during a cross-bridge cycle

A
  1. ATP attaches to the myosin head energizing the molecule. This occurs as the link between myosin and actin weakens and detaches.
  2. ATP is split into ADP and Pi. The myosin head is energized allowing it to attach to actin
  3. Myosin head attaches to the actin myofilament, forming a cross bridge
  4. Inorganic phosphate from previous contraction cycle is released, initiating the power (working) stroke sliding the actin filament toward the M line. ADP is then released
27
Q

Explain the Sliding Filament Hypothesis of Huxley

A
  • Muscle shortens by the interactions between actin and myosin where myosin heads pull onto actin towards the M line creating a larger overlap between the filaments
  • The sarcomere shortens
  • I band shortens
  • H zone shortens
  • A band stays constant in length
  • Distance between Z disks shorten
28
Q

Identify and describe the specific roles of ryanodine and dihydropyridine receptors in the release of calcium.

A

The action potential runs along the Sarcolemma through the Transverse Tubule which gets detected by the Dihydropyridine receptor. It acts as a voltage sensor which causes the ryanodine receptor in the SR to open it’s Ca2+ channels.

30
Q

What is the significance of Calsequestrin?

A

Site where Ca2+ binds in the SR

31
Q

Describe Malignant Hyperthermia, its treatment, and it’s relation to muscular contraction.

A

Malignant hyperthermia is a rare disorder where anesthesia causes a rapid rise in body temperature, muscle rigidity, muscle damage, and death.

It is caused by an abnormal Ryanodine receptor that releases excessive amounts of calcium

Treated by Dantrolene, a muscle relaxant that blocks the Ryanodine Receptor

32
Q

Dantrolene

A

Muscle relaxant that blocks the ryanodine receptor

33
Q

Describe the energy sources use and their processes during muscle contraction (ATP, Creatine Phosphate, Glycogen Breakdown)

A

The muscle fiber stores ATP and Creatine phosphate intracellularly.

Creatine Kinase turns Creatine phosphate + ADP into ATP and Creatine.

Dietary Creatine can increase muscle Creatine phosphate levels

ATP comes from Aerobic Oxidative metabolism of glucose, glycogen, and fatty acids. When oxygen supply is low, anaerobic glycolysis creates ATP

34
Q

Describe Rigor Mortis Disease

A

High serum levels of Creatine Kinase is a useful indicator of muscle disease. This is an indication of inadequate ATP

In the absence of ATP, myosin heads cannot detach from actin causing death from Rigor Mortis

35
Q

Describe the timing of Electrical and Mechanical events of a single muscle twitch

A
  1. Motor Neuron depolarizes from -70->30
  2. During repolarization of the neuron, Muscle fibers depolarize from -90->30 (2ms)
  3. Tension begins to increase dramatically during contraction and then decreases during relaxation (10-100ms)
36
Q

Define the following:
Isotonic Contraction
Isometric Contraction
Eccentric Contraction

A

During Isotonic contraction, tension increases until it is equal to the weight to be lifted. Then the muscle shortens and the tension stays constant => isotonic
NOTE: This is also known as a concentric contraction

During Isometric contraction, tension is developed but the overall length of the muscle does not change. Same length => Isometric

Eccentric Contraction is where tension is developed but the muscle lengthens due to external force

=> Isotonic (concentric) shortens, Isometric stays the same, Eccentric lengthens

37
Q

Describe, in detail, the length-tension relationship that exists in skeletal muscle

A

When a muscle contracts isometrically, the tension developed depends on the initial length of the muscle before it contracted.

The initial length-tension relationship curve is constructed by varying the muscle length at rest and measuring the isometric tension when the muscle is maximally stimulated at length

Optimal length is the length at which tension development is maximal and there is optimal cross bridge overlap. This is shown by the inverted U-shape curve in the Huxley model.

When length increases beyond this point, tension decreases. The tension is determined by the amount of cross bridge overlap

38
Q

Describe what Summation and Tetanus are and how they occur in skeletal muscle

A

Clostridium Tetani Infection causes Tetanus where there is uncontrollable spasms of skeletal muscles.

The toxin produced by this bacterium blocks inhibitory synapses in the central nervous system so that there is increased activity of the motor nerves to skeletal muscle

The muscle action potential of skeletal muscle cells lasts for about 5 milliseconds but the muscle cell twitch lasts for a few hundred => if the muscle is stimulated more faster than a twitch can be completed, there will be no refractory period and hence there is Summation of tension at high frequencies of activation.

When this buildup of tension reaches its maximum, it is called complete tetanus

39
Q

Explain what the Staircase Phenomenon is (Treppe) and how it occurs

A

When a muscle is stimulated repetitively at a frequency below what causes summation (Stimulus occurs less than once every 10-100 ms), there is a progressive increase in the tension developed with each twitch until a maximum twitch is reached

40
Q

List 3 examples of Multiunit and 3 examples of Visceral Smooth Muscle

A

Multiunit: Cilliary muscle, Iris, Piloerector muscles, Large arteries and veins, Atriovenous shunt vessels, Bronchial smooth muscle

Visceral: Intestine, Uterus, Bladder, Ureters, Ducts of Exocrine Glands, Precapillary Sphincters, Small blood vessels (Arterioles)

41
Q 
Differentiate between Multiunit and Single-unit (Visceral cells) in smooth muscle
Controlled by?
Innervation?
Neuromuscular junction
Spontaneous activity?
Electrical transmission?
Action potential?
A

Multiunit vs Visceral
1. Neurogenic (controlled by nerves) vs Myogenic (controlled by local factors, stretch, and hormones)

  1. Rich Innervation vs Sparse Innervation
  2. Well developed neuromuscular junction vs poorly developed neuromuscular junction
  3. No spontaneous activity vs Some pacemaker cells
  4. No electrical coupling between cells vs Gap junction
  5. No action potentials vs Action potentials and slow waves
42
Q

Describe what plasticity is and the role it plays in smooth muscle

A

Smooth muscle tension has an irregular relationship with length. Stretch causes contraction (eg. autoregulation of blood flow) but sustained stretch causes relaxation (eg. urinary bladder)

43
Q

Define, describe, and differentiate between excitation-contraction coupling in smooth muscle and heart muscle (Compared to skeletal muscle)

A

Smooth Muscle:

  • Smooth muscle has no striations because actin and myosin are less regularly arranged.
  • Actin filaments are anchored to dense bodies. - There is no T system, no troponin, and usually a poorly developed SR.
  • Most of the Ca2+ for contraction comes from extracellular fluid
    1. Ca2+ binds to Calmodulin -> activates Myosin Light Chain Kinase -> activates Myosin head allowing cross bridge formation
    2. Phosphorylation Myosin heads perform the power stroke (contraction) => shortening
    3. Relaxation occurs by pumping Ca2+ out of the cell allowing myosin phosphatase to inactivate myosin
    4. Myosin ATPase activity is slow and hence muscle contraction is slow and sustained

Cardiac/Heart Muscle:

  • Regular actin/myosin arrangement giving striated appearance
  • Cells joined at intercalated discs which have gap junctions of low electrical resistance => the muscle is not a structural but a functional syncytium (Works in sync as a unit)
  • Compared to skeletal and smooth muscle, the SR is intermediate in development
  • There is only one terminal cisternae per T-tubules that occur at the Z line/disc => only one triad per sarcomere
  • Ca2+ comes from both extracellular fluid (during action potential) and the SR
    1. The Dihydropyridine receptor allows Ca2+ form the T system into the cell where it activates the Ryanodine receptor to release Ca2+ from the SR
    2. Events during cross bridge are similar to skeletal (brownie points if you can restate them)
    3. Ca2+ exits the cell mainly by Na/Ca exchanger
44
Q

Describe the role of extracellular calcium in smooth and heart muscle compared to that of skeletal muscle

A

The skeletal muscle contractile mechanism is not directly affected by extracellular Ca2+ concentration. Hypocalcaemic Tetany is the spasm of skeletal muscle due to increased motoneuron excitability

Smooth and Cardiac muscle are very sensitive to extracellular Ca2+ and to agents which affect Ca2+ entry into cells Ca2+ channel blocking drugs will reduce the contractility of the heart and dilate blood vessels

Extra info: This is due to the fact that skeletal muscles rely on SR Ca2+ whereas Smooth muscle and cardiac muscle rely more on the extracellular as their SR is not developed or moderately developed respectfully

45
Q

Describe the length-tension relationship that determines muscle mechanics in the heart muscle

A
  • The heart muscle demonstrates the length-tension relationship and the staircase phenomenon.
  • It does NOT show summation or tetanus
  • Filling of the ventricle is equivalent to preload and aortic pressure is equivalent to afterload.
46
Q

Apply Frank-Starling’s law to muscle mechanics in heart muscle

A

The heart normally operates on the upstroke (positive slope) of the length-tension curve. Therefore, the heart ejects what it receives

Example: During diastole, the blood entering the ventricle stretches the ventricle (muscle) and as the preload increases, so does the stretching of the ventricle. When the ventricle contracts, after receiving a nerve impulse from the AV node, the force of contraction will be proportional to the volume of preload i.e. stretch.

47
Q

Explain why heart muscle cannot be tetanised

A

The twitches of heart muscle cells cannot summate or tetanize because the action potential is so long that the muscle has begun to relax BEFORE the end of the absolute refractory period

48
Q

Describe the significance of Troponin-complex levels in the blood

A

A part of the troponin complex is unique to the heart muscle and is released into the blood following myocardial infarction. This is a useful measure of heart damage

49
Q

Define what a Motor Unit is and Define its properties and list the factors that increase muscle contraction

A
  • A motor unit consists of a motor neuron and all of the muscle fibers it innervates (A motor neuron innervates several muscle fibers)
  • Some motor units are large such as postural muscles and some are small such as hand muscles which require precise control
  • When a motor neuron is excited, all of the fibers in the motor unit contract
  • The force of muscle contraction is increased mainly by two means:
    1. By activating more motor units
    2. By increasing stimulus frequency to cause summation or tetanus of individual motor neurons (activator motor units more)
50
Q

Briefly Describe the technique of Electromyography

A

The electrical activity of skeletal muscles can be recorded using a Electromyogram or EMG. This is done by having a recorder connected to an amplifier connected to electrodes located in or near the muscle to read action potential/depolarization.

51
Q

Differentiate between fast and slow muscles

  • Speed of contraction
  • length of sustainment/fatigue ness
  • Type of metabolism
  • Color
  • Motor neuron size
  • Muscle diameter
  • Ca2+ pump speed
  • Glycogen store
  • Oxidative capacity
  • Myoglobin
  • Myosin ATPase
A

Slow Muscles are

  • Adapted for slow, sustained, tonic (used all the time), fatigue-resistant contractions e.g. postural muscles
  • Adapted for aerobic metabolism
  • Are red due to mitochondria, myoglobin, and vascularity
  • Motor neuron size is small
  • Muscle diameter is small
  • Ca2+ pump is slow
  • Low glycogen store
  • Myoglobin is low
  • Myosin ATPase is slow

Fast muscles are

  • Adapted for rapid, intense, phasic (occasionally used), easily fatigues contractions e.g. gastrocnemius
  • Adapted for anaerobic metabolism
  • Are white due to lack of mitochondria, myoglobin, and vascularity
  • Motor neuron size is large
  • Muscle diameter is large
  • Ca2+ pump is fast/rapid
  • High glycogen storage (glycolysis)
  • Myoglobin is high
  • Myosin ATPase is fast
52
Q

Describe the effects of Denervation on Skeletal Muscle

A
  1. A lesion of the motor nerves to skeletal muscle (lower motor neuron lesion) causes flaccid paralysis
  2. This causes Fasciculations or Visible twitching caused by release of ACh from degenerating motor neurons
  3. This leads to the gradual development of Denervation Hypersensitivity due to spread of ACh receptor from the motor neuron endplate (but now in the extracellular fluid from step 2) which results in fibrillations or uncoordinated individual cell contraction
    - Nerve regeneration reverses this and can restore function
    - Failure to regenerate results in type I and II fiber atrophy where muscle fibers begin to deteriorate
53
Q

Describe what Atrophy and Hypertrophy are with some reasons they occur

A

Atrophy is muscle deterioration
Type I and II Atrophy occurs from:
1. Denervation of muscle fibers
2. Peripheral Neuropathy, lack of use, Parkinson’s disease

Type II atrophy associated with Duchenne muscular dystrophy and aging

Hypertrophy is muscle building
Type II Hypertrophy occurs with weight training

54
Q

How are muscles deemed to be fast or slow?

A

Whole muscles are describes as fast or slow if the majority of its cells are fast or slow respectively

55
Q

Which type of muscle fibers is

  • more excitable
  • Recruited first during moderate contractions
  • Recruited first during more intense contractions
A

Slow fiber
Slow fiber
Fast Fiber

56
Q

Slow Fibers are also known as

A

Type I muscle fibers

57
Q

Fast fibers are also known as

A

Tube II-b muscle fibers

58
Q

How can a faste muscle turn into a slow muscle and vice versa?

A

Electrical intervention/nerve stimulation

Low frequencies => Slow to fast
High frequencies => Fast to slow

59
Q

What is the effect of training on the number of fast and slow muscle fibers

A

Training has no effect lmao

Elite sprinters are born with high fast fibres

Elite endurance athletes have high numbers of slow fibres

60
Q

What is the effect of training on the size of muscle fibers

A

Training increases size. Easy no?

61
Q

What are Fasciculations?

A

Visible twitching caused by release of ACh from degenerating motor neurons

62
Q

What is Fiber Atrophy

A

Muscle deterioration

63
Q

What is Fiber Hypertrophy

A

Muscle building

68
Q

Describe the process of Excitation-contraction coupling in muscle

A
  1. Action potential propagates along the Sarcolemma and T system
  2. This causes the release of Ca2+ from the terminal cisternae so that sarcoplasmic Ca2+ concentration increases
  3. Troponin binds Ca2+ causing conformational changes which allow cross bridge formation with actin and release of ADP and phosphate from myosinATPase
  4. Further conformational changes move the cross bridges, thereby pulling the actin filaments towards the center of the A band
  5. Myosin ATPase binds ATP causing the dissociation of the cross-bridges, hydrolysis of ATP, and return to the “cocked” position for further cycles
  6. Relaxation occurs when the sarcoplasmic Ca2+ concentration returns to normal by active transport of Ca2+ back into the sarcoplasmic reticulum where it is bound to Calsequestrin

Medicine Year 1 Semester 1 (23 decks)

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