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TOB > Muscle > Flashcards

Muscle Flashcards

1
Q

What is the Sarcolema?

A

Outer membrane of a muscle cell

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2
Q

What is the sarcoplasm?

A

Cytoplasm of a muscle cell

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3
Q

What is the sarcoplasmic reticulum?

A

Smooth er of a muscle cell

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4
Q

What is a sarcomere?

A

Unit of striated muscle. Distance from one z band to the next.

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5
Q

What are the bands in striated muscle? What are the two filaments?

A

MHAZI, m line is in the h band which is in the a band. The z band is in the I band. A band is the dark band, I band is the light band.
Actin filament is thin filament
Myosin filament is thick filament

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6
Q

What are the h bands?

A

Wherever the actin filaments don’t overlap with myosin filaments. When the muscle contracts this gets smaller as more overlap and when it relaxes it gets bigger due to the Sliding filament.

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7
Q

What altogether forms the actin filament?

A

Actin, troponin, tropomyosin molecules, skeletal and cardiac muscle only.

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8
Q

How is the actin filament arranged?

A

A troponin complex is attached to each tropomyosin molecule covering the binding sites for the myosin filament.

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9
Q

What does the myosin filament consist of?

A

Many myosin molecules, whose heads protrude at opposite ends.

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10
Q

How does contraction begin?

A

Increased amounts of ionic calcium bind to the TnC of troponin and a conformational change moves tropomyosin away form the actins binding site. This displacement allows myosin heads to bind to actin and contraction begins.

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11
Q

What are the 5 stages of contraction?

A 
Attachment
Release
Bending
Force generation
Reattachment
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12
Q

What happens in step 1 of contraction - attachment?

A

Rigour configuration - myosin heads are tightly bound to actin. In death lack of ATP perpetuates this binding (rigour mortis)

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13
Q

What happens in step 2 of contraction - release?

A

ATP binds to the myosin head causing it to uncouple from the actin

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14
Q

What happens in step 3 of contraction - bending?

A

Hydrolysis of ATP causes the uncoupled myosin head to bend and advance a short distance

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15
Q

What happens in step 4 of contraction - Force generation?

A

The myosin head binds weakly to the actin filament causing the release of inorganic phosphate which strengthens the binding and causes the power stroke in which the myosin head returns to its former position. This advances the actin filament.

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16
Q

What happens in step 5 of contraction - reattachment?

A

The myosin head binds tightly again and the cycle can repeat. Individual myosin heads attach and flex at different times causing movement.

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17
Q

How is the contraction cycle initiated?

A
  1. Upon arrival of action potential from axon at pre synaptic neuron terminal at n’muscular junction, voltage dependent calcium channels open and Ca2+ ions flow into this area.
  2. Influx of calcium ions causes acetyl choline containing vesicles to fuse with the presynaptic membrane and Ach is released into the synaptic cleft.
  3. Ach diffuses across cleft and binds to the nicotine Ach receptors on the motor end plate, these are folded to increase SA for more receptors.
  4. When the receptors are bound to Ach they open, allowing Na+ to flow in and K+ out of the Sarcolemma, depolarising it which also spreads to the T tubules.
  5. Voltage sensor proteins of the T tubule membrane change their conformation.
  6. Gated Ca2+ release channels of adjacent terminal cisternae from sarcoplasmic reticulum are activated and proteins change in conformation.
  7. Ca2+ is rapidly released from the terminal cisternae into the sarcolpasm.
  8. Ca2+ binds to the TnC subunit of the troponin.
  9. Contraction cycle is initiated and Ca2+ is returned to SR.
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18
Q

Where do you find neuromuscular junctions? What does building muscle do to these?

A

On every muscle cell. Build up of muscle also builds up the number of these.

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19
Q

How many nicotine Ach receptors have to be occupied for full muscular contraction?

A

25% to open all the sodium channels

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20
Q

How does the Ach release change during the contraction of a muscle?

A

Lots at first and then reduced to a sustained level as only 25% of receptors need to be filled for full muscular contraction.

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21
Q

How many times are calcium ions needed in the initiation of the contraction cycle?

A

Twice

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22
Q

What are the characteristics of white skeletal fibres and where are they found?

A

Fast contraction and fatigue. Lots of neuromuscular junctions. Sprinters legs

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23
Q

What are the characteristics of red skeletal fibres?

A

Slower contraction and fatigue, fewer n’muscular junctions.

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24
Q

Are skeletal, cardiac and smooth muscle voluntary or involuntary?

A

S - voluntary

C and Sm - involuntary

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25
Q

What is the macrostructure of skeletal muscle?

A

Muscle (surrounded by epimysium) is composed of fascicles (surrounded by perimysium, connective tissue carrying nerves and blood vessels) which are composed of muscle fibres/cells (surrounded by endomysium) which are composed of micro fibrils which are composed of myofilaments (actin and myosin).

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26
Q

How does skeletal muscle interact with tendons?

A

Interdigitates with the tendon collagen bundles at myotendinous junctions. Sarcolemma always lies between collagen bundles and muscle fibres myofilaments.

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27
Q

What do you see if you cut skeletal muscle transversely/longitudinally?

A

T- peripheral nuclei

L- see nuclei in rows

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28
Q

How is the skeletal muscle formed?

A

Mesodermally derived multipotent myogenic cells give rise to myoblasts. Near synchronous fusion of myoblasts forms primary myotube with lots of nuclei/cell. Multiple nuclei at periphery as newly synthesised actin and myosin myofilaments displace them.

29
Q

What is the nature of repair in skeletal muscle?

A

Cells can’t divide but tissue can regenerate by mitotic activity of satellite cells (which can become muscle cells). So that hyperplasia follows injury.
Satellite cells can also fuse with existing muscle cells to increase mass (hypertrophy).

30
Q

How is gross damage repaired in skeletal muscle?

A

Repaired by connective tissue which leaves a scar.

31
Q

What happens if the nerve or blood supply to skeletal muscle is interrupted?

A

Muscle fibres degenerate and are replaced by fibrous tissue.

32
Q

What are the three types of muscle?

A

Skeletal
Cardiac
Smooth

33
Q

What is the nature of repair in cardiac muscle?

A

Incapable of regeneration and so, following damage, fibroblasts invade and lay down scar tissue.

34
Q

What is the nature of repair of smooth muscle?

A

Cells retain their mitotic activity and so can form new smooth muscle cells.
For example in pregnant uterus where the muscle wall becomes thicker by hypertrophy and hyperplasia if individual cells.

35
Q

What are the functions of skeletal muscle?

A

Movement
Posture
Stability of joints
Heat generation

36
Q

How is cardiac muscle controlled?

A

ANS and hormones

37
Q

What are the features of cardiac muscle?

A

Striations
Branching
Centrally position nuclei, 1/2 per cell
Intercalated discs for electrical and mechanical coupling with adjacent cells
Gap junctions at 90 degrees for electrical coupling so all cells contract at the same time.
Adherens-type junctions to anchor cells and provide anchor for actin.

38
Q

Where is smooth muscle found?

A

Gut wall, blood vessel walls, dermis, secretory glands.

39
Q

What are the two kinds of modified smooth muscles cells and where are they found?

A

Myoepithelial, form basket work around secretory unit of some exocrine glands (eg sweat, mammary, salivary) and contract to assist secretion of product into the duct.
Also in iris to dilate pupil.
Myofibroblasts, site of wound healing, produce collagenous matrix and contract. Prominent in drawing wound edges together.

40
Q

What are the features of smooth muscle?

A

Spindle shaped (Fusiform) cells with 1 central nucleus.
Not striated, no sarcomeres, no tubules
Contraction still relies on actin and myosin interactions but is slower, more sustained and requires less ATP.
Capable of being stretched.
Respond to stimuli in form of nerve signals, hormones, drugs or local conc of blood gases.
Form sheets, bundles or layers.
Thin and thick filaments are arranged diagonally within cell spiralling down so contracts in a twisting way.

41
Q

How does the ANS affect the smooth muscle?

A

Release their neurotransmitter from Varicosities when they swell into a wide synaptic cleft.

42
Q

What do purkinje fibres do and what do they contain?

A

Transmit action potentials to the ventricles from the AV node.
Abundant with glycogen, sparse myofilaments, extensive gap junction sites.

43
Q

How do purkinje fibres differ from regular cardiac muscle and what does this mean?

A

They conduct action potentials rapidly which enables the ventricles to contract in a synchronous manner.

44
Q

In relation to replacement and destruction, what is hypertrophy and atrophy?

A

Atrophy is destruction>replacement

Hypertrophy is destruction

45
Q

What are the three reasons for atrophy?

A

Disuse, age and denervation.

46
Q

What causes denervation?

A

Neuro causes

47
Q

What is disuse atrophy?

A

Lack of movement against resistance causes muscle fibres to shrink and weaken. Decrease in diameter.

48
Q

Why does age cause atrophy? What can this lead to?

A

Past age of 30 muscle mass starts to decrease. 50% loss by age of 80.
Sarcopenia can Affect their mobility to do basic things like get out of a chair.
Affects temp reg as use skeletal muscles to shiver, less mass, can’t maintain temp as well.

49
Q

What happens in denervation?

A

Muscles no longer receive contractile signals required to maintain normal size. Lead to weakness, flaccidity, degeneration of muscle fibres. If innervation isn’t reestablished within 3 months v poor recovery.
Muscles replaced with fibrous and fatty tissue. Fibrous leads to contractures and muscle shortens.

50
Q

What happens in hypertrophy and what metabolic changes occur?

A

Increase in muscle mass from work against load lead to more actin and myosin so increased fibre diameter.
M- increased enzyme activity for glycolysis, increased number of mitochondria, increase stored glycogen, increased blood flow
Altogether greater O2 utilisation.

51
Q

What is acetylcholine terminated by?

A

Acetylcholinesterase

52
Q

What is myasthenia gravis?

A

Autoimmune destruction of end plate Ach receptors by IgG antibodies. Loss of junctional folds at end plate so loss of SA for receptors. Widening of synaptic cleft so further for Ach to diffuse.

53
Q

When is the crisis point for myasthenia gravis?

A

When it affects respiratory muscles

54
Q

What are the symptoms of myasthenia gravis and why?

A

Fatigability and sudden falling due to reduced Ach release- harder to maintain the muscle contraction as not enough receptors will be occupied.
Drooping eyelids
Double vision- eyes don’t move in sync

55
Q

What is myasthenia gravis also affected by?

A

General state of health and emotion.

56
Q

How do you treat myasthenia gravis?

A

Acetylcholinesterase inhibitors.
Less Ach broken down in cleft so can bind to receptors multiple times to maintain the contraction for longer.
Immunosuppressants to stop the body destroying itself.
Remove the harmful antibodies from the patients serum.

57
Q

What affect does botulism have on the body?

A

Toxins block Ach release

58
Q

What affect does organophosphate have on the body?

A

Irreversibly inhibits Acetylcholinesterase, therefore Ach remains in the receptors and muscle stays contracted.

59
Q

What is the General pathophysiology of muscular dystrophy?

A

Genetic faults cause the absence or reduced synthesis of specific proteins that anchor the actin filaments to the sarcolemma, the muscle fibres may then tear themselves apart on contraction.

60
Q

Which is the most serious and life threatening form of dystrophy?

A

Duchenne muscle dystrophy

61
Q

What causes duchenne…?

A

Complete absence of dystrophin so there is nothing linking the actin filament to the sarcolemma. The muscle fibres tear themselves apart on contraction as the sarcolemma doesn’t move with the contraction as its not connected to the actin. Enzyme creatine (phospho)kinase liberated into serum. Calcium enters cell causing cell death. Pseudohypertrophy (swelling) before fat and connective tissue replace muscle fibres.

62
Q

Why does ice treat drooping eyelids?

A

It decrease activity of Acetylcholinesterase

63
Q

What are the signs and symptoms of duchenne.. .?

A

Early onset, gowers sign (hands on knees to generate strength)
Contractures

64
Q

How do you treat duchennes?

A

Steroid therapy (prednisolone) not anabolic steroids

65
Q

What is malignant hyperthermia?

A

Rare autosomal dominant disorder that is a life threatening reaction to certain drugs used for GA.

66
Q

What are the drugs used for GA that can cause malignant hyperthermia?

A

Volatile anaesthetic agents and neuromuscular blocking agent succinylcholine. S inhibits the action of Ach acting non competatively on the nicotine receptors. Degraded by butyrylcholinesterase but much more slowly than degradation of Ach.

67
Q

What happens in those susceptible to reacting to the GA drugs?

A

Drugs induce a drastic Nd I controlled increase in skeletal muscle oxidative metabolism, quickly overwhelming the body’s capacity to supply O2, remove CO2 and regulate body metabolism. Eventually lead to circulatory collapse and death of not treated quickly.

68
Q

How can you treat malignant hyperthermia?

A

Correction of hyperthermia, acidosis and organ dysfunction, discontinuation of triggering agents and admin of dantrolene, a muscle relaxant that works by preventing release of calcium.

TOB (6 decks)

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