Lecture 9- Muscle tissue introduction Flashcards

1
Q

‘myos’

A

muscle

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2
Q

myalgia

A

muscle pain

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3
Q

myasthenia

A

weakens the muscle

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4
Q

myocardium

A

muscular component of the heart

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5
Q

myopathy

A

any disease of the muscles

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6
Q

myoclonus

A

sudden muscle spasm

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7
Q

myoclonus

A

sudden muscle spasm

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8
Q

two types of muscle

A

striated and non-striated

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9
Q

striated

A

skeletal muscle

cardiac muscle

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10
Q

non-striated

A

smooth muscle

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11
Q

skeletal muscle is under

A

voluntary control

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12
Q

nerve muscle interactions in skeletal muscle

A

direct nerve-muscle communication

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13
Q

cardiac muscle is under

A

involuntary control

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14
Q

nerve-muscle interaction in cardiac muscle

A

indirect nerve-muscle communication

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15
Q

is myoglobin present in striated muscle

A

YES

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16
Q

is myoglobin present in non-striated muscle

A

NO

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17
Q

is smooth muscle under involuntary control

A

NO

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18
Q

nerve-muscle communication in smooth muscle

A

No direct nerve-muscle communication

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19
Q

myoglobin is a what colour protein

A

red

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20
Q

myoglobin is structural similar to

A

Hb (single unit)

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21
Q

myoglobin function

A

oxygen string molecule which provides oxygen to working striated muscle

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22
Q

at low pH Hb ..

A

gives up oxygen to myoglobin

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23
Q

when striated muscles dies (necrosis)

A

myoglobin is released onto the bloodstream

24
Q

what removes myoglobin from the blood

A

the kidneys

- excreted in the urine- myoglobinurea

25
Q

excess myoglobin in the blood can

A

damage kidneys

26
Q

sarcolemma

A

outer membrane of muscle cell

27
Q

sarcoplasm

A

cytoplasm of a muscle cell

28
Q

sarcosome

A

mitochondrion

29
Q

sarcomere

A

contraction unit in striated muscle

30
Q

sarcoplasm retioculum

A

smooth endoplasmic reticulum of a muscle cell 9high [Ca2+]

31
Q

what is the contraction unit in striated muscle

A

the sarcomere

32
Q

which types of muscle are under voluntary control

A

skeletal muscles

33
Q

which types of muscle have dire nerve- muscle communication

A

skeletal

34
Q

each muscle fibre contains

A

myofibrils

35
Q

myofibrils are made up of

A

repeating subunits called sarcomeres

36
Q

myofibrils are made up of which proteins

A
  • actin
  • myosin
  • tropomyosin
37
Q

thin filaments

A

composed of actin

38
Q

thick filaments

A

composed of myosin

39
Q

thin and thick filaments

A

partially overlap and form functional units called sarcomeres (why myofibrils ahem dark and light bands- striated)

40
Q

how do myofibrils bring about muscle contraction

A

via the sliding-filament theory

41
Q

the sarcomere A band

A

dark band composed of thick filaments and some thin filaments

42
Q

the sarcomeres H band

A

centre of the A band- only thick filament present

43
Q

I band

A

light bands composed of actin (thin) alone

44
Q

Z band

A

found at the centre of I bands

45
Q

Z bands are made of

A

alpha-actinin

- anchors actin filaments and acts as a boundary between sarcomere units

46
Q

z to z=

A

width of sarcomere

47
Q

contraction energy source

A

glycogen- glucose storage meolcile

48
Q

what provides phosphate for ADP-ATP

A

creatine phosphate

49
Q

glycogen is converted to ATP through

A

glycolysis and aerobic resp

50
Q

contraction of sarcomere powered through

A

hydrolysis of ATP–> ADP and inorganic phosphate

51
Q

when muscle are at rest

A

there is an incomplete overlap between the thick and thin filaments with some areas containing only one of the two types

52
Q

when muscle are at rest the ATP molecule is attached to

A

globular myosin head on myosin filaments

53
Q

when muscles are contracting

A

the sarcomeres shorten in length due to the thick and thin filaments sliding over each other resulting in greater overlap between the filaments and a narrowing of the H zones

  • the I bands will come closer together
  • Size of the A band will stay the same
54
Q

MOA: muscles contraction

A
  1. Ca2+ binds to troponin C on the actin filament (thin)- causing a conformational change in troponin
  2. This causes Tropomyosin to move allowing interaction of actin and myosin (tropomyosin previously blocking myosin binding site on actin)
  3. ATP molecule attached to myosin head is hydrolysed, changing its conformation
  4. Myosin head binds actin and forms cross bridge and ‘power stroke occurs
  5. Calcium is transported back to SR by (SERCA ATPase) and the muscle relaxes due to active site on actin being blocked by tropomyosin once again
55
Q

outline Excitation-contraction coupling (long)

A
  1. Action potential at NMJ causes Ach release at synaptic cleft- depolarises the sarcolemma
  2. Action potential propagated down t-tubule of muscle
  3. Depolarisation triggers conformation change in L-type channels which opens Ryanodine receptors
  4. Ryanodine receptors open causing calcium from the SR to flood into the sarcoplasm
  5. Ca2+ binds to troponin C on the actin filament (thin)- causing a conformational change in troponin
  6. This causes Tropomyosin to move allowing interaction of actin and myosin (tropomyosin previously blocking myosin binding site on actin)
  7. ATP molecule attached to myosin head is hydrolysed, changing its conformation
  8. Myosin head binds actin and forms cross bridge and ‘power stroke’ occurs
  9. Calcium is transported back to SR by (SERCA ATPase) and the muscle relaxes due to active site on actin being blocked by tropomyosin once again