Muscles Flashcards

1
Q

What are T-tubules?

A

Extensions of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells.

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2
Q

What is excitation-contraction coupling?

A

How the muscle gets an external signal from the nerve to excite it and propagate an AP to contract. Acetylcholine is usually the neurotransmitter.

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3
Q

what is DHPR?

A

Dihydrophyridine receptor is a L-type voltage-gated calcium channel.

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4
Q

What happens with the hormones when the AP is activated?

A

DHPR changes shape and interacts with RYR, causing it to open and allow calcium to flow out into cytoplasm. Calsequestrian holds Ca2+ in terminal cisternae to generate a concentration gradient (although not high affinity for calcium).

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5
Q

What two things are needed to allow a muscle to contraction?

A

Calcium and ATP. if no calcium then cannot bind actin and myosin so muscle remains relaxed. If no ATP, myosin ends up in resting state and rigorous mortis occurs (contracted/rigid) and Calcium goes into cytoplasm.

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6
Q

What is SERCA?

A

Pump found on membrane which pumps calcium back into SR to restore calcium (2 per ATP molecule).

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7
Q

why might some twitches be fast or slow?

A

Due to different muscle fibres/proteins being expressed/present.

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8
Q

why does it take twice as long for skeletal muscle to relax than contraction?

A

During relaxation calcium leaves. It takes longer to pump calcium into SR against concentration gradient than easily flowing out.

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9
Q

Why is the refractory period longer in the heart?

A

Got to wait much longer for the next AP to propagate as it is essential that the muscle properly relaxes to allow the heart to fill up properly. Tetany would prevent the heart from pumping.

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10
Q

What does thin filament regulated mean in regards to skeletal and cardiac muscle?

A

Actin needs to be activated by calcium to allow the contraction to occur.

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11
Q

How can we control how much calcium is stimulated?

A

Sympathetic/hormonal stimulation of Beta-adrenergic receptors.

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12
Q

What happens during exercise to the heart?

A

Change in sensitivity to calcium.

Change in level of actin-myosin interactions (reduced space of filaments).

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13
Q

What is the main differences in the smooth muscle contraction?

A

Thick filament regulated. Different myosin present which behaves differently. Actin and myosin arranged differently. Doesn’t contract in ONE direction.

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14
Q

What do muscles use ATP for?

A

Energise the power stroke of the myosin cross bridge.
Disconnect the myosin cross bridge form the actin binding site.
Energise the calcium pump for transport of calcium ions back into SR.

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15
Q

What are the 3 possible routes for ATP generation?

A
  1. Direct phosphorylation
  2. Anaerobic pathway
  3. Aerobic pathway
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16
Q

what happens to the NADH and pyruvate made in glycolysis?

A

Shuttled into mitochondrial matrix to complete aerobic oxidative glycolysis
OR
Converted to lactate and NAD+ in the cytosol (non-oxidative glycolysis).

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17
Q

What are the four stages of the aerobic pathway?

A
  1. Glycolysis
  2. Pyruvate decarboxylation
  3. Krebs cycle
  4. Oxidative phosphorylation
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18
Q

what occurs during the fed state?

A

Glucose in blood stream and excess if stored as glycogen.

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19
Q

What occurs during the fasted state?

A

Fatty acids are used up. Glycogen stores are broken down. Gluconeogenesis occurs to create new glucose.

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20
Q

What is McCardle disease?

A

Muscle cells can’t break down glycogen after strenuous exercise so causes muscle cramp.

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21
Q

What is lipid storage disease?

A

Due to CPT deficiency. Causes muscle cramp after prolonged exercise.

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22
Q

What us a agonist/prime mover?

A

A muscle that contracts to create the desired action.

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23
Q

What is a synergist?

A

A muscle that helps the agonist.

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24
Q

What us an antagonist?

A

A muscle that opposes the action of the agonist, thus undoing the desired action.

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25
Q

what is the function of connective tissue layers in muscle?

A

Prevent over stretching, organisation, elasticity, attach to bone and surrounding tissue.

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26
Q

what does a force transducer do?

A

Measures the pull of the muscle by measuring its length, stimulating it and seeing tension it gives.

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27
Q

what is an isometric concentration?

A

The muscle develops force but doesn’t shorten (length constant) e.g. standing still

28
Q

what is a Isotonic contraction?

A

Concentric -muscle shortens e.g. lifting a load.

Eccentric - muscle contracts but lengths e.g. lowering a load/running down hill. Force is constant.

29
Q

what is preload?

A

The resting force on the muscle. If the length increases then the preload increases.

30
Q

What is the after-load?

A

The force the muscle must generate above the preload in order to shorten. Increasing weight increases after-load.

31
Q

What can skeletal blood vessels do?

A

Can auto regulate and have a basal tone (flow remains constant)

32
Q

What happens during strenuous exercise?

A

Intracellular oxygen falls, anaerobic glycolysis predominates and lactic acid production increases and causes pain due to stimulation on nociceptive C fibres.

33
Q

What is exercise hyperaemia usually due to?

A

A fall in vascular resistance.

34
Q

How many bones in the human body?

A

206 bones.

35
Q

what bone is an exception and why?

A

Hyoid bone - doesn’t connect to or form a joint.

36
Q

What is the function of joints?

A

Holds skeletal bones together, allow flexibility for movement and makes bone growth possible.

37
Q

describe the functional classifications of joints?

A

Synarthroses - immovable
Amphiarthroses - little movement
Diarthroses - lots of movement

38
Q

Describe the structural classifications of joints?

A

Fibrous - immovable, held together CT, grow and fuse together.
Cartilaginous - slightly moveable due to cartilage.
Synovial - freely moveable, hip joint, 6 types.

39
Q

Facts about the synovial membrane?

A

Lined by connective tissue (no epithelial lining) so cells are spaced out.
Rich capillary network and has good regenerative powers. Some cells have projections. Contains synoviocytes.

40
Q

What do Type A synoviocytes do?

A

They remove debris and contribute to fluid production. They are macrophagelike and are found in the bone marrow.

41
Q

What do Type B synoviocytes do?

A

Main producer of synovial fluid. Rough ER? Fibroblast-like.

42
Q

how does articular cartilage receive nutrients?

A

Nutrients from blood supply at the end of the bone next to joint. Some nutrients from synovial fluid.

43
Q

what do muscle spindles do?

A

detect rapid rates of change - determine stretch and gather sensory information.

44
Q

what do Golgi tendon receptors do?

A

Measure tension in tendons to detect force generated by the muscle.

45
Q

what types of receptors can determine joint angulation?

A

Skin receptors, Pacinian corpuscles (pressure), Ruffini’s endings (joint position). Free nerve endings create pain sensations.

46
Q

what is osteoarthritis?

A

breakdown of joint cartilage and underlying bone. caused by stress on joint and inflammatory processes.

47
Q

what is rheumatoid arthritis?

A

Autoimmune disorders that affects joints. Genetic and environmental factors. Inflammation of the synovial membrane. Increase in fibroblast-like synoviocytes.

48
Q

what is the function of short bones?

A

stability, support and some motion (carpals)

49
Q

what is the function of flat bones?

A

Point of attachments for muscles (ribs and cranium). Spongy bone is surrounded by compact bone.

50
Q

what is the function of irregular bones?

A

Protect internal organs (facial bones)

51
Q

what is the function of sesamoid bones?

A

Protect tendons from flattening during forces (patellae). Prevents friction. Named after function NOT shape.

52
Q

what is the bone matrix comprised of?

A

Organic portion - 35% - collagen protein fibres and proteoglycans. Provides flexibility.

Inorganic portion - 65% - calcium and phosphate salts. Provides strength.

53
Q

what do osteoblasts do?

A

Synthesise and secrete the collagen matrix and calcium salts. They lack mitotic activity.

54
Q

what do osteocytes do?

A

maintain the mineral concentration of the matrix via the secretion of enzymes.

55
Q

what do osteoclasts do?

A

Break down bone and release matrix back into the blood. They move around so direct blood supply. Good for raising blood calcium levels.

56
Q

what is osteogenesis/ossification?

A

Bone tissue formation in the foetus - occurs throughout life. Can have a genetic influence or be affected by hormones GF’s and signals.

57
Q

what regulates bone growth an remodelling?

A

Genetics, Hormones, Physical activity, environmental factors and nutrition.

58
Q

What are IGFS?

A

Insulin-like growth factors - produced by bone and liver. Promote cell division at epiphyseal plate and enhance synthesis of bone proteins. Production of IGF’s stimulated by hGH. It is important during childhood.

59
Q

What are hGH’s?

A

Produced by anterior pituitary. Stimulates epiphyseal activity and osteoblast activity and osteoclast activity. Activity of hGH is modulated by thyroid hormone.

60
Q

What are PTH’s?

A

Parathyroid Hormones. Stimulates osteoclasts to degrade bone matrix to release Calcium. Stimulates synthesis of vitamin D calcitonin. Stimulates osteoblasts to deposit calcium salts. Inhibits osteoclast activity.

61
Q

what is gene therapy?

A

A direct use of genetic material to treat a disease in a patient. Limited to somatic cells.

62
Q

what happens during heart failure?

A

Part of muscle is starved from oxygen, causing the muscle to die and scar tissue is formed. Has to compensate for lack of contraction now due to less muscle.

63
Q

how does the heart compensate for less contractile force during heart failure?

A

Chambers enlarge, muscle is thinner.

64
Q

What happens to calcium when the heart is pumping?

A

Relaxation - calcium enters into extracellular space.

Contraction - Calcium must disappear to allow relaxation again, so pumps it back into ER. This is regulated by SERCA2a.

65
Q

what happens in HF patients in relation to SERCA2a?

A

Activity decreases.

Peaks are wider on ECM.