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Sem 3 > neuromuscular/case 9 > Flashcards

neuromuscular/case 9 Flashcards

1
Q

What is fitness?

What types of fitness?

A

physically and psychologically able to meet demands of your environment

health related fitness
skill related fitness

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2
Q

What is endurance? (aerobic and muscular)

A

aerobic: ability of body to sustain a high work rate, maintain technical quality and concentration throughout a training session or event without fatigue
muscular: ability of muscles to carry our repeated contractions without fatigue

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3
Q

How is chemical energy generated?

A

ATP through:

  • anaerobic resp: glycolysis in absence of 02 (produces lactate)
  • aerobic respiration (in presence of 02)
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4
Q

What are the different anaerobic systems?

A
  • lactate

- ATP-PC (ATP-phosphocreatine)

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5
Q

What are the different stages in training load?

A

stimulus
fatigue
compensation
overcompensation (when you do better than initial fitness)

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6
Q

What is overtraining syndrome?

A

training loads too intense and fitness becomes a negative improvement (instead of pos improvement)

  • -> physical changes such as stress fractures
  • -> emotional and behavioural changes
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7
Q

What is VO2 max?

A

rate of volume of oxygen consumption while working at maximal capacity ml/O2/Kg/min

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8
Q

What does VO2 max show?

A

innate ability to perform endurance sports

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9
Q

What is the anaerobic threshold?

A

change from using mitochondrial pathways to glycolytic pathways

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10
Q

How does anaerobic threshold relate to recovery from surgery?

A

the higher it is, the better you will do post surgery

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11
Q

What is isometric contraction?

A

maintain constant length, but increase in tension

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12
Q

Why can’t muscles contract beyond their optical length?

A

actin and myosin have been pulled so far apart/ too squished

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13
Q

What is isotonic contraction?

A

muscle shortens but constant load

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14
Q

What is fine control?

A

few muscle fibres per motor unit

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15
Q

What is coarse control?

A

many muscle fibres per motor unit

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16
Q

large motor unit:
motor neuron
muscle fibres
activity

A

large, fast conduction, hard to excite
many, type 2 (glycolytic)
recruited if strong, contraction is required, usually inactive

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17
Q

small motor unit:
motor neuron
muscle fibres
activity

A

small, slow conduction, easy to excite
few, type 1 (oxidative)
first to be recruited, frequently active

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18
Q 
lower motor neurone lesion:
muscle strength
paralysis
muscle tone
reflexes
A

weakness
flaccid
hypotonia
hyporefelxia

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19
Q 
upper motor neurone lesion:
muscle strength
paralysis
muscle tone
reflexes
A

weakness
spastic (up regulation of Ach receptors: respond to stray Ach)
hypertonia (muscles hard to move, feel heavy)
hyperreflexia (CNS is not inhibiting reflexes)

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20
Q

What happens in the stretch reflex?

A

tendon tap - stretch muscle - stimulate muscle spindles -excite motor neurone/excites inhibitory interneurone - agonist muscle contraction/antagonist muscle relaxation

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21
Q

What distance does the muscle shorten at every contraction?

A

4nm

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22
Q

What are the ELC and RLC parts of myosin? Where are they found?

A

ELC: essential light chain (also called Alkali)
RLC: regulatory light chain

light chains

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23
Q

What is a myofibril?

A

collection of sarcomeres

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24
Q

What regulates binding of myosin to actin?

A

troponin T, C and I molecules
alpha-tropomyosin: wraps around actin and covers actin binding sites (release and binding of Ca to troponin uncovers binding sites)

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25
Q

What roles do troponin T, C and I have in muscle proteins contraction?

A

globular protein

troponin C: Ca binding site: makes conformational change in TnI

troponin T: binds to tropomyosin and forms troponin-tropomyosin complex + inhibits actin-myosin binding unless Ca present

troponin I: binds to actin: holds troponin-tropomyosin complex in place

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26
Q

How many cycles of binding and detachment to actin does a muscle go through every time it twitches?

A

100-1000

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27
Q

What is the striatal muscle contraction cycle?

A
  1. ATP binds to myosin head, causing the dissociation of the actin-myosin complex
    - -> released state
  2. ATP is hydrolysed, causing myosin heads to return to their resting conformation (ADP+ P)
    - -> cocked state
  3. a cross-bridge forms and the myosin head binds to a new position on actin
    - -> cross bridge state
  4. P is released. myosin heads change conformation, resulting in the power stroke. the filaments slide past each other
    - -> power-stroke state
  5. ADP is released
    - -> attached state
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28
Q

What is myasthenia gravis?

A

long term neuromuscular disease that leads to varying degrees of skeletal muscle weakness due to autoimmune disease: have an antibody to the Ach receptors: muscles fatigue very quickly (inactive the receptor): CNS has to make huge demand on muscle to get a normal response

29
Q

Why are T tubules important?

A

spreads excitation deep into cell: for even contraction of the cell

30
Q

What is the sarcoplasmic reticulum and what does it contain?

A

folded bit of membrane that contains a lot of calcium

31
Q

What are the different receptors of the Sarcoplasmic reticulum?

A
  • RoR (ryanodine receptors): detect change in membrane potential and in response with release calcium from SR
  • dihydropirine receptor
32
Q

What happens when an AP reaches the sarcolemma until contraction?

A
  • cytoplasmic calcium increases
  • calcium interacts with troponin
  • twitch force (slight delay)
  • -> as long as there is Ca and ATP, there will be repeated cycling of myosin heads
33
Q

what is actin?

A

40KD globular protein that associates to form filaments: major component of thin filament

34
Q

What is tropomyosin?

A

thin filament component binding to actin

35
Q

What is myosin?

A

200kD globular head coupled to long coiled-coil tail + hinge
+ two 20kD light chains
–> binds and hydrolyses ATP, undergoing a conformational change in the head

36
Q

What is alpha-actinin?

A

cross-links actin filaments at the sarcomere Z line/disks: need it to create muscle fibres

37
Q

What is titin?

A

very long filamentous protein, links Z lines to M lines (largest protein that exists)

38
Q

What are myomesins?

A

binds to titin

generate hexagonal packing of thick filaments

39
Q

What does vinculin bind to?

A

alpha-actinin

40
Q

What does cap-Z do?

A

caps the +ends of actin filaments at the Zline/disk

41
Q

What does tropomodulin do?

A

caps the -ends of thin filaments

42
Q

What does desmin do?

A

links together myofibrils at the Zdisk/line

43
Q

What does dystrophin do?

In what disease is it mutated/absent?

A

links actin filaments to the muscle cell outer membrane

mutated/absent in Duchenne Muscular Dystrophy

44
Q

What does Nebulin do?

A

determines the length of thin filaments

45
Q

What determines the types of muscle cell it becomes (type 1, 2A or 2B)?

A

gene expression is governed by firing pattern of motor neurone

46
Q

When do you start expressing more than one type of myosin?

A

embryogenesis and early life

47
Q

How many ATP molecules are made from one 02 molecule?

A

38

48
Q

How many ATP molecules are made from glucose by substrate level phosphorylation?

A

2

49
Q

What is the Cori cycle?

A

oxygen is used by liver to produce glucose from lactate (regeneration of glucose)

50
Q

What are the different energy store use in muscles from seconds to minutes/hours?

A
  • ATP-PC
  • anaerobic glycolysis
  • oxidative system (mitochondria)
51
Q

How does exercise affect mitochondria?

A
  • increase muscle mitochondria biogenesis via
    1. Ca signalling pathway in the cell
    2. chronic imbalance of ATP demand virus production by mitochondria which case activation of signalling protein kinases
52
Q

What are the effects of lack of exercise (in relations to muscle atrophy?

A

drop in :

  • protein levels
  • fibre diameter
  • force production
  • fatigue resistance

–> increase protein degradation and reduce protein synthesis pathways contribute to muscle loss due to misuse

–> programmed biological process due to lack of exercise

53
Q

What pathway is involved in muscle atrophy? What transcription factors?

A
  • proteolytic (ubiquitin-proteasome, lysosomal and calpaan)

- NF-KB and myostatin (transcription factors)

54
Q

Why is the presynaptic neurone of a neuromuscular junction wrapped in Schwann cell?

A

-stops extracellular ions, blood etc depolarising cell and changing cellular activity

55
Q

Why are junction folds used in post-synaptic terminals of neuromuscular junctions?

A

increase quantity of receptors: not miss any transmitters (make transmission as robust as possible

56
Q

What are the different steps in depolarisation?

A
  • sodium channels open
  • sodium moves in (down concentration and electrical gradient)
  • AP reaches top peak, Na channels turn themselves off (ball and chain inactivation)
57
Q

What are the different steps in depolarisation?

A
  • sodium channels close
  • potassium channels open (open slower than Na channels)
  • potassium moves out along concentration gradient
  • return of electrical potential to neg inside
  • takes 1 ms of ATPase to bring membrane to its normal resting potential (hyper polarised)
58
Q

What are the different steps of neurotransmission at NMJ?

A
  1. AP
    - depolarised pre-synaptic terminal
    - activated voltage gated Ca channels
  2. Ca2+ entry
    - triggers vescicole fusion
  3. vesicle fusion
  4. Ach release
  5. ACh receptor activation
  6. current propagation
  7. ACh removal
59
Q

What happens in vesicle fusion?

A

SNARE hypothesis: (proteins)

  • v-SNAREs (vesicle): synaptobrevin, synaptotagmin
  • t-SNAREs (target membrane): syntax, SNAP-25
  • -> as Ca comes in: binds to synaptotagmin, pulling proteins tighter and membranes to fuse

-happens at active zone (T bars): micro domain

60
Q

What are the different steps in and following ACh receptor activation?

A
  1. ACh release
  2. ACh bind to receptor and open ligand gated sodium channels (only respond to ligand or neurotransmitter: conscious pathway)
  3. Na enters cell though electrical and concentration gradient (microdoamins causing depolarisation-)
  4. voltage gated sodium channels open in response (allowing more Na in (micro domain)
  5. Start an AP in muscle and spread down transverse tubule
  6. Ca channels open (due to AP):
    -slight increase in intracellular AP
    + release from SR
    –> interaction of myosin and actin
  7. muscle contraction
61
Q

What is acetylcholine made from? What synthesis it?

A
  • choline
  • acetyl coenzyme A

-ChAT (choline acetyltransferase)

62
Q

What is the vesicle ACh transporter?

A

VAChT (vesicular ACh transporter)

63
Q

What breaks ACh down? What ACh broken down into?

A

-AChE (ACh esterase)

  • choline
  • acetic acid
64
Q

What happens to choline and acetic acid?

A
  • choline: gets transported back into presynaptic by choline transporters
  • acetic acid is screwed as liquid waste though kidneys
65
Q

What are the different types of ACh receptors?

  • location
  • agonist/antagonists
  • type
A 
-nicotinic
skeletal muscles
agonist: nicotine
antagonists: curare
type: inotropic (Na, fast excitatory)
  • muscarinic
    agonist: muscarine
    antagonist: atropine
    type: metabotropic (K permeability, slow excitatory and inhibitory)
66
Q

What is EPP and what does it do?

A

end plate potential

triggers AP is muscle fibre

67
Q

Which toxins affect the NMJ?

A 
botulinum toxin
tetanus
tetrodotoxin (TTX)
curare
bungarotoxin
Sarin/VX
68
Q

What do the botulinum toxin and tetanus do?

A

enzymatically cleaves synaptobrevin

69
Q

What does Sarin/VX do?

A

irreversible inhibitor of AChE

Sem 3 (20 decks)

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