key concepts Flashcards

1
Q

contraction cycle - 6 steps

A

1) neuromuscular junction propagates signal
2) acetylcholine is released
3) Ca is released
4) T-tubules dive into muscle & relay action potential along t-tubule
5) Ca binds to troponin & releases tropomyosin for actin & myosin cross bridge
6) myosin heads pull thin filaments in user power stroke = contraction

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2
Q

3 ways to produce ATP

A
  1. creatine phosphate - fastest
  2. anaerobic pathway- glycolysis
  3. aerobic pathway- TCA - slowest
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3
Q

3 ways ATP is metabolized

A
  1. Na / K ATPase pump - uses ATP to pump 3 Na out & 2 K in
  2. Ca ATPase pump- uses ATP to pump Ca back into cell / SR
  3. ATP hydrolysis - during muscle contraction to release it for actin
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4
Q

2 factors that influence amount of force control

A

1) increased frequency of stimulus
2) increased motor unit recruitment

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5
Q

How does AChE cause paralysis

A

AChE breaks down acetylcholine which is needed for contraction cycle to occur - releases Ca needed for action potential

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6
Q

2 reasons why action potentials are unidirectional

A

1) refractory period - prevents another AP
2) no sensor at pre-synapse so it can’t pick up a stimulus and transfer AP backwards

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7
Q

muscle contraction in smooth vs skeletal muscle

A

1) smooth- uses myosin light chain - phosphorylated myosin which allows it to bind to actin
2) skeletal- troponin & tropomyosin cross bridge sites

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8
Q

How does a neuron reset after an action potential

A

after depolarization, Na channels close so membrane can return to resting potential & neuron enters refractory period

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9
Q

sliding filament mechanism

A

muscle fibers contract when myosin pulls actin closer & causes sarcomeres to shortn

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10
Q

power stroke mechanism

A

myosin bends to pull thin filaments in, detaches and rebinds further on fibre to pull it more

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11
Q

what is the function of troponin

A

exposes myosin binding sites

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12
Q

what is the function of tropomyosin

A

blocks actin cross bridge sites & prevents interaction between myosin & actin for muscle contraction

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13
Q

what is cross bridge cycling

A

repeated motions that drive thin filaments in towards each other

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14
Q

3 mechanisms that influence NT concentration after release at synapse

A
  1. diffusion
  2. re-uptake
  3. enzyme degradation
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15
Q

contraction & relaxation of smooth muscle

A

contraction- increased calcium results in a chain of biochemical events & myosin becomes phosphorylated which allows it to interact with actin & produce movement

relaxation- myosin becomes dephosphorylated through the light chain and it follows biochemical reactions for calmodulin to unbind Ca and allow relaxation

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16
Q

how is an action potential initiated & propagated

A

initiated by a stimulus that reaches threshold to open Na gates & cause depolarization where 3 Na enter the fiber -> dendrites receive signal & conducts the AP along axon to axon terminal where NT are released -> 2 K leave fiber to repolarize -> hyperpolarization allows return to resting state & gates are closed

17
Q

How is muscle fatigue affected by ATP metabolism

A

ATP concentration decreases as it is consumed by muscles -> favours transfer of phosphate to phosphocreatine from ADP -> forms ATP + creatine for contractions

drop in ATP-> cannot pump Na, K or Ca and cannot perform ATP hydrolysis b/c these metabolic mechanisms require ATP - without ATP = no mechanisms can occur = no ATP for muscle use = muscle fatigue

18
Q

temporal vs spatial summation

A

temporal- several inputs from 1 axon that stimulates another response

spatial- same synapse type with more than 1 input

19
Q

a decrease in pH leads to what shift?

A

right shift- bohr effecr

20
Q

2 concepts that give s shaped curve

A

1) sigmoidal curve- O2 drops very fast during 20-40 = steep increase = O2 drops off slower 60-100 =s shape

2) postage stamp hypothesis- takes more energy to make 2 cuts on the 1st O2 (steep curve section) and only 1 cut for the 2nd, 3rd & 4th O2 (flattens curve) = s shaped

21
Q

what produces EPO

A

kidneys

22
Q

inflammation mechanism (4 steps)

A

1) brings fluid to site of damage
2) macrophages recognize pathogen
3) mast cells release histamine to widen gaps
4) neutrophils & monocytes enter & fight

23
Q

hemostasis steps

A

1) vascular spasm: blood vessels constrict to prevent excess blood loss
2) platelet plug formation: platelets stick to collagen & secrete ADP to cause other platelets to stick to them
3) blood coagulation: fibrinogen is converted to fibrin which forms a clot & prevents platelet plug from moving

24
Q

why do you want low concentration of factor 12 in the blood?

A

factor 12- creates clot

want low concentration so there is no accidental clotting - especially in lungs so TPA is high to ensure no random clotting

25
Q

depolarization ions

A

Na enters

26
Q

repolarization ions

A

K leaves

27
Q

hyperpolarization ions

A

K leaves

28
Q

resetting phase ions

A

3 Na out & 2 K in

29
Q

2 things that slow down conduction speed

A

decreased myelination
decreased fibre diameter

30
Q

Rigor mortis

A

no ATP available to release cross bridges = stuck in contraction