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E ( PHYS ) > MIDSEM PREP (E) > Flashcards

MIDSEM PREP (E) Flashcards

1
Q

What is general cell RMP (intracellular)?

A

-70mV

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2
Q

What is AR cell RMP?

A

-60mV

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3
Q

What is AR cell threshold level (mV)?

A

-40mV

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4
Q

What is AR cell depolarised MP (mV)?

A

0mV

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5
Q

What is myocardial cell RMP?

A

-90mV

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6
Q

What is myocardial threshold level (mV)?

A

-70mV

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7
Q

What is myocardial cell depolarised MP (mV)?

A

+30mV

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8
Q

What is contained within the following region of the sarcomere:
I band.

A

I band:

Actin and titin (thin filament only).

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9
Q

What is contained within the following region of the sarcomere:
H zone.

A

H zone:

Myosin and titin (thick filament only).

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10
Q

What is contained within the following region of the sarcomere:
Z line.

A

Z line:

Actin and titing (attachment or anchoring point).

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11
Q

What is contained within the following region of the sarcomere:
M zone.

A

M zone:

Myosin and proteins holding it in place (thick filament attachment to cytoskeleton).

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12
Q

What is contained within the following region of the sarcomere:
A band.

A

A band:

Entire length of thick filament, may contain thin filament depending on stage of contraction.

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13
Q

Provide 2 examples of SYMPORT across cell membrane, stating whether this is an active or passive process.

A
  1. SGLT - 2 sodium and one glucose in; 2AT.

2. One Na and one AA in; 2AT.

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14
Q

Provide 2 examples of ANTIPORT across cell membrane, stating whether this is an active or passive process.

A
  1. NaK ATPase - 3 Na+ out 2 K+ in; active.

2. Sodium hydrogen exchanger - 3 Na+ in one H+ out; active.

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15
Q

Provide 2 examples of UNIPORT across cell membrane, stating whether this is an active or passive process.

A
  1. Voltage gated K channels - efflux, 2AT.

2. Voltage gated Na channels - influx, 2AT.

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16
Q

Which substances are PERMEABLE to the cell membrane; and what properties deem them so? Provide examples.

A

Lipophillic (hydrophobic, non-polar) substances permeable - such as gases, urea, steroids.

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17
Q

Which substances are IMPERMEABLE to the cell membrane; and what properties deem them so? Provide examples.

A

Lipophobic (hydrophillic, polar) substances impermeable - such as sugars, AA, water.

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18
Q 
For the following stage of sarcomere contraction, state the position (or movement) of the following regions: 
RELAXED... 
H zone - 
I bands - 
Z disks - 
A bands -
A 
RELAXED... 
H zone - largest. 
I bands - largest. 
Z disks - furthest apart. 
A bands - NO CHANGE.
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19
Q 
For the following stage of sarcomere contraction, state the position (or movement) of the following regions: 
CONTRACTING... 
H zone - 
I bands - 
Z disks - 
A bands -
A 
CONTRACTING... 
H zone - narrowing. 
I bands - narrowing. 
Z disks - move towards each-other. 
A bands - NO CHANGE.
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20
Q 
For the following stage of sarcomere contraction, state the position (or movement) of the following regions: 
CONTRACTED... 
H zone - 
I bands - 
Z disks - 
A bands -
A 
CONTRACTED... 
H zone - disappeared. 
I bands - smallest. 
Z disks - closest together as they get. 
A bands - NO CHANGE.
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21
Q

What’re the 3 functional benefits to a cell, granted by it having a negative RMP?

A

Overall - ability to store potential energy.

  1. Cell signalling.
  2. Nerve transmission.
  3. Muscle contraction.
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22
Q

What is the general cell RMP (extracellular)?

A

0mV.

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23
Q

What % of membrane potential is made up by the efforts of NaK ATPase.

A

20%.

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24
Q

Overall, how is membrane potential established? (4)

A
  1. Effect of NaK ATPase.
  2. Na movement in isolation.
  3. K movement in isolation.
  4. Concurrent effects of Na and K.
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25
Q

Briefly explain the effect of NaK ATPase on membrane potential.

A

NaK pump moves 3Na+ out and 2K+ in; antiport. The majority of its effect is through the electrochemical gradient it establishes, and subsequent 2AT which it allows. Individually, it accounts for 20% of membrane potential.

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26
Q

What is the main influencer of membrane potential, Na or K, and why?

A

K+ is main influencer of membrane potential simply because the membrane is far more permeable to K then it is to Na. Subsequently, cell membrane potential is very close to the equilibrium potential for K+, at 70mV.

This being said Na movement DOES affect the RMP (working in the opposite direction, due to sodiums higher [] extracellular it brings positive charge in). The leakage of ions in both directions (as K and Na are both freely able to move across membrane) is offset by the work of the NaK pump.

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27
Q

Describe what is meant by the following term(s):

Nersnt potential.

A

Nersnt potential details the relationship between the magnitude of membrane electrical potential and the difference in ion concentration.

(basically - calculating membrane potential by accounting for charge in ions and there abundance)

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28
Q

The nernst potential increases by approx 60mV for each __x increase in concentration ratio.

(where [ratio] is the concentration of substance extracellular divided by concentration of substance intracellular)

A

10x.

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29
Q

What’re the 2 main points which can be concluded from the nernst potential relationship?

A
  1. A relatively small electrical potential difference can balance a large concentration difference across the membrane.
  2. Existence of a concentration gradient across a membrane in NOT evidence that work has to be done to move a particular species.
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30
Q

State the general speed of an action potential.

A

100 m/s.

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31
Q

What is the “equilibrium potential for K+”?

A

-70mV, this is reflected by the fact that K+ is the predominantly responsible for establishing RMP (as there are more K+ channels then Na+ channels).

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32
Q

Explain the general steps involved with voltage gated Na+ channels.

A
  1. Membrane at rest - (equilibrium potential for K) at -70mV. Activation gate is CLOSED; no Na current.
  2. Stimulus arrives - stimulus causes partial depolarisation, causes activation gate to open and Na to flow in down its electrochemical gradient.
  3. Positive feedback - self amplifying process, sodium continues to enter cell until +30mV achieved
  4. Na current reaches a maximum in 0.5msecs then rapidly falls to zero (despite cell membrane still being depolarised). This is due to abrupt closing of sodium channels, as the inactivation gate closes the channel.
  5. Na channel does not re-open until membrane potential returns to resting level (-70mV, the sodium channel has to be ‘reset’).

This whole process takes a few ms to complete.

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33
Q

Explain the general steps involved with voltage gated K+ channels.

A
  1. Potassium channels open slower then Na channels, at +30mV.
  2. K+ current (out of cell) reaches maximum after Na channel inactivated.
  3. K+ efflux returns membrane potential to -70mV quickly (channel opens slow but works fast).
  4. This works on the basis of ‘time delay’; K channel is delayed to allow for depolarization -> repolarisation

(note: K is slower to open but its effect is strong and long lasting - bringing membrane back to resting potential. Then, relative amounts of ions are maintained by NaK pump).

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34
Q

How long does it take for sodium inactivation gate to become active?

A

~0.5 ms.

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35
Q

What occurs in a nerve cell where it becomes depolarised, but only to a level BELOW threshold level?

A

If a nerve cell is depolarised below threshold there is a passive spread of electrical signal which deteriorates in strength at distance.

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36
Q

Explain what is meant by the following term(s):

Graded potential.

A

Graded potentials are small deviations from resting potential (-70mV). These signals (be they depolarisation or hyperpolarisation) are graded in that they vary in there amplitude depending on the strength of the stimulus, and are localised.

  • small
  • local
  • strength dependent on stimulus
  • most often occur in cell body/ dendrites.
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37
Q

a. ) Explain how nerve conduction speed varies in UNMYELINATED fibres?
b. ) By how much would conduction speed increase in an UNMYELINATED fibre, if there were a 100x increase in fibre diameter?

A

a. ) In unmyelinated regions there is a direct relationship between conduction velocity and axon diameter. This is as the larger the axon, the less resistance to current.
b. ) 100x increase of fibre diameter causes 10x increase in conduction velocity.

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38
Q

Do nodes of ranvier have a higher, or lower density of ion channels compared to unmyelinated fibres?

A

Higher; this in conjunction with saltatory conduction is responsible for the much higher velocity of impulse in myelinated fibres.

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39
Q

Provide 2 functional advantages of myelin.

A
  1. AP travels faster in small sized axons (such as optic nerve).
  2. Metabolic energy is conserved as active excitation is confined to nodes of ranvier.
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40
Q

Is axon diameter still a factor to consider when assessing speed of transmission through a myelinated axon? Why/ why not?

A

YES - as the greater the fibre diamter the greater the distance between the nodes, thus less nodes are required.

The less nodes that are present the faster the action potential, as the jump of electrical transmission over myelinated areas is way faster then the movement of ions into and out of the cell in unmyelinated areas.

This being said the greatest advantage of myelinated fibres is that nerves can be small and still have fast propagation times, such as in the optic nerve.

41
Q

Explain what is meant by the following term(s):

Absolute refractory period.

A

ARP is the duration following an action potential where second action potential cannot be elicited regardless stimulus strength; from threshold potential to repolarisation at 60mV.

42
Q

Explain what is meant by the following term(s):

Relative refractory period.

A

RRP is the duration after action potential where a second action potential may be elicited, provided a GREATER THEN USUAL stimulus is applied; excitability increase as RRP progresses.

43
Q

Unmyelinated fibres transmit messages by whats called _______ conduction.

A

Continuous conduction.

44
Q

In terms of ion movements, why is it that…

a. ) The neuron can be re-stimulated during the RRP?
b. ) The AP elicited during RRP is weaker in amplitude?

A

a. ) It is possible to induce AP during RRP as the sodium inactivation gate has closed (post repolarisation; -60mV), and so stimulus is able to trigger open the sodium activation gate once again.
b. ) The AP is weaker as K+ activation gate is still open during this period and so K+ is constantly moving out of the cell, working against the depolarising effect of Na+ moving into the cell.

45
Q

State the distances of the following synapses:

a. ) Chemical synapse
b. ) Electrical synapse

A

a. ) Chemical synapse - 20 nm gap (synaptic cleft”).

b. ) Electrical synapse - 2nm gap.

46
Q

Explain the basic occurrences which occur at a chemical synapse, as an impulse is transmits from an electrical -> chemical -> electrical form.

A
  1. Electrical - AP reaches the axon knob, where the change in electrical potential stimulates the opening of voltage gated calcium channels. Calcium subsequently rushes into the axon knob, thus inducing the release of neurotransmitters, which travel within there vesicles to the edge of the presynaptic membrane.
  2. Chemical - the vesicles fuse with the presynaptic membrane and the neurotransmitters contained within are released into the synaptic cleft. These NT’s diffuse across the synaptic cleft and toward the postsynaptic membrane.
  3. Electrical - neurotransmitters (ie. ACh) then bind to receptors on the postsynaptic membrane, triggering opening of Na and K channels in postsynaptic neuron, and a subsequent AP to occur.
47
Q

Approximately, how many synaptic connections exist within a human’s CNS?

A

10^9 synaptic connections.

48
Q

As axonal transport occurs (of NT, proteins. lipoproteins etc), transport also occurs simultaneously in the opposite direction. What is typically found going in this opposite direction?

A

Endocytotic proteins imbided from the ECF.

49
Q

What are the mechanisms for axonal transport?

A

Microtubules of the axoplasm.

50
Q

State the general diameter of synaptic vesicles.

A

3-4nm.

51
Q

How many molecules of ACh are found in each synaptic vesicle?

A

~10 000.

52
Q

ACh is broken down by acetylcholinesterase in the synaptic cleft. How is it then reabsorbed into the terminal end of the axon?

A

Cotransport (symport) with sodium.

53
Q

Which chemical is responsible for most often inducing secretion?

A

Calcium.

54
Q

Why are mitochondria present in the terminal button?

A
  1. Energy is used to convert CoA into acetyl CoA, which can then be used to combine with choline to form ACh.
  2. To clear excess Ca+2 in terminal button.
55
Q

What’re the 3 ways which ACh may be disposed of?

A
  1. AChase breaks it down, and its recycled.
  2. Diffuses into blood.
  3. Taken up by glial cell.
56
Q

Is a ‘time delay’ present in electrical synapses, chemical synapses or both? Why is this so?

A

Time delay characteristic to chemical synapses only; as this is the time it takes for a signal to convert from electrical -> chemical -> electrical form. For the mostpart, it is the time for diffusion to occur; however it is only a fraction of a second.

57
Q

How is it that postsynaptic potentials differ to presynaptic potentials?

A
  1. Smaller amplitude.

2. Longer duration (10-100x).

58
Q

The magnitide of a postsynaptic potential depends on what?

A

PostSP magnitude is directly proportional to amount of NT released. This explains why the PostSP rises rapidly (lots of NT present initially) and then slowly tapers off (as NT gradually broken down/ disposed of).

59
Q

PostSP’s are generally much smaller in amplitude; the result of this is that a single AP from a presynaptic neuron is rarely sufficient to trigger an AP in the postsynaptic neuron. Explain the mechanism in place to overcome this phenomena.

A

SUMMATION: several presynaptic bulbs release their NT’s at the same time onto the same postsynaptic membrane, resulting in enough NT being present to reach threshold potential. Summation may be TEMPORAL or SPATIAL.

60
Q

Explain what’s meant by temporal summation.

A

Subsequent impulses from SAME AXON arrive before the preceeding PostSP has fully decayed, augmenting it’s effect. This is a FREQUENCY MODULATED effect; as it is the constant frequency with which AP’s from this neuron arrive which stack for the final effect.

61
Q

Explain what’s meant by spatial summation.

A

The same as temporal summation however NT’s from DIFFERENT AXONS augment to reach threshold level.

62
Q

Contrast the effects of excitatory and inhibitory NT’s.

A

Excitatory - opens ligand gated Na channel.

Inhibitory - opens ligand gated K/ Cl channels.

63
Q

Explain what is meant by the following general term(s):
Presynaptic inhibition.
(note: is this a selective, or non-selective process)

A

PRESYNAPTIC INHIBITION - SELECTIVE. This synapse is the one which occurs between presynaptic axon terminal and target cell:
The inhibitory fibre connects directly to the terminal button of the excitatory fibre, causing it to hyperpolarise.
As a result the impulse that arrives in the excitatory neuron causes a less then usual amount of neurotransmitter to be released, causing a reduced PostSP. This PostSP is lower in amplitude and does not reach threshold level, resulting in no AP.

64
Q

Explain what is meant by the following general term(s):

Postsynaptic inhibition.

A

POSTSYNAPTIC INHIBITION - NON-SELECTIVE.
This synapse occurs between postganglionic neuron and all its target cells:
The inhibitory fibre connects directly to cell body of the postganglionic neuron. There is competition between the excitatory and inhibitory fibres, resulting in a modulated signal which is below threshold. The result is no AP being initiated at trigger zone (axon hillock).

65
Q

State the main site of action for the following receptor:

α1.

A
  • vascular SM (skin/ gut)

- gut sphincters

66
Q

State the secondary messenger(s) for the following receptor:
α1.

A

G proteins; activation of phospholipase C to increase [Ca+2].

67
Q

State the main site of action for the following receptor:

α2.

A

Presynaptic adrenergic nerve terminals.

68
Q

State the secondary messenger(s) for the following receptor:
α2.

A

G proteins; inhibitions of adenyl cyclase to decrease [cAMP].

69
Q

State the main site of action for the following receptor:

β1.

A

Heart.

70
Q

State the secondary messenger(s) for the following receptor:
β1.

A

G proteins; activation of adenyl cyclase to increase [cAMP].

71
Q

State the main site of action for the following receptor:

β2.

A
  • vascular SM (sk muscle and heart)

- bronchioles

72
Q

State the secondary messenger(s) for the following receptor:
β2.

A

G proteins; activation of adenyl cyclase to increase [cAMP].

73
Q

What’re the 4 myofibrils making up skeletal muscle? Include there classification (thin or thick).

A
  1. Actin (thin).
  2. Troponin (thin).
  3. Tropomyosin (thin).
  4. Myosin (thick).
74
Q

What’re the 2 other protein molecules which aren’t thin or thick filament, but contribute to the sarcomere? State their function also.

A
  1. Titin (elastic anchor) - returns sarcomere to original length, stabilises position of contractile proteins.
  2. Nebulin (non-elastic anchor) - helps align actin molecules.
75
Q

State the diameter of sk muscle fibres.

A

0.1 - 0.01 mm.

76
Q

State the length of a sarcomere.

A

2.5 qm (in a relaxed muscle; the distance between Z lines).

77
Q

Describe the structure of myosin.

A

Myosin appears as a thin rod with a double globular head. The thin rod is made of 2 entwined heavy protein chains, and have an elastic hinge region on them for the attachment of the globular heads. This elastic hinge region allows the globular heads to swivel around their point of attachment.

78
Q

Describe the structure of tropomyosin, including it’s position to the backbone of the thin filament (actin).

A

Tropomyosin is a long, thin thread like molecule which lies in the grooves on the actin molecule (the grooves of the double helix made of G-actin subunits).

79
Q

Explain what is meant by the following general term(s):

F-actin polymer.

A

An F-actin polymer is many G-actin subunits (bead like structures) strung together to form a double helix. Colloquially, this is just understood as the ‘actin’ molecule.

80
Q

What does troponin bind to, and why is it such a significant molecule?

A

Troponin molecules bind to each tropomyosin molecule. These are important as when calcium is present, they undergo a conformational change revealing the binding site on the tropomyosin.

81
Q

State 2 unique functional properties which cardiac muscle possesses, compared to skeletal.

A
  1. Functions as syncytium - due to gap junctions, contraction in one area rapidly spreads.
  2. Refractory period.
82
Q

What is the function of intercalated discs?

A

Maintain cell to cell adhesion.

83
Q

t/f: smooth muscle contains little troponin.

A

true.

84
Q

Smooth muscle contains high concentrations of a specific calcium binding protein, known as what?

A

Calmodulin.

85
Q

Outline the steps involved with contraction of skeletal muscle.

A
  1. AP travels down terminal axon of motor neuron (toward MEP).
  2. Depolarisation at terminal axon opens voltage gated calcium channels, allowing Ca+2 to flow into the terminal button.
  3. Increased [Ca+2] triggers release of synaptic vesicles from motor end plate, ACh diffuses across synaptic cleft (20nm).
  4. ACh binds to ligand-gated receptor on sarcolemma of muscle (region which this occurs in known as neuromuscular junction).
  5. Binding of ACh induces opening of Na gated ion channels in muscle cell, Na rushes into muscle cells depolarising it and inducing an AP.
  6. AP travels across sarcolemma of muscle inducing muscular contraction.
86
Q

How does contraction occur simultaneously in all muscle fibres, considering communication dependant on diffusion of a chemical?

A

Due to the ULTRASTRUCTURE of muscle..

  1. T-system (complex tubule system).
  2. Sarcoplasmic Reticulum (system of flattened vesicles).

When impulse arrives at motor end plate depolarisation of the sarcolemma of muscle follows, this depolarisation continues into the T-system allowing for rapid communication of the stimulus. The SR increases speed by vast supply of Ca+2, which is necessary for the drift to threshold of muscle cells.

87
Q

Describe the steps in the contraction cycle. (9), and the series of events leading up to this (a-e).

A

a. ) AP arrives at MEP on muscle.
b. ) T-tubule system carries AP throughout muscle belly (into interior also; invaginations).
c. ) AP (which is mainly Na+ flow) induces opening of voltage gated DHP receptor on surface of T tubule. This allows calcium to flow into the sarcoplasm.
d. ) DHP receptor mechanically linked to RyR receptor on SR, which when activated further releases calcium.
e. ) Calcium activates ATP hydrolysis, and binds to troponin causing it’s confirmational change.

  1. ATP hydrolysis.
  2. Calcium binds to troponin, conformational change to troponin causes tropomyosin to be pulled out of way.
  3. Myosin attach to actin forming crossbridge.
  4. Power stroke as myosin head swivels.
  5. ADP + Pi released.
  6. New ATP arrives.
  7. Detachment of myosin from actin.
  8. ATP hydrolysis (repeat of step 1 really).
  9. Myosin prepares to re-attach to actin.
88
Q

Name the calcium binding protein found within the sarcoplasmic reticulum.

A

Calsequesterin.

89
Q

Explain what is meant by the following general term(s):

Motor unit.

A

A motor neuron and all the muscle fibres it innervates.

90
Q

Explain what is meant by the following general term(s):

Recruitment.

A

The process of increasing the number of active motor units in a muscle.

91
Q

Explain what is meant by the following general term(s):

Latent period.

A

The time between application of a stimulus and the beginning of a response in a muscle fibre.

92
Q

How long is the absolute refractory period of skeletal muscle?

A

5ms.

93
Q

How long is the absolute refractory period in cardiac muscle?

A

300ms.

94
Q

What’s the difference between ISOMETRIC and ISOTONIC muscle contraction?

A

Isometric - muscle length constant.

Isotonic - load on muscle constant, but muscle itself shortens.

95
Q

In smooth muscle, myosin ATPase activity is low, and actin/ myosin are thus inactive unless for the presence of what?

A

Calcium-linked activator.

96
Q

Describe what is meant by EQUILIBRIUM POTENTIAL, providing example(s).

A

The equilibrium potential for an ion is the membrane potential where the net flow through open channels is 0. Therefor, the chemical and electrical forces acting on this ion are in balance.
EqP for K+ = -84mV (150mM in cell, 5mM out).
EqP for Na+ = +60mV (15mM in cell and 150mM out).

97
Q

Describe what is meant by RESTING POTENTIAL, providing example(s).

A

The resting potential is the ‘real life’ situation of membrane potential, taking into account the effect of all the different ion’s equilibrium potentials. This being said, the resting potential for most neurons is around -70mV, which approximates the equilibrium potential for K+. This is as K+ has the predominant influence on RMP, as the cell membrane is far more permeable to K+ then any other ion (lots of K+ channels).

98
Q

Which ion has an equilibrium potential exactly equal to RMP?

A

Cl-.

note: chance event

E ( PHYS ) (6 decks)

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