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A&P Test 4 > 10/30 > Flashcards

10/30 Flashcards

1
Q

What does ischemia usually mean?

A

That there is a small part of the heart injured, or not getting the energy that it needs.

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2
Q

In what direction would you expect the current of injury to be moving in this picture?

A

Down and towards the left foot

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2
Q

Draw an EKG strip of Lead 2 that shows this type of injury.

A
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3
Q

Is the ST segment segment physically depressed in ST segment depression d/t ischemia

A

No, it just looks that way because the TP segment is elevated.

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4
Q

Why do we only choose 2 of the leads to decide the current of injury and/or mean electrical current?

A

Because of Einthoven’s law. Leads 1+3=lead 2
that makes lead 2 erroneous

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5
Q

what would you expect to see on an EKG if you had a small area of ischemia in the left ventricle?

A

ST segment depression

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6
Q

Which area in the heart is the most likely to be ischemic and why?

A

The sub endocardial layer of the left ventricle.
The tissue there is very deep, is subjected to a lot of pressure, and has the longest action potential

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7
Q

What is the T-P segment?

A

The official name for the segment between the end of the T wave and beginning of the P wave

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8
Q

What does an infarct mean?

A

A large part of the ventricular wall is affected by ischemia. It is no longer defined by just the sub endocardium, and the whole wall is usually involved.

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9
Q

How does the current of injury look different in an infarct vs ischemia?

A

In infarct the vector has a larger magnitude (longer) and it will be pointed in the opposite direction than in ischemia.

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10
Q

Why is it important for us to be able to be able to “zero out” an EKG by finding the J point and comparing it to the current of injury?

A

It’s an equipment issue. Today’s equipment isn’t able to zero out EKGs at the J point, and this is how we determine current of injury.

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11
Q

If you could design software to reasonably, consistently, identify the J point you would be

A

rich and famous

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12
Q

Which gate on a fast sodium channel is the inactivation gate?
Where is this found?

A

H gate
inside of cell

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13
Q

Which gate on a fast sodium channel is the activation gate?
Where is this found?

A

M gate
outside of the cell

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14
Q

How long are both the M and H gate opened at the same time?

A

a very very short amount of time

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15
Q

What do we have to do to reuse a slow L-type Ca++ channel after it has been inactivated?

A

Repolarize it. This would close the D gate and open the F gate

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16
Q

What are the names of our L type Ca++ channels gates?

A

Inactive(F)- found inside the cell
Active(D)- found outside the cell

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16
Q

What state are we in when the activation(D) is closed and the inactivation(F) is open

A

Resting

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17
Q

What is the result of an AP depolarizing a VG Na+ channel or VG slow L-type Ca++ channel?

A

The Outside gate (M gate on Na+ and D gate on Ca++ channel) opens.
Now the cell is open and the ion can flood into the cell.

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18
Q

What makes the D gate on a VG Ca++ channel open?

A

depolarization

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19
Q

The speed at which a d gate opens on a L type slow Ca++ channel compared to a fast Na+ channel is

A

slower

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20
Q

How long does it take the D and F gate to close on a L type Ca++ channel?

A

longer than the fast Na+ channel gates

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21
Q

What stage are we in when the D gate is open and the H gate is closed on the VG slow L-type Ca++ channel?

A

Inactivated

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22
Q

Which gate on a VG L-Type Slow Ca++ channel is the activation gate?

A

D gate

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23
Q

What are the differences in a Fast Na+ channel’s gates and a slow L-Type Ca++ channel’s gates?
(Vague answer)

A

name and timing

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24
Q

Which gate on a VG L-Type Slow Ca++ channel is the inactivation gate?

A

F gate

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25
Q

Delete

A

Me

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26
Q

Resting membrane potential in the ventricular myocyte

A

-80

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27
Q

What is the normal resting membrane potential in the SA node?
What is the normal threshold in the SA node?

A

-55
-40

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28
Q

Delete

A

Me

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29
Q

Delete

A

Me

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30
Q

SA node has what kind of AP?

A

Slow

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31
Q

fastest part of the AP in the SA node?

A

phase 4

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32
Q

what decides if an AP is fast or slow?

A

the slope of phase 0

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33
Q

What kind of ions are in a slow L-Type Ca++ channel in the SA node?

A

Phase 4: Ca++
Phase 0: Ca++
Phase 3: K+

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34
Q

The SA node doesn’t have any _____. This is why it has “slow” AP

A

fast Na+ channels

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35
Q

What are the 2 theories as to why there isn’t any fast Na+ channel activity in the depolarization phase of nodal tissue

A
  1. No VG fast Na+ channels in the nodal tissue
  2. There are VG fast Na+ channels but they don’t function because the VRM isn’t negative enough
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36
Q

slow L type Ca++ channel VRM is probably more ______ than Fast Na+ channels

A

positive

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37
Q

What is an important difference between Fast Na+ channels and Slow L Type Ca++ channels?

A

reset voltage is different
fast Na+ channels need more voltage to reset

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38
Q

Purkinje AP have what kind of phase 4?

A

A slight slope to phase 4, eventually it would self depolarize but would take a long time

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39
Q

in the fast AP what does phase 0 look like?

A

straight up and down

40
Q

when does Ca++ come in during a fast AP?

A

Phase 1 (fast T type Ca++) and phase 2(slow L type Ca++)

41
Q

slope of phase 0 in muscle tissue in the heart is directly related to what?

A

how many Fast Na+ channels we have in that tissue

42
Q

If our VRM has changed to a more positive number in the ventricular tissue what would happen?

A

You would lose fast Na+ channels. This leads to the slope of phase 0 decreasing and the peak of phase 1 would not be as positive or high

43
Q

Can you get too high of a VRM that there aren’t any fast Na+ channels involved in phase 0 of a fast AP?

A

Yes.
This would turn your fast AP into a slow AP.

This makes sense with the theory that nodal tissue upstream like in the SA node doesn’t have any fast na+ channels because the VRM is too high (-55 vs -80). In this case, the Na+ channels aren’t repolarized and therefore aren’t being used,( if there are Na+ channels there in the first place.)

44
Q

why can we still have a decent AP in the ventricles of heart if the VRM is so positive that we don’t have any fast Na+ channels involved?

A

Ca++ coming in stimulates Ca++ release from the SR which can give us a slow AP

45
Q

where is the one pace in the heart that doesn’t have any gap junctions?

A

AV node

46
Q

If we have a ton of sodium coming into the cell, it usually doesn’t have any problem going from cell to cell, why?
When our VRM is to high and we loose fast Na+ channels, how does this affect conduction?

A

gap junctions
It is slower and not as strong d/t Ca++ being big and clunky. it moves through the gap junctions but not as efficiently as Na+.

47
Q

what can cause conduction problems in the heart related to AP?

A

a higher VRM

48
Q

waiting for Ca++ to go through gap junctions is slower because

A

Ca++ is big and clunky and doesn’t fit through gap junctions well

49
Q

what is the back up system in the heart when fast Na+ channels aren’t working?

A

Ca++ channels

50
Q

Can you get so positive of a VRM that you lose Ca++ channels?

A

yes. This results in a lack of an AP and you would just have a squiggly line.

51
Q

Slow conduction problems can cause issues with the _____

A

pumping performance of the heart

52
Q

What causes a more positive VRM than normal in the ventricles?

A

Hyperkalemia
acidosis (leads to energy deficit)
MI(leads to energy deficit)

53
Q

How does acidosis affect repolarization?

A

The enzymes in our cells function optimally at a pH of 7.4.
If pH is less than 7.4 then the enzymatic reactions that normally occur no longer happen at an optimal speed. These reactions are involved in resetting the cell and providing energy for the cell. If you have an energy deficit then you won’t be able to reset the cell normally.

53
Q

normal pH for A&P?

A

7.4

54
Q

The slope of phase 0 is dependent on

A

The amount and type of ion channels located there

54
Q

How does a MI affect repolarization?

A

This leads to the cells not getting the energy that they need to be able to reset. Energy deficit.

54
Q

How do -cain drugs work?

A

Block fast Na+ channels which reduce the slope of phase 0

55
Q

at rest nodal tissue is very leaky to

A

Ca++ through leak channels

56
Q

During the AP Ca++ permeability is high in which types of AP?

A

Fast and slow

57
Q

What is the order (greatest to least) of tissues that are permeable to Ca++ in the resting heart during phase 4?

A

SA
AV
Perkinje Fibers

58
Q

In the perkinje fibers how much Ca++ permeability is there in phase 4?

A

Not a ton of

59
Q

what is the primary way that nodal tissue maintains or adjusts, fine tunes, determines VRM?

A

opening of K+ channels through activation of mACh-r

60
Q

What types of receptors are found in the cell wall of a heart cell?

A

GPCR mACh-R that opens K+ channels
GPCR mACh-R that have an alpha subunit that is inhibitory to Adenylyl cyclase
GPCR Beta-R that have an alpha subunit that is stimulatory to Adenylyl cyclase
GPCR Beta-R that interacts with HCN channels directly and opens them

61
Q

where is adenylyl cyclase found in a cell?

A

in the cell wall

62
Q

Blocking of a mACh-R would result in what in the heart?

A

Less K+ channels being opened
Less K+ able to leave the cell
More positive VRM
Faster HR

63
Q

Why is Guanylyl cyclase called soluble and Adenylyl cyclase is not?

A

soluble means it is floating around in the cell where Adenylyl Cyclase is stuck in the cell wall

64
Q

What does Adenylyl cyclase do?

A

Turns ATP into cAMP

65
Q

what makes B adrenergic stimulation dangerous?

A

L-Type Ca++ channels being phosphorylated by PKA

Too much beta adrenergic activity can lead to heart attacks in people who are increasing their activity (80yo shoveling snow). If these L-type Ca++ channels become too sensitive d/t increases in PKA then they can open at the wrong time, allowing Ca++ to come in at the wrong time which makes the heart beat at the wrong time.

66
Q

What is an EAD

A

early after depolarizations

67
Q

What is a DAD

A

delayed after depolarizations

68
Q

EAD and DAD are d/t

A

L-type Ca++ channels being PO4 by PKA and making them open at the wrong time. This can lead to MI’s

69
Q

What would you expect to see on an EKG when the Left ventricle has infarcted?

A

ST segment elevation

70
Q

What does it tell us when you have a negative deflection in the T-P segment? (The T-P segment is lower than normal)

A

That there is ST segment elevation

71
Q

What does it tell us when you have a positive deflection in the T-P segment? (The T-Psegment is higher than normal)

A

That there is ST segment depression

72
Q

What current of injury is this?

A

Negative current of injury

73
Q

What current of injury is this?

A

No current of injury

74
Q

What current of injury is this?

A

Positive current of injury

75
Q

Draw the current of injury for this EKG strip

A
76
Q

What kind of depolarization is this in V2?
What does it mean?

A

Negative current of injury
It is an anterior infarct

77
Q

What is the current of injury in this EKG?

A

No current of injury

78
Q

What is the current of injury in this EKG?

A

Negative current of injury

79
Q

What is the current of injury in this EKG?

A

Negitive current of injury

80
Q

What is the current of injury in this EKG?

A

Positive current of injury

81
Q

Plot the current of injury for this picture

A
82
Q

In a plot of current of injury, what does the direction of the net electrical current arrow tell us?

A

It is pointed away from the area of injury, this tells us where the injury is. (Opposite of the arrow)

83
Q

Which part of the heart is injured based off of this picture?

It is an anterior or posterior problem?

A

Apex of the heart

Posterior

84
Q

What causes the F gate to close?

A

It can close on it’s own (like it is on a very short timer)
Or can close in response to depolarization

85
Q

What is another name for the self depolarizing slope 4 in the SA node?

A

Diastolic depolarization

86
Q

What is another name for the self depolarizing slope 4 in the SA node?

A

Diastolic depolarization

87
Q

What does stimulation of the GPCR mACh-R attached to Adenylyl cyclase in the heart do?

A

Slows down Adenylyl cyclase which decreases cAMP which decreases HR

88
Q

When an agonist binds to the beta receptor with an alpha subunit in the heart, what happens?

A

The stimulatory alpha subunit stimulates Adenylyl cyclase to increase in speed which increases cAMP which increases HR

89
Q

When an agonist binds to Beta receptors tethered to HCN channels what happens?

A

They open the HCN channels with allows Na+ and Ca++ to come into any of our pacemaker cells during phase 4

90
Q

What are two ways that HCN channels can open in the heart?

A

Through an agonist binding to the Beta receptors linked to the HCN channels
OR
Through an increase in cAMP(agonist binding to mACh-R with Gs, or agonist binding to Beta-R with Gs)

91
Q

The more cAMP we have around we increase the activity of ____

A

PKA

92
Q

What are the targets of PKA?
What happens when these targets are phosphorylated?

A

L- type Ca++ channels. PO4 them which makes them more sensitive and easier to open= more Ca++ coming in = faster HR

Troponin. PO4 Troponin I which increase the contractile protein sensitivity to Ca++=increase cycling rate of cross bridge generating filaments= faster HR

Phospholamban(inhibitor of the SERCA pump). PO4 increases the speed of SERCA pump=faster resetting of the cell=faster HR

93
Q

How is cAMP degraded?

A

It can fall apart on its own, or we can break it down with phosphodiesterase (PDE)

94
Q

What does PDE do?

A

It breaks down cAMP into AMP. This reduces the amount of cAMP we have around which reduces PKA which reduces the effects of PKA

95
Q

What happens when you inhibit PDE?

A

You have an increase cAMP which increases PKA which increases the effects of PKA.

A&P Test 4 (7 decks)

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