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CVS A > Session 4 Lecture 1 > Flashcards

Session 4 Lecture 1 Flashcards

1
Q

What sets up the resting membrane potential in a cardiac myocyte?

A

Potassium

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2
Q

Initially in the cardiac myocyte, what ion is in a higher concentration inside the cell?

A

Potassium

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3
Q

Initially in the cardiac myocyte, what ion is in a lower concentration inside the cell?

A

Sodium

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4
Q

Why does resting membrane potential not equal potassium equilibrium potential?

A

Because the cardiac myocyte has a very small permeability to other ion species at rest

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5
Q

In a ventricular action potential graph, what causes the upstroke?

A

Opening of the voltage gates Na+ channels

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6
Q

In a ventricular action potential graph, what causes the initial repolarisation?

A

Transient outward K+ channels

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7
Q

In a ventricular action potential, what causes the plateau?

A

Opening of voltage gated calcium channels (L type)

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8
Q

In a ventricular action potential, what causes the repolarisation?

A

Efflux of K+ through voltage gated K+ channels

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9
Q

What is the SAN action potential also known as?

A

The pacemaker potential

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10
Q

In the SAN action potential, what is the initial slope due to?

A

Funny current

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11
Q

What initiates the cardiac action potential

A

Pacemaker cells

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12
Q

What is the initial depolarisation also known as?

A

Pacemaker potential

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13
Q

What is the pacemaker potential due to?

A

The population of channels that open relatively slowly and are permeable to Na+ ions

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14
Q

How are these slow Na+ channels different to fast Na+ channels?

A

The slow ones activate more with hyper polarisation and are sometimes referred to as funny current

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15
Q

What are these slow Na+ channels called?

A

HCN

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16
Q

What does HCN stand for?

A

Hyper polarisation activated cyclic nucleotide gated channels

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17
Q

What causes the upstroke in the SA node action potential?

A

The opening of the calcium channels

18
Q

What causes the downstroke in the SA node action potential?

A

Opening of the voltage gated potassium channels

19
Q

Is there a plateau in the SA node action potential?

A

No

20
Q

What is

the normal plasma K+ concentration?

A

3.5 - 5.5 mol/L-1

21
Q

What is hyperkalaemia?

A

Plasma K+ conc too high

22
Q

What is hypokalaemia?

A

Plasma K+ conc too low

23
Q

Why are cardiac myocytes so sensitive to changes in the K+ conc?

A

Because they have a very negative resting membrane potential which is close to the potassium equilibrium potential

24
Q

What affect dos hyperkalaemia have on the cardiac myocytes?

A

Depolarise the myocytes and slows down the upstroke of the action potential

25
Q

Why does hyperkaelamia slow the upstroke?

A

If you raise K+ then Ek gets less negative so the membrane potential depolarises a bit. This inactivates some of the voltage gated Na+ channels

26
Q

What risks are associated with hyperkalaemia?

A

The heart can stop - asystole.

27
Q

What treatment is used for hyperkalaemia?

A

Calcium gluconate

Insulin+glucose

28
Q

What effect does calcium gluconate have?

A

Makes heart less excitable

29
Q

What effect does Insulin+glucose have?.

A

Insulin promotes potassium to move into the cells

30
Q

Why is KCl used in heart surgery?

A

In order to stop the heart from beating

31
Q

What effect does hypokaelamia have?

A

Lengthens the action potential and delays repolariation

32
Q

What are the effects of a long action potential?

A

Can lead to early after depolarisation (EADs) which leads to oscillations in membrane potential and results in ventricular fibrillation

33
Q

What happens in cardiac myocytes after depolarisation?

A

Depolarisation opens L type Ca2+ channels in the T tubule system

34
Q

What effect does calcium have on cardiac myocytes?

A

Ca2+ binds to troponin C and this shifts tropomyosin to reveal the myosin binding site on the actin filament.

35
Q

How do cardiac myocytes relax?

A

Must return Ca2+ to resting levels

36
Q

How is the Ca2+ returned to normal levels?

A

Most pumped back in SR by SERCA. Some exits across cell membrane.

37
Q

How is contraction regulated in vascular smooth muscle?

A

Ca2+ binds to calmodulin and activates MLCK which phosphorylates the myosin light chain to permit interaction with actin. Relaxation as Ca2+ levels decline

38
Q

What is MLCK?

A

Myosin Light Chain Kinase

39
Q

What needs to happen to the myosin light chain to enable actin myosin interaction?

A

Myosin light chain must be phosphorylated

40
Q

What effect does PKC have on MLCK?

A

PKC inhibits the action of MLCK because it inhibits the phosphorylation of MLCK.

41
Q

If phosphorylation of MLCK is inhibited, what happens?

A

Inhibits contraction

CVS A (18 decks)

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