Electrical Activity Flashcards

1
Q

Define depolarisation

A

Cell becomes less polarised. The inside of cell is less negative than normal

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2
Q

How do pacemaker cells / autorhythmic cells generate action potentials spontaneously?

A

Because it has an unstable resting membrane potential.

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3
Q

Which two ion channels are responsible for the unstable resting membrane potential of authorhythmic cells? Describe the movement of ions.

A

Funny channels = slow entry of Na into cell (causes depolarisation)
T type calcium channels = transient calcium influx

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4
Q

Which ion is higher in concentration outside the cell compared to inside? Calcium, potassium or sodium?

A

Sodium and calcium. K is more concentrated inside

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5
Q

When do the funny channels close?

A

Half way through the pacemaker potential. Once closed, T-type calcium channels open, which allows for further depolarisation until the threshold is reached.

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6
Q

Which ion and ion channel is responsible for the rapid depolarisation of autorhythmic cells?

A

L-type calcium channels open, allowing for large influx of calcium.

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7
Q

Which ion and ion channel are responsible for the repolarisation of autorhythmic cells?

A

At peak of depolarisation, voltage gated K channels open, allowing for large K efflux

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8
Q

Which ion channel maintains the stable resting membrane potential of contractile cells?

A

A leaky K channel. Slow K efflux

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9
Q

Once the flow of current arrives via gap junctions, what causes the depolarisation of contractile cells?

A

Voltage gated Na channels = rapid Na influx

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10
Q

Explain the two ion channels contributing to the plateau of the contractile cell’s action potential

A

Transient K channels open, allowIng quick but brief K efflux. Causes slight repolarisation, then channel closes
L-type Ca channels open, allowimg slow Ca influx, which prolongs the peak of thr action potential

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11
Q

What causes the repolarisation of contractile cells?

A

L-type calcium channels close, causing voltage gated K channels to open. Fast K efflux repolarises cell

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12
Q

Primary, secondary and tertiary pacemaker of heart?

A

SA node
AV node
Purkinje fibres

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13
Q

What happens when damage to AV node causes purkinje fibres to become primary pacemaker?

A

Complete heart block.
Caused by no electrical signal tranduction between atria and ventricles
Purkinje fibre AP rate is also far too slow

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14
Q

Define an ectopic focus

A

When purkinje fibres become faster than SA node. Causes premature heart beats and PVC

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15
Q

Define PVC

A

Premature ventricular contraction

= less blood ejected

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16
Q

Causes of ectopic focus?

A

Alcohol, nicotine, stress, caffiene, anxiety, etc

17
Q

What is the major connection between atria and ventricles?

A

AV node

18
Q

Why is there a delay of transduction at the AV node?

A

To allow the atria to finish contracting before the ventricles start

19
Q

Why is the refractory period of a cardiomyocyte longer than regular muscle cells?

A

To ensure each contraction is followed by enough time to ensure the chambers refill before the next contraction. Prevents tetanus contractions

20
Q

Where does the electrical signal travel after SA node and AV node?

A

Bundle of his, then apex of ventricle

21
Q

After the electrical signal reaches the ventricle apex, where does it go?

A

To the purkinje fibres, then to the rest of the ventricle

22
Q

P wave of ECG =?

A

Atrial depolarisation + contraction

23
Q

QRS complex =?

A

Venctricular depolarisation + contraction + simultaneous repolarisation of atria

24
Q

T wave =?

A

Ventricular relaxation + repolarisation

25
Q

What would ventricle fibrillation look like on ECG?

A

Rapid, disorganised and irregular signals

26
Q

Describe atrial flutters

A

Increased rate of atrial contractions. Doesnt allow for ventricles to fill properly. Ventricles will not contract with every atrial contraction (e.g. 3:1)

27
Q

Describe complete heart block

A

AV node impairment, resulting in ventricles not being stimulated. The atria will contract normally, but the ventricles will generate their own pulses that are much slower than atria pulses / contractions.

28
Q

Complete heart block appearance on ecg?

A

Normal P wave (due to normal atrial contractions)
Slow QRS and T waves (slow, but still regular)
Extra lines may appear which represent atrial repolarisation (normally masked by QRS complex, but they are no longer simultaneous)

29
Q

PSNS effect on ions and HR?

A

Opens K channels, causing hyperpolarisation, meaning takes longer to reach threshold. = slower HR

30
Q

SNS effect on HR and ions?

A

Increases closure of K channels, meaning threshold is reached sooner.
Increases HR

31
Q

PSNS vs SNS transmitter?

A
Acetylcholine = PSNS
Adrenaline = SNS