Cardiac Contraction Flashcards

1
Q

What do cardiomyocytes make up?

A

Branching myofibres

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2
Q

What does each myocyte contain?

A

Multiple rod-like cross branched strands that run the length of repeating sarcomeres

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3
Q

What are t tubules?

A

Invagination of the muscle cell membrane that penetrates into the centre of cardiac muscle cells

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4
Q

What does the cytoplasm between the myofibrils contain?

A

The single, centrally located nucleus, mitochondria and sarcoplasmic reticulum

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5
Q

What are sarcomeres?

A

Cause muscle contraction when the actin and myosin filaments move relative to each other

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6
Q

What is proportional to intracellular calcium?

A

Force of contraction

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7
Q

What are the 5 steps in cardiac muscle contraction?

A
  • sodium channels open allowing sodium to enter and depolarise the cell
  • voltage gated calcium channels open
  • plateau phase calcium influx and calcium induced calcium release
  • calcium channels close and potassium channels open fully allowing potassium to leave and repolarise the cell
  • stable sodium/potassium pump when cell is at rest
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8
Q

Where would you find ryanodine receptors?

A

Intracellular calcium channels

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9
Q

What does troponin T bind to?

A

Tropomyosin

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10
Q

What does troponin I bind to?

A

Actin filaments

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11
Q

What does troponin C bind to?

A

Calcium

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12
Q

What does binding of calcium to troponin C lead to?

A

Conformational changes of tropomyosin and exposure of actin binding sites

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13
Q

How does the calcium concentration decrease in myocytes?

A
  • action potential repolarises t tubules, and the voltage gated calcium channels and decreased calcium influx
  • no calcium influx-> no calcium induced calcium release
  • extrusion of calcium from cell by Na/Ca exchanger
  • calcium uptake into sarcoplasmic reticulum via SR membrane
  • calcium is taken into the mitochondria
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14
Q

What is intrinsic stretch a result of?

A

Increased pressure or volume

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15
Q

What is extrinsic control due to calcium conc rise a cause of?

A

Some pressure or volume but increased contractility

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16
Q

What are drugs needed for clinically?

A

To increase the contractility of the heart

17
Q

What do sympathetic mimetic drugs do?

A

Increase the voltage gated calcium channel activity

18
Q

What do cardiac glycoside drugs do?

A

Reduce calcium extrusion

19
Q

What do positive ionotropes do?

A

Increase the strength of contraction

20
Q

What do beta 1 adrenoreceptors induce?

A

Increased contractility

21
Q

What does increased pKA lead to?

A
  • increased calcium channel so higher calcium level and greater contraction
  • increased potassium channel opening so faster repolarization and shorter action potential leads to a faster heart rate
  • increased sarcoplasmic reticulum calcium ATPase, so uptake of calcium into storage by SR allowing fresh relaxation
  • overall stronger faster contractions, same diastolic time to allow for filling with blood and coronary perfusion
22
Q

Why are cardiac glycosides not used often now?

A

Side effects

23
Q

What is digitoxins mechanism of action?

A

It inhibits the sodium potassium ATPase

  • Na build up lowers the concentration gradient
  • less calcium epulsion by sodium/potassium exchanger , so it is taken up into stores
24
Q

What drugs are used in acute heart failure?

A

Dobutamine and dopamine

25
Q

What drug is used in acute heart failure when taking beta blockers (and how does it work)?

A

Glucagon

Acts as a GPCR, stimulates Gs pathway, and increases cAMP and pKA activity

26
Q

What is amrinone?

A

Phosphodiesterase inhibitor