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1. Theme 3 > T3 L18: Molecular control of the heart > Flashcards

T3 L18: Molecular control of the heart Flashcards

1
Q

What is the difference between extrinsic and intrinsic regulation of force contraction in the heart?

A

Intrinsic is at the cellular level, extrinsic involves compounds from other cells and making the cross bridge formation stronger

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2
Q

What does greater overlap of sarcomeres cause?

A

Stronger force of contraction

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3
Q

How quick is the isolated/denervated heart rate?

A

100 beats per minute

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4
Q

Why is the normal resting heart rate lower than the isolated denervated heart rate?

A

Normal heart rate is toned by parasympathetic stimulation

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5
Q

What effect does noradrenaline have on the funny current?

A

It increases the funny current. The pacemaker potential will increase via beta-receptors

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6
Q

What do pacemaker cells do?

A

Control the rate of contraction of cardiomyocytes

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7
Q

What does an increase in Ca2+ do to cardiomyocytes?

A

Increases force of contraction

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8
Q

What does an increase in K+ do to cardiomyocytes?

A

It shortens the action potential so allows a faster heart rate

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9
Q

When do HCN channels open and what do they do?

A

They open when the membrane becomes negative and they help control the slope of the pacemaker potential

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10
Q

What do alpha-1 adrenergic receptors do?

A

Work using the Gq pathway to increase Ca2+ and cause vasoconstriction

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11
Q

What do alpha-2 adrenergic receptors do?

A

Work using Gi pathway to increase glucagon and decrease insulin

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12
Q

What do beta-receptors do?

A

Work using the Gs pathway to increase heart contractility, heart rate, bronchodilation

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13
Q

What type of stimulation does the vagus nerve carry?

A

Parasympathetic

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14
Q

What effect does vagal stimulation have on heart rate and how?

A

It releases ACh to increase K+ which hyperpolarises the membrane and slows down heart rate

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15
Q

What does atropine do?

A

It blocks vagal stimulation so heart rate can increase

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16
Q

What ion is involved in delayed rectifier channels in the heart?

A

K+

17
Q

What ion is involved in inward rectifier channels in the heart?

A

K+

18
Q

What is E-C coupling?

A

The link between excitation and the consequent huge influx in cytosolic Ca2+

19
Q

What do RyR do?

A

Release Ca2+ from the sarcoplasmic reticulum

20
Q

What does SERCA do?

A

Pumps Ca2+ back into the sarcoplasmic reticulum

21
Q

What can Ca2+ overload cause?

A

Ectopic beats and arrhythmias because Ca2+ spill out of the SR

22
Q

What does the drug Amlodipine do and what is it used for?

A

Its a Ca2+ blocker used to treat angina and arrhythmias

23
Q

What does the drug Verapamil do and what is it used to treat?

A

Ca2+ blockers used for arrhythmias because it slows down nodal rate

24
Q

What does the drug Diltiazem do and what is it used to treat?

A

A Ca2+ blocker used to treat angina and arrhythmia because it slows down nodal rate and reduces workload

25
Q

What does the drug Digoxin do?

A

It increases stroke volume and contractility so is used for heart failure. It works by inhibiting Na+/K+ channels and by stimulating the vagus nerve

26
Q

What is the preferred treatment for heart failure?

A

Beta-blockers because there a lower mortality rate compared to Digoxin

27
Q

Where is NO released from?

A

The endothelium

28
Q

What 2 things does the endothelium detect?

A

Stretch and plasma proteins

29
Q

Which protein initiates VSMC (vascular smooth muscle cell) contraction?

A

Myosin light chain kinase (MLCK)

30
Q

How does MLCK work?

A

It phosphorylates mysoin at its light chain

31
Q

What is MLCK activated by?

A

Calcium calmodulin (Ca2+ bound to protein)

32
Q

What is the drug Glyceryl Trinitrate (GTN) used for?

A

For vasodilatation because it degrades to NO within the body but tolerance can be built so its taken in pulses

33
Q

What does Bradykinin do?

A

It vasodilates but constricts bronchi and GI tract smooth muscle

34
Q

Which drugs prevent degradation of bradykinin?

A

ACE inhibitors. They cause a dry cough when the bradykinin accumulates

35
Q

When would Troponin (Tn) be released?

A

Released from cardiomyocytes during necrosis

36
Q

What increases Creatine Kinase (CK)?

A

Released from cardiomyocytes during necrosis

37
Q

Wat increases C reactive protein (CRP)?

A

Increases during inflammation

1. Theme 3 (19 decks)

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