*Physiology 2 (lecture 2) Flashcards

1
Q

Is cardiac muscle striated or non-striated?

Why?

A

Striated

Due to the regular arrangement of contractile protein

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2
Q

What part of the intercalated disc provides mechanical adhesion between adjacent cardiac cells?

A

The desmosomes

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3
Q

What are myocytes made up of?

A

Myofibrils which contain actin and myosin

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4
Q

Out of actin and myosin, what is the thicker filament and what is the thinner filament?

A
Thicker = myosin (darker appearance)
Thinner = actin (lighter appearance)
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5
Q

What is the actin and myosin in myofibrils arranged into?

A

Sacromeres

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6
Q

What are sarcomeres?

A

The functional unit of muscle

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7
Q

Does actin slide over myosin or does myosin slide over actin?

A

Actin slides over myosin

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8
Q

Is ATP required for the contraction or relaxation of cardiac muscle fibres?

A

Contraction and relaxation

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9
Q

What happens to the myosin head when ATP is present but there is no Ca2+ present?

A

It is energised but since there is no Ca2+, it does not bind to actin

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10
Q

What happens to the myosin head when both ATP and Ca2+ are present?

A

The myosin head is energised and since there is Ca2+ present, it can bind to actin and creates a bending movement called a power stroke causing the release of energy and ADP + Pi

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11
Q

What must be available for myosin to detach from actin?

A

ATP

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12
Q

What 2 molecules are found attached to actin?

A

Troponin

Tropomyosin

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13
Q

How does the presence of Ca2+ lead to myosin being able to bind to actin?

A

Ca2+ binds to topping which causes a conformational change which slides the troponin-tropomyosin complex away from the binding site on actin (if we don’t have Ca2+ this does not happen and therefore the troponin-tropomyosin complex stays covering the binding site)

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14
Q

What is the intracellular store of calcium in a cell?

A

In the sarcoplasmic reticulum

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15
Q

how is calcium released from the sarcoplasmic reticulum?

A

Due to the presence of extracellular calcium = calcium induced calcium release

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16
Q

How does the length of the action potential and muscle contraction compare between cardiac smooth muscle and skeletal muscle?

A

much longer in cardiac smooth muscle (refractory period is also longer)

17
Q

What is the refractory period?

A

The period following stimulation in which it is not possible to produce another action potential

18
Q

Why is the long refractory period good for the heart?

A

It is protective, preventing generation of titanic (sustained) contraction

19
Q

What is the stroke volume?

A

The volume of blood ejected from each ventricle per heart beat

20
Q

SV = ?

A

SV = end diastolic volume - end systolic volume

21
Q

What are the 2 categories of mechanisms by which the stroke volume can be regulated?

A

Intrinsic (within the heart itself)

Extrinsic (nervous and hormonal control)

22
Q

What are the intrinsic factors affecting stroke volume?

A

Changes in diastolic length of myocardial fibres

This is determined by the volume of blood in each ventricle at the end of diastole (end diastolic volume)

23
Q

What is the cardiac preload?

A

Length of sarcomeres/ tension in cardiac muscle prior to contraction

24
Q

What determines the cardiac preload?

A

The end diastolic volume

25
Q

What determines the end diastolic volume?

A

Venous return to the heart

26
Q

Starling’s law/ Frank-Starling curve?

A

The more the ventricle is filled with blood during diastole (end diastolic volume), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume) - as we increase the end diastolic volume, we increase the stroke volume unless we stretch the heart too much

27
Q

How is the optimal length of cardiac muscle achieved?

A

By stretching the muscle

28
Q

What is the afterload?

A

Resistance into which the heart is pumping

29
Q

What can happen if an increased afterload persists e.g. untreated hypertension?

A

the ventricular muscle will increase to overcome the resistance = ventricular hypertrophy

30
Q

What type of nerve supplies the ventricular muscle?

A

Sympathetic nerves

31
Q

What happens when the sympathetic nerves suppying the ventricular muscle is stimulated?

A

It increases the force of contraction - positive ionotropic effect

32
Q

How does the force of ventricular contraction increase due to sympathetic stimulation?
What mediates this effect?

A

Due to increased activation of Ca2+ channels - peak ventricular pressure rises, rate of pressure change during systole also increases, rate of ventricular relaxation also increases due to increased rate of Ca2+ pumping
cAMP

33
Q

What are the 2 axis on the frank starling curve?

A

EDV

Stroke volume

34
Q

What effect does sympathetic stimulation have on the Frank-stirling curve?

A

Shifts it to the left and peak is increased

35
Q

What effect does heart failure have on the frank-starling curve?

A

Shifts it to the right - negative ionotropic effect - less stroke volume for same EDV due to lower force of contraction

36
Q

Effect of parasympathetic nerve on ventricular contraction?

A

Very little innervation of ventricles by ages in man therefore little, if any, direct effect on SV (large impact on rate but not force or contraction)

37
Q

what hormones have a chronotropic and ionotropic effect?

A

Adrenaline and noradrenaline released from the adrenal medulla (effects normally minor)

38
Q

What is the cardiac output?

A

The volume of blood pumped by each ventricles per minute

39
Q

What is the equation for cardiac output?

A

CO = SV X HR