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B2 > CV Week 1 > Flashcards

CV Week 1 Flashcards

1
Q

Which of the following is not a role or function of the cardiovascular system?

a) dispose of CO2 and other byproducts of metabolism
b) vehicle for hormone transport and regulation of specific functions on target tissues
c) maintenance of body fluid
d) regulation of body temperature
e) provide adequate O2 supply and essential nutrients to select tissues

A

E - ALL TISSUES

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2
Q

The heart composed of two pumps organized in ______ and flow is described as ______

A

series, unidirectional

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3
Q

Elasticity of arteries has one impact on the intermittent nature of blood flow from heart?

A

reduces the force (attentuates)

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4
Q

Elasticity allows for a more _____ flow to tissues due to their ____ during the relaxation phase of the cardiac cycle

A

continuous, recoil

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5
Q

How is blood provided to the heart?

A

In systole, aorta and large arterial branches store part of energy by mechanical distension then in diastole energy is released like a rubber band when ventricles are relaxing back to heart.

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6
Q

True/False: All blood vessels control their internal diameter via precise control of smooth muscle

A

FALSE - capillaries don’t!

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7
Q

Arteries have a thicker wall, are stiffer, and have a strong contractile apparatus due to what two features?

A

presence of elastic fibers and a more prominent smooth muscle layer

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8
Q

Why does pressure fall more quickly in the terminal segments of small arteries and arterioles in comparison to large arteries?

A

Increase in frictional resistance and increase in cross sectional area from extensive branching and multiplication

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9
Q

What causes dampening of pulsatile arterial flow at capillary level?

A

Distension of large arteries (compliance) and resistance of small arteries and arterioles - non-pulsatile flow

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10
Q

As cross-sectional area _______, velocity of blood flow _______

A

area, decreases [watch out!!! increases in respect to diameter tho!]

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11
Q

Where is the majority of blood found in CVS and why?

A

Majority of blood found in the veins and venules (67%) because systemic veins and venules act as a large reservoir of blood that can be rapidly mobilized upon demand

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12
Q

True/False: In the pulmonary vascular bed, most of the blood is found in the veins

A

FALSE - equally distributed btwn arteries, veins and capillaries

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13
Q

Why is the right ventricular wall much thinner and weaker than the left ventricular wall?

A

Left ventricle sustains pressures in the order of 100mmHg at rest whereas right ventricle pressures are around 15mmHg

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14
Q

What directly measures blood pressure?

A

pressure in the aorta

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15
Q

When is the LUB or S1 produced?

A

When the AV valves close

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16
Q

When is the DUB or S2 produced?

A

When the aortic and pulmonary valves close

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17
Q

What may produce S3?

A

rapid filling of the ventricles

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18
Q

What may produce S4?

A

Contraction of the atrium to get final bits of blood out

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19
Q

Where is the SA node located?

A

The SA node is located in the right atrium on the upper lateral side near the superior vena cava

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20
Q

The effective pumping of blood into the circulatory system depends on the ______

A

SA node

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21
Q

Arrhythmias can compromise mechanical performance and lead to life threatening decreases in ?

A

cardiac output and blood pressure

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22
Q

Action potential acts as a trigger for contraction of individual cardiac muscle cells through _______. This is important because it synchronizes contraction of the whole heart.

A

excitation-contraction coupling

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23
Q

How are action potentials (and resting membrane potentials in myocytes generated?

A

Via the opening and closing of ion channel proteins - reason why important target for therapeutic drugs

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24
Q

Which myocytes are specialized for conduction of electrical impulse? (5)

A

SA node, cells of internal conduction track, AV node cells, Bundle of his, Purkinje Cells

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25
Q

Why is SA node considered the primary pacemaker of the cell?

A

It is SPONTANEOUS

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26
Q

The _______ carry electrical impulses that initiate atrial contraction

A

cells of internal conduction track

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27
Q

Describe the pathways of the cells of internal conduction track

A

Flow through 3 internal pathways and one interatrial conduction tract to activate AV node and left atrium

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28
Q

Where is the AV node located?

A

at the junction between the right atrium and IV septum

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29
Q

What is the delay time for AV node activation of ventricles?

A

120 ms

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30
Q

Purkinje fibers run along the _________ surface and penetrate about 1/3 into ventricular tissue

A

endocardial

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31
Q

What happens when there is a left bundle branch block?

A

Excitation of left ventricle will be slower. The excited right ventricle will propagate its signal to left ventricle (delayed). Pattern of excitation will be shifted rightward.

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32
Q

Which electrical impulse cell generates impulses at the fastest rate? The slowest?

a) SA
b) AV
c) His
d) Purkinje

A

SA is fastest, Purkinje is slowest

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33
Q

What are the differences between cardiac muscle and skeletal muscle cells?

A

Cardiac muscle is interconnected electrically and mechanically - acts as synctium. Cardiac contraction is phasic and cannot summate into tetanus. Skeletal muscles contract individually and need more recruitment of fibers to generate a greater force.

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34
Q

Why can’t cardiac contraction summate into tetanus?

A

Action potential duration and refractory period is very long

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35
Q

Which cells are considered pacemaker cells?

A

SA node, AV node, Purkinje

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36
Q

Which cells are more depolarized at rest?

a) Purkinje
b) Bundle of His
c) SA node
d) AV node
e) Atrial cells

A

C,D - exhibit a relatively slower upstroke than atrial, purkinje, ventricular

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37
Q

The resting membrane potential is determined by ______

A

conductance of K+

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38
Q

True/False: The RMP in ventricles, atria and AV node is about -80 to -90 mV

A

FALSE - true for ventricles, atria and PURKINJE SYSTEM

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39
Q

The equilibrium potential for K+ is -92mV. Why is the RMP for ventricles, atria and purkinje cells slightly more positive?

A

Differences in permeability to Na+ - more significant in nodal cells

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40
Q

What is the Na+ concentration influenced by?

A

Na+/K+ pump

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41
Q

Describe the ions pumped by the Na+/K+ pump

A

Pumps in 2K+ for every 3 Na+ pumped out - net loss of a positive charge –> slight hyperpolarization of membrane

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42
Q

How much the Na+/K+ pump contributes to the RMP is directly related to what two attributes?

A

pump activity and membrane resistance - system can contribute as much as -5 to -10 in RMP of ventricular cells

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43
Q

K+ channel activity (and thus permeability of K+) is very sensitive to what? This causes PNa/PK ratios calculated via GHK concentration to be higher than expected.

A

extracellular K+ concentration

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44
Q

True/False: Cl- and Ca++ ions contribute significantly to RMP of ventricular, atrial and purkinje cells

A

FALSE

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45
Q

What is the main reason why cardiac cells such as ventricular, atrial and purkinje cells have such long action potentials (about 300 ms)?

A

large drop in Pk to almost 0 during phase 0 when Na+ channels open. [In neurons, the Pk rises quickly during the action potential.

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46
Q

Describe phase 0 in ventricular, atrial and purkinje cells.

A

Phase 0 is the upstroke caused by an increase in Na+ conductance and depolarization of the membrane.

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47
Q

In what membrane potential range are Na+ channels active?

A

-80mV to -50mV

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48
Q

How does extracellular K+ accumulation as a result of ischemia affect RMP? How will this affect Vmax and overshoot?

A

it becomes more positive (depolarized). decreases Vmax and overshoot.

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49
Q

What occurs if Na+ channels when the membrane potential depolarizes?

A

Na+ channels become less available for activation

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50
Q

The slow response caused by Na+ channel inactivation in ventricular, atrial and purkinje cells is analogous to what?

A

upstroke of action potential in SA node as it involves Ca++ current

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51
Q

True/False - The availability of Ca++ channels is influenced by extracellular potassium concentration

A

FALSE - NOT INFLUENCED

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52
Q

How are Ca++ channels regulated

A

via voltage gated mechanisms - activated at voltage higher than -50mV

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53
Q

What happens when Na+ channel inactivation is incomplete in ventricles, atrial, and purkinje cells

A

Longer action potentials occur which favor the development of early after depolarizations (such as in long QT syndrome)

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54
Q

Why are EAD’s dangerous?

A

can lead to severe arrhythmias such as torsades de pointes or v-fibrillation

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55
Q

The Vmax (rate of depolarization of the membrane is proportional to ______ and leads to a high _______

A

number of sodium channels open, conduction velocity

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56
Q

Membrane potential reaches a positive value of +20 to +30mV. Time past 0mV is called the ______

A

overshoot

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57
Q

Describe phase 1 of the action potential in ventricles, atrial cells and purkinje cells

A

Brief period of initial repolarization caused by outward current of K+ ions and decreased Na+ conductance

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58
Q

What K+ channels are involved in the phase 1/ initial repolarization phase of action potential in ventricles, atrial cells and purkinje cells?

A

Kto channels

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59
Q

Describe phase 2 of the action potential in ventricles, atrial cells and purkinje cells

A

Plateau caused by a transient increase in Ca++ conductance but also increase in K+ conductance that cancel each other out

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60
Q

What K+ channels are involved in the plateau phase of action potential in ventricles, atrial cells and purkinje cells?

A

Delayed rectifier K+ channels (Kir)

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61
Q

Delayed rectifier K+ channels (Kir) are _____ acting and have an activation threshold of ____

A

slow, 20mV

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62
Q

True/False Delayed rectifier K+ channels activate during a maintained depolarization

A

false

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63
Q

The duration and potential level of the plateau phase determines the amount of _______ developed by cardiac muscle

A

force

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64
Q

Describe phase 3 of action potential in ventricular, atrial and purkinje cells

A

repolarization phase caused by decrease in Ca++ conductance and increase in K+ conductance which predominantes (Ik current)

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65
Q

During phase 3 / repolarization phase what channels are unmasked and at what voltage?

A

IK1 channels at -20mV. IK1 is time and voltage dependent.

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66
Q

Why are IK1 channels not detected at high voltages?

A

Regulated by internal Mg++ polyamides which block channels at higher voltages

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67
Q

Describe phase 4 of action potential in ventricles, atria, and purkinje cells

A

Resting membrane potential. Inward and outward Ik currents equal

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68
Q

The stable membrane potential in phase 4 (RMP) of the action potential in ventricles, atria and purkinje cells is caused by what?

A

high K+ permeability across IK1 channels

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69
Q

The delay in activation of ventricular action potential is important to control _______ and prevent __________

A

conduction velocity, deleterious conditions favoring abnormal reentrant excitation and ventricular arrhythmias

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70
Q

What phases are missing from action potential in the SA node and why?

A

phase 1 and 2 because the activation of ICa combined with progressive activation of IK leads to rapid repolarization

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71
Q

The resting membrane potential in the SA node is unstable and exhibits ______

A

automacity

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72
Q

Intrinsic rate of phase 4 depolarization and heart rate is fastest in the _______ and slowest in the _____

A

SA node, His-Purkinje

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73
Q

In contrast to other heart cells, what is phase 0 in the SA node caused by?

A

an increase in Ca++ conductance rather than Na

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74
Q

Do Na+ channels contribute to phase 0 in SA node action potential?

A

NO

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75
Q

Ca++ current in phase 0 of SA node action potential is dependent on what two factors?

A

time and voltage

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76
Q

Phase 3, repolarization, in SA node ends via the closing of what channels? What channels are activated?

A

IK channels close, If channels open

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77
Q

Describe phase 4 of SA node action potential

A

Slow depolarization due to Na+ conductance

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78
Q

The increase in Na+ current in phase 4 of SA node is called _____

A

Ifunny

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79
Q

What turns on “Ifunny” in phase 4 of the SA node action potential?

A

Repolarization of the membrane potential during the preceding action potential

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80
Q

SA nodal action potential exhibits only a small (if any) overshoot due to slow onset of voltage-activated __________

A

delayed rectifier K+ (Ik current)

81
Q

______ is the pacemaker channel of th eherat and is stimulated by _____

A

Ifunny, hyperpolarization below -40mV

82
Q

True/False: Ifunny can be activated by depolarization

A

FALSE

83
Q

Once Ifunny is activated, it is ______ and allows what two molecules to flow in equally?

A

non-selective, Na+ and K+. Na+ influx causes rise seen in phase 4.

84
Q

Describe action potential in the AV node.

A

Upstroke (phase 0) caused by an inward Ca++ current such as in SA node

85
Q

________ reflects the time required for excitation to spread through cardiac tissue

A

conduction velocity

86
Q

Where is conduction velocity quickest and slowest?

A

Quickest in Purkinje, slowest in AV node

87
Q

If conduction velocity in the AV node were to be increased, what would this result in?

A

ventricular filling may be compromised

88
Q

What three characteristics does conduction velocity depend on?

A

fiber diameter (directly proportional), maximum upstroke of action potential and overshoot of action potential

89
Q

Conduction velocity is inversely proportional to __________

A

RMP

90
Q

When the membrane is depolarized, RMP increases which ______ Na+ availability and therefore _____ rate of phase 0 in non-pacemaker and AV nodal cells

A

reduces, reduces

91
Q

________ is a decrease in conduction velocity when conduction spreads

A

decremental conduction

92
Q

Current is passed between cells via cardiac ________

A

gap junctions

93
Q

________ is the ability for cardiac cells to initiate action potentials in respond to inward, depolarizing current

A

excitability

94
Q

__________ are changes in excitability throughout the course of the action potential

A

refractory periods

95
Q

What is the difference between absolute and effective refractory periods?

A

Both start at the upstroke of action potential but effective is a slightly longer. Absolute ends after the plateau.

96
Q

Refractory periods depend on what four factors?

A

sodium conductance, membrane potential, recovery from inactivation and magnitude of outward K+ current during repoarlzation

97
Q

What is excitability in non-pacemaker cells related to? In Pacemaker cells?

A

increase in Na+ conductance. In pacemaker, would be Ca++

98
Q

What are the three classes of ion channels?

A

channels activated or suppressed by a ligand, voltage-dependent, or background/leak channels

99
Q

What are the three basic mechanisms to alter pacemaker activity?

A

change of slope of phase 4 diastolic, change in maximum diastolic potential, change in threshold potential

100
Q

How does vagal output slow down pacemaker activity? [in terms of pressure and slope]

A

Lowers mean diastolic pressure and decreases slope of phase 4

101
Q

What is the mechanism for how vagal output slows down pacemaker?

A

Ach binds and activates ligand-gated K+ channels which results in hyperpolarization of SA node cell membrane potential

102
Q

What are the effects of vagal response on the atria?

A

Reduction in action potential duration by Ach-mediated activation of K+ channels

103
Q

What are the effects of vagal output on ventricles?

A

little effect, antagonizes the stimulator effects of beta-adrenergic stimulation DOE

104
Q

What are the effects of vagal output on the AV node?

A

reduces excitability and thereby reduces transmission through ventricles –> ventricular escape in purkinje fibers

105
Q

What are the effects of sympathetic stimulation in SA node?

A

increases firing rate of pacemaker cells, increases current of all and slope of phase 0, faster upstroke velocity

106
Q

What are the effects of sympathetic stimulation on atria and ventricles?

A

increased contractibility

107
Q

What are the effects of sympathetic stimulation on AV node?

A

increased excitability and transmission of impulse –> increased conduction velocity

108
Q

True/False : Sympathetic stimulation lengthens action potential duration

A

FALSE

109
Q

What happens to cardiac excitability in hyperkalemia in ventricles, atria and purkinje cells?

A

Hyperkalemia leads to membrane DEPOL in ventricular, atrial and purkinje cells which reduces action potential amplitude (due to inactivation of sodium channels), increases conduction velocity, and increases repolarization activity (IK1 channels) in phase 3

110
Q

What happens to automaticity of SA nodal cells in hyperkalemia?

A

Decreases

111
Q

What happens to cardiac excitation in hypokalemia in ventricles, atria, and purkinje cells?

A

Depending on how low K+ is, could lead to instability of resting potential which can lead to ventricular arrhythmias (dangerous)

112
Q

What happens to automacity of AV nodal cells in hypokalemia?

A

enhanced

113
Q

Variation in PR interval is caused by what?

A

variation in conduction velocity through AV node (inversely proportional)

114
Q

The negative Q wave represents initial depolarization of the _____ whereas the negative S deflection represents initial depolarization of the _____

A

septum, base

115
Q

What does the QT interval represent?

A

Entire period of depolarization of the ventricles

116
Q

What does the ST segment represent?

A

period when the ventricles are depolarized

117
Q

What does the T wave represent?

A

ventricular repolarization

118
Q

What does each thick line on the Y axis represent?

A

0.1 mV

119
Q

The heart can be viewed as a _____ in terms of EKG and a given set of loads will detect the _______

A

dipole, vectorial sum

120
Q

Where are the positive and negative electrodes found in lead I? Degrees?

A

Positive is on left arm, negative is on right arm. 0 degrees (horizontal)

121
Q

Where are the positive and negative electrodes found in lead II? Degrees?

A

Positive is on left foot, negative is on right arm. 60 degrees.

122
Q

Where are the positive and negative electrodes found in lead III? Degrees?

A

Positive on left foot, negative on left arm. 120 degrees.

123
Q

What are the unipolar leads? The bipolar leads?

A

Unipolar are AVF, AVL, AVR. Bipolar are I, II, and III

124
Q

Where is the positive electrode on AVF?

A

left foot, 90 degrees

125
Q

Where is the positive electrode on AVL?

A

left arm, 330 degrees.

126
Q

Where is the positive electrode on AVR?

A

right arm, 210 degrees

127
Q

In ________ the voltage is measured relative to a common ground obtained by connecting the three electrodes together

A

V1-V6 precordial leads

128
Q

What are two types of supraventricular arrythmia?

A

atrial flutter and atrial fibrillation

129
Q

What are the 4 types of arrhythmias from junctional origin?

A

AV blocks, premature junctional contractions, junctional escape rhythm, junctional tachycardia

130
Q

What are the four types of ventricular arrhythmias?

A

PVC’s, v tach, v fib, ventricular asystole

131
Q

What may a right axis deviation indicate?

A

Obstructive lung disease or pulmonary hypertension because of chronic increase in afterload imposed on right ventricle (lungs not letting blood in)

132
Q

What may a left axis deviation indicate?

A

Can be caused by LVH - LVH can be physiological as seen in athletes or pathological due to increased afterload (aortic stenosis or systemic HTN)

133
Q

How would an impaired artery appear on an EKG?

A

ST segment will be depressed or elevated; T waves will have variations in amplitude, shape and polarity. In general, axn potentials will be depressed and exhibit a lower RMP and reduced duration

134
Q

An _______ is any disorder of rate, rhythm, origin or conduction of impulses with the heart

A

arrhythmia

135
Q

Why of the following does not commonly cause arrhythmias?

a) myocardial infarction
b) digitalis
c) running
d) anesthesia

A

c

136
Q

_______ are abnormal sites of excitation

A

ectopic foci

137
Q

What are the two general categories of arrhythmias?

A

abnormal impulse formation and disorders of impulse conduction

138
Q

An _____________ is a delayed repolarization that favors reopening of Ca++ channels with a second phase of depolarization occurring during the relative refractory period

A

early after depolarization

139
Q

A ___________ is an abnormal Ca++ release event which includes transient membrane depolarization after final phase of repolarization

A

delayed after depolarization

140
Q

What would cause an early after depolarization?

A

reduced activity of K+ channels or enhanced acitivity of Na+ or Ca+ channels, long QT syndrome –> Torsades de Pointes

141
Q

What would cause a delayed after depolarization?

A

seen in conditions favoring Ca++ overload

142
Q

A arrhythmia of impulse conduction without reentry would be classified as a ______

A

AV block

143
Q

What are the requirements of a slowed conduction arrhythmia with reentry? (3)

A

a unidirectional block and conduction time around alt pathway must be longer than ERP/ARP

144
Q

What would NOT favor slowed conduction with reentry?

a) long reentrant pathway
b) slow conduction
c) rapid effective refractory period
d) short effective refractory period

A

C

145
Q

What are the three types of reentry arrhythmias?

A

reflection, circus movement, phase 2

146
Q

What is an example of an anatomical block for circus movement arrhythmia?

A

inexcitable valve

147
Q

What is an example of a non-anatomical block for circus movement arrhythmia?

A

functional block such as a region not being excitable any longer due to severe ischemia –> strong depol of membrane

148
Q

What are the three types of non-anatomical block circus movement arrhythmias?

A

leading circle, figure of 8, spiral wave

149
Q

The _________ is the temporal change in concentration of free intracellular Ca++ concentration during one cardiac beat

A

Ca++ transient

150
Q

What does the amplitude of the Ca++ transient regulate?

A

contractile force

151
Q

What plays a primary role in determining the size of the Ca++ transient?

A

action potential

152
Q

When the plateau level of the action potential is elevated, what happens to the Ca++ transient?

A

it increases

153
Q

Describe the positive staircase phenomenon.

A

When the frequency of stimulations is increased, contraction of the heart increases only progressively before reaching a new steady state.

154
Q

True/False: Most of Ca++ transient is from direct Ca++ entry through voltage and time dependent Ca++ channels

A

FALSE, only 10% at most

155
Q

Where does the majority of Ca++ influx in the Ca++ transient come from?

A

Ca++ induced Ca++ release (CICR)

156
Q

Describe the mechanism of CICR.

A

Ca++ influx triggers Ca++ release from SR. Ca++ channels are juxtaposed with a different class of Ca++ channels in the t-tubules. Ca++ binds and opens these channels.

157
Q

What are the Ca++ channels found on t-tubules called

A

Ryanodine receptors (RyR)

158
Q

Ca++ binding opens Ryr channels. What closes them?

A

decreased driving force for Ca++ and intrinsic inactivation

159
Q

______ is the main Ca++ transporter involved in relaxing the Ca++ transient

A

Ca++ ATPase in the SR membrane

160
Q

Describe the action of Ca++ ATPase in the SR membrane

A

it drives Ca++ back into the SR

161
Q

______ is a Ca++ transporter found in the t-tubules and sarcolemma that does not require ATP

A

3Na+/Ca++ transporter, pumps Ca++ out

162
Q

True/False: 3Na+/Ca++ transporter is the major mechanism for balancing Ca++ entry

A

TRUE

163
Q

How does intracellular Ca++ stimulate contraction?

A

Free Ca++ binds to troponin C which initiates acto-myosin bridge cycling

164
Q

Myocardial cells are packed with ________ which are regular arrays of filamentous proteins

A

myofibrils

165
Q

What are myofibrils made up of?

A

actin, myosin, and structural proteins

166
Q

Myofilaments are surrounded by the _______ which is an extensive intracellular membrane network

A

sarcoplasmic reticulum

167
Q

_______ surround the myofibrils and make up ___ of muscle cell volume

A

mitochondria, 35%

168
Q

The plasma surface of cardiac myocytes is called the _______

A

sarcolemma

169
Q

At fixed intervals, the sarcolemma protrudes into the cell and forms the ________

A

transverse t-tubules [interior contigious with extracellular space]

170
Q

True/False: Transverse t-tubules are much wider in skeletal muscle cells than cardiac cells

A

FALSE CARDIAC CELLS

171
Q

The close juxtaposition of _____ with the ____ forms the dyad

A

portions of the SR and t-tubules

172
Q

What is the portion of the SR involved in the dyad called? What is the rest of the SR called?

A

In the dyad, it is the subsarcolemmal cisternae. The rest of the SR is the sarcotubular network

173
Q

The ______ are the clear light areas composed of thin filaments, mostly actin

A

I

174
Q

The _______ is the thin dark line in the middle of the I band

A

Z line

175
Q

The space between two Z lines is called the _____

A

sarcomere

176
Q

The _________ is an opaque, dark area consisting of ordered overlap between thick filaments (mainly myosin)

A

A band

177
Q

How do cardiac glycosides improve mechanical performance of the heart?

A

Inhibit the Na+/K+ pump. Therefore, increase in intracellular Na+. Na/Ca exchanger does not pump Ca out as a result so Ca++ intracellular increases which is then uptaken by SR and is available for release during an action potential through CICR

178
Q

How does norepinephrine from terminal ending and epi from adrenal gland stimulation increase cardiac contraction?

A

Stimulates production of AC –> cAMP –> PKA activation - enhances Ca++ channel open probability which increases efficacy as a trigger for CICR

179
Q

How does NE/epi affect Ryr in the SR?

A

stimulates Ca++ influx to increase Ryr channel activity which improves Ca++ release

180
Q

How does NE/epi affect phospholamban (PLB)?

A

represses activity of Ca++/ATPase pump and therefore inhibits relaxation of Ca++ transient

181
Q

How does NE/epi affect troponin?

A

phosphorylation reduces affinity of troponin complex for Ca++ which facilitates relaxation

182
Q

Which sympathetic stimulation mechanism is most important in increasing the size of the Ca++ transient and contraction?

A

Ca++ influx to increase Ryr channel activity

183
Q

The basic unit structure responsible for contraction of striated muscle is the _________

A

sarcomere

184
Q

Shortening of muscle results from interaction between ________ and ______ in the sarcomere

A

thin (actin) and thick (myosin)

185
Q

True/False: Thick filaments are made of actin

A

FALSE - made of myosin

186
Q

The __________ of myosin reacts with actin

A

globular region - made up of two heavy chains wound around each other

187
Q

The globular regions of myosin exhibit ________

A

ATPase activity (cross bridge cycling?!)

188
Q

Myosin filaments are arranged how?

A

globular regions oriented opposite of each other

189
Q

F-actin polymer composed of two chains wound around each other in a coiled conformation by means of _________ makes up thin filaments of actin

A

disulfide bonds

190
Q

Each actin chain made up of a monomer called ________

A

G-actin

191
Q

What are the regulatory proteins bound to actin that couple Ca++ transient to acto-myosin bridge cycling? (4)

A

tropomyosin, troponin complex - trop C, trop I, trop T

192
Q

Describe the function of tropomyosin

A

allow or prevent interaction of actin and myosin.

193
Q

The ___________ is found tightly packed on thin filaments, evenly spaced

A

troponin complex

194
Q

Describe the function of troponin C.

A

Troponin C binds to Ca++. Two globular regions.

195
Q

Each globular region of troponin C contains two divalent cation binding sites labeled I through IV. Describe actions.

A

I and II are Ca++ specific, II is acceptor site. III and IV bind both Ca++ and Mg++ and stabilize the troponin complex.

196
Q

Describe the function of troponin I.

A

Troponin I is located between TnC and TnT and inhibits interaction between myosin and actin (although weaker than tropomyosin)

197
Q

What enhances the inhibitory activity of troponin I?

A

phosphorylation by PKA - accelerates relaxation - responsible for inhibiting acto-myosin bridge cycling during diastole

198
Q

Describe the function of troponin T

A

Binds to TnI and Tropomyosin. Maintains structural integrity of complex.

B2 (15 decks)

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