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Physiology > Section 2 Review 2 > Flashcards

Section 2 Review 2 Flashcards

1
Q

Responses to a therapeutic level of a cardiac glycodeside?

A

inc SV, ince MAP, inc Art PP

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2
Q

Response to an agent that selectively reduces arteriolar resistance:

A

inc SV, dec MAP, inc PP

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3
Q

Which patron best describes the response to hemmorhage?

A

dec Sv, dec MAP, dec PP

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4
Q

Inc both MAP and PP means you what increased:

A

inc SV

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5
Q

In response to hemmorhage HR is increased by:

A

activation of b-1 recipes on SA-node

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6
Q
  • 2 vasc beds in parallel, flow through each is the same. Cut the R of 1 in half and double the R in the other, total flow:
A

will be greater than the control ?

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7
Q

Effect of metabolites released into tissues on flow and mean cap p:

A

increase total flow and inc mean cap P in the tissue

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8
Q

How will blood flow to the myocardium change with increased fitness levels?

A

coronary blood flow will decrease

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9
Q

T or F? inc HR is most responsibel for the inc in the working of the heart m. during exercise.

A

T

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10
Q

How would the PV loop be changed with the addition of a pos inotropic agent?

A

same preload, inc P build up during isovolumetrtic contraction, increased Sv

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11
Q

How is PV loop effected with chronic reduction in the inotropic state of the heart (dev. of heart failure)

A

heart can’t pump as much, increased preload, graph shifted to the R and smaller in the y direction

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12
Q

If a drug dec MAP and inc PP, what is the mode of action?

A

dec art R

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13
Q

How will arterial pulse pressure be effected with a decrease in arteriolar R?

A

it will increase

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14
Q

Will the application of a M rec agonist lead to an increase or decrease venous compliance?

A

decrease

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15
Q

Will going from laying down to a standing position lead to an increase or decrease venous compliance?

A

decrease

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16
Q

Would a beta recep agonist lead to an increase or decrease venous compliance?

A

increase

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17
Q

Would a selective agonist for precap a-1 recpes lead to an increase or decrease venous compliance?

A

increase

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18
Q

Would a a-1 recep antagonist lead to an increase or decrease venous compliance?

A

increase

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19
Q

Are metabolites vasodilators or vasoconstrictors?

A

vasodilators. this makes sense, if anything builds up that normally isn’t there, you’re body wants to clear it)

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20
Q

In the presence of sever hemorrhage the baro-reflex mediated mechanism most responsible for the recruitment of myocyte cross bridges is:

A

Activation of beta-1 receptors on myocytes.

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21
Q

Effect of inc HR on SV:

A

decreases SV

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22
Q

Effects of cardiac glycosides:

A

increase force of contraction, dec HR

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23
Q

How do cardiac glycosides work?

A

inhibit the Na-K pump, inc activator pool of Ca, inc force of ven contraction, inc intracellular Na levels (initiating depol.)

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24
Q

Which is troponin dependent, sk m. or s.m.?

A

sk. m.

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25
Q

Calcium binding protein involved in s.m. contraction:

A

calmodulin

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26
Q

What is invloved in the phosphorylation of myosin in s.m. cell contraction?

A

MLKC

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27
Q

3 methods to dec Ca conc in s.m. cell after contraction is over:

A

ATP in SR, ATP out of cell, Na Ca exchanger (against Ca gradient)

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28
Q

The only way to activate sk.m. contraction:

A

AP

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29
Q

how to activate s.m. contraction:

A

AP, NTs, hormones, paracrines, NE, AcH, stretch

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30
Q

What type of rec does IP3 interact with:

A

G-protein coupled rec

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31
Q

How is Ca released from the SR?

A

Ca-induced-Ca release

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32
Q

What type of channels are involved in entry of Ca into s.m. cells?

A

voltage gated (L-type)

33
Q

What would cause blood flow to normal regions of the myocardium to be increased, while blood flow distal to the stenotic artery to not change if a pt w/ stenosis was given a vasodilator agent?

A

The arterioles in the stenotic region were already maximally dilated due to chronic under-perfusion and build up of vasodilator metabolites.

34
Q

How will a circulation model tracing change with an inc in art R?

A

same HR, more forceful contract (larger amplitude wave on bottom and top of tracing)

35
Q

body response to an alpha-1 receptor agonist:

A

Dec HR and inotropic state of the myocardium

36
Q

What do an increase in venous hydrostatic pressure lead to?

A

edema

37
Q

Will vasoconstriction lead to edema?

A

yes

38
Q

When do you hear the first heart sound?

A

at the end of ventricular filling

39
Q

What would happen to a P-V loop if the Ca channels of the cardiac working muscle were blocked?

A

the preload would increase, the Sv decrease, and the force of contraction decreases. these would make the loo[p narrower, shorter and shifted to the R. The U L portion of the graph will never touch toe solid curve bc it can’t generate the nec. force

40
Q

How would the P-V loop be effected if you block the alpha-1 receptors of systemic arterioles?

A

no resistance in the systemic arterioles, decrease in arterial pressure, decrease in after load, more blood returning faster so an increase in preload.

41
Q

Activation of a-1 receps in s.m. leads to __ while activation of B-2 receps in s.m. leads to:

A

vasodilation, vasoconstriction

42
Q

define hyperemia:

A

increased tissue flow, in excess of metabolic demand, following the release for arterial occlusion

43
Q

How would partial inhibition of the Na-K pump affect the cell?

A

increase intracellular Ca levels

44
Q

Would increasing vasomotor tone increase or decrease SV?

A

dec (inc vasomotor tone –> inc arterial BP –> inc afterload

45
Q

response to hemorrhage

A

a primary dec cardiac output, a secondary dec in art P and inc in HR and R

46
Q

a drug causes an inc in art systolic P and dec in art diastolic P (inc in art pulse P). What physiological responses account for these changes?

A

inc SV and inc art R

47
Q

What does the P wave correspond with on the EcG?

A

right before the little hill that represents the atrial, extra push of blood into the L ventricle

48
Q

Why is a person w/ a stenosis asymptotical initially?

A

the R2 coronary R (art R) decreases to compensate or the inc R1 R (the stenosis)

49
Q

How to calculate PP:

A

s-d

50
Q

how to calculate mean arterial P:

A

[1/3(PP) + d] …… (PP=s-d)

51
Q

Slow depol during this phase enable pacemaking activity by the cell:

A

Phase 4 (RMP)

52
Q

This phase is assoc with QRS complex of the ECG:

A

Phase 0 (rapid depolarizaton)

53
Q

This phase is imp in excitation-contraction coupling:

A

Phase 2 (plateau)

54
Q

What is phase 1?

A

Partial repolarization

55
Q

What is phase 3?

A

repolarization

56
Q

T or F? The RMP is prop to the ratio of the K conc across the membrane for both cardiac and sk.m..

A

T

57
Q

T or F? The force of m. contraction is prop to the cytosolic Ca conc. for both cardiac and sk.m..

A

F.

58
Q

Through which heart structure does the AP travel most slowly through?

A

AV node fibers

59
Q

What will a dec in MAP w/ reflexes intact result in?

A

inc in HR

60
Q

Does atropine decrease or increase HR?

A

increase

61
Q

What change happens in the cap bed if the arterioles are constricted?

A

reabsorption > filtration

62
Q

What physiological changes alter MAP?

A

SV, HR, arterial resistance (not sig. though)

63
Q

What causes hyperemia in sk. m. during light exercise?

A

an inc in vasodilator metabolites

64
Q

T or F? Coronary blood flow is primarily under neural control.

A

F. characterized by autoregulation

65
Q

T or F? A persons HR decreases when they stand.

A

F

66
Q

T or F? The central V.P. will inc when a person stands.

A

F

67
Q

Does R atrial P increase or dec with exercise?

A

dec

68
Q

What can an ECG tell you about cardiac activation?

A

Hr, sequence of activation of the myocardium, delay bw the excitation of the atria and the ventricles, duration of the ventricular excitation

69
Q

2 beds in parallel: double R in one and halve the other. Net flow?

A

Greater than control ( Flow = 1/R(a) + 1/R(b) )

70
Q

T or F? Ca binds troponin-C subunit of actin in s.m.

A

F. in sk. m., not s.m.

71
Q

What would happen if you block the a-1 receps on venous s.m. cells?

A

constriction (act of these leads to vasodilation)

72
Q

What would phosphorylation of volt-gated Ca channels in cardiac ventricular cells lead to?

A

dilation

73
Q

Mech responsible for adjusting HR from laying down to standing:

A

dec activation of muscarinic receps on the SA-node cells (removing para sym depression and allowing to rise to the rate it would be w/o any influence?)

74
Q

How would a dec in art P and an inc in venous compliance affect SV?

A

it wouldn’t. It would remain the same

75
Q

Changes resulting form the loss of a limb:

A

Resting metabo decreases, resting CO dec, resting MAP remains the same, total BV dec

76
Q

These dec if a limb is lost:

A

resting metabo, resting CO, total BV

77
Q

How is resting MAP effected with the loss of a limb?

A

it’s not

78
Q

What physio change can lead to a dec in MAP and an inc in arterial PP?

A

dec art R

79
Q

Cardiac glycoside does what to working heart cells?

A

partial inhibition of the SL Na-K pumps, inc activator pool of Ca, inc force generation during S, inc intra Na conc

Physiology (55 decks)

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