Physiology Sparks Review Questions

Front 1

1. There are a number of risk factors for hypertension. Which of the following risk factors cannot be controlled?
A. Excess weight.
B. Inactivity
C. Sodium intake.
D. Excessive alcohol intake.
E. Family history.

Back 1

E. Family history.

Front 2

2. There are a number of risk factors for hypertension. Which of the following pairs of risk factors can be controlled?
A. Age and race.
B. Race and family history.
C. Sodium intake and race.
D. Excess weight and sodium intake.
E. Age and tobacco use.

Back 2

D. Excess weight and sodium intake.

Front 3

3. There is a pressure gradient in the systemic circulation. The greatest drop in mean pressure occurs in the:
A. Arteries.
B. Arterioles.
C. Capillaries.
D. Venules.
E. Veins.

Back 3

B. Arterioles.

Front 4

Which is the correct calculation of pulse pressure (PP)?
A. PP = U – V
B. PP = U – Z
C. PP = W – Y
D. PP = U – Y
E. PP = W – Z

Back 4

B. PP = U – Z

Front 5

6. Systolic arterial pressure is determined by:
A. Total Peripheral Resistance and Heart Rate
B. Total Peripheral Resistance and Stroke Volume
C. Stroke Volume and Aortic Compliance
D. Stroke Volume and Heart Rate
E. Aortic Compliance and Heart Rate

Back 5

C. Stroke Volume and Aortic Compliance

Front 6

7. Diastolic arterial pressure is determined by:
A. Total Peripheral Resistance and Heart Rate
B. Total Peripheral Resistance and Stroke Volume
C. Stroke Volume and Aortic Compliance
D. Stroke Volume and Heart Rate
E. Aortic Compliance and Heart Rate

Back 6

A. Total Peripheral Resistance and Heart Rate

Front 7

8. The main site of Total Peripheral Resistance is the systemic:
A. Arteries
B. Arterioles
C. Capillaries
D. Venules
E. Veins

Back 7

B. Arterioles

Front 8

9. The following constrict systemic arterioles:
A. Sympathetic nerves
B. Neurons that release nitric oxide
C. Atrial natriuretic peptide
D. Adenosine
E. Bradykinin

Back 8

A. Sympathetic nerves

Front 9

10. The following dilate systemic arterioles:
A. Sympathetic nerves
B. Neurons that release nitric oxide
C. Angiotensin II
D. Vaspressin
E. Endothelin

Back 9

B. Neurons that release nitric oxide

Front 10

12. An increase in arterial pressure leads to a decrease in blood volume by increasing:
A. Sympathetic nerve firing to the sinoatrial node.
B. Sympathetic nerve firing to veins.
C. Sympathetic nerve firing to cardiac muscle.
D. Urinary loss of sodium and water.
E. Urinary retention of sodium and water.

Back 10

D. Urinary loss of sodium and water.

Front 11

14. Angiotensin converting enzyme catalyzes the following reaction:
A. Angiotensinogen to angiotensin I
B. Renin to angiotensinogen
C. Angiotensin I to angiotensin II
D. Angiotensin II to aldosterone
E. Angiotensin II to angiotensin I

Back 11

C. Angiotensin I to angiotensin II

Front 12

15. The renin-angiotensin-aldosterone system increases arterial pressure by increasing:
A. Total peripheral resistance and cardiac output.
B. Vasoconstriction and urinary sodium loss.
C. Systemic arteriolar constriction and urinary sodium loss.
D. Renal salt and water retention and arteriolar dilation.
E. Arteriolar dilation and urinary salt and water loss.

Back 12

A. Total peripheral resistance and cardiac output.@

Front 13

16. The renin-angiotensin-aldosterone system is activated by:
A. Decreased delivery of NaCl to the macula densa of the renal tubules.
B. Decreased sympathetic nerve activity to the kidney.
C. Increased arterial pressure.
D. Increased glomerular filtration rate.
E. Increased stretch of renal arterioles.

Back 13

A. Decreased delivery of NaCl to the macula densa of the renal tubules.

Front 14

17. Physiological hypertrophy of the left ventricle occurs in response to:
A. Aortic stenosis
B. Chronic hypertension.
C. Myocardial infarction.
D. Chronic exercise.
E. Aortic banding.

Back 14

D. Chronic exercise

Front 15

18. When compared to pathological hypertrophy, left ventricles undergoing physiological hypertrophy caused by chronic exercise exhibit:
A. More expression of natriuretic peptides.
B. More fibrosis (connective tissue).
C. Less myocyte width (diameter).
D. More receptor tyrosine kinase activity.
E. More phospholipase C activity.

Back 15

D. More receptor tyrosine kinase activity.

Front 16

19. Renal artery stenosis causes hypertension by decreasing:
A. Excretion of salt and water.
B. Renin release by the kidney.
C. Angiotensin I formation.
D. Angiotensin II formation.
E. Aldosterone secretion by the adrenal cortex.

Back 16

A. Excretion of salt and water.

Front 17

20. Renal artery stenosis causes hypertension by increasing all of the following EXCEPT:
A. Angiotensin I formation.
B. Renin release by the kidney.
C. Excretion of salt and water.
D. Total peripheral resistance.
E. Aldosterone secretion by the adrenal cortex.

Back 17

C. Excretion of salt and water.

Front 18

21. Renal handling of sodium involves:
A. Glomerular filtration and tubular secretion.
B. Tubular reabsorption and tubular secretion.
C. Glomerular filtration, tubular secretion and tubular reabsorption.
D. Glomerular filtration and tubular reabsorption.
E. Active transport across the glomerular capillaries.

Back 18

D. Glomerular filtration and tubular reabsorption.

Front 19

22. Aldosterone reduces urinary loss of sodium by:
A. Increasing filtration of sodium.
B. Increasing the copies of sodium/potassium pumps and sodium channels in cortical collecting duct cells.
C. Decreasing arterial pressure.
D. Decreasing blood volume.
E. Decreasing the transport of water in collecting duct cells.

Back 19

B. Increasing the copies of sodium/potassium pumps and sodium channels in cortical collecting duct cells

Front 20

23. Excess aldosterone causes hypertension by:
A. Increasing the excretion of sodium and water.
B. Inhibiting whole body autoregulation.
C. Inhibiting arteriolar growth.
D. Stimulating cardiac hypertrophy.
E. Decreasing blood volume.

Back 20

D. Stimulating cardiac hypertrophy.

Front 21

25. In hypertension, arterial medial hypertrophy results from:
A. Decreased norepinephrine.
B. Decreased angiotensin.
C. Increased nitric oxide.
D. Increased arterial pressure.
E. Inhibition of growth of smooth muscle and fibroblasts.

Back 21

D. Increased arterial pressure.

Front 22

26. In hypertension, arterial medial hypertrophy results from:
A. Decreased norepinephrine.
B. Decreased angiotensin.
C. Increased nitric oxide.
D. Decreased arterial pressure.
E. Growth of smooth muscle and fibroblasts.

Back 22

E. Growth of smooth muscle and fibroblasts.

Front 23

27. Hypertension can be caused by mutation of a single gene. An example of such a mutation is:
A. Gain of function mutation of the enzyme responsible for the formation of nitric oxide in endothelial cells.
B. Loss of function mutation for gene encoding angiotensinogen in liver cells
C. Gain of function mutation for the apical sodium channel in cortical collecting duct cells.
D. Loss of function mutation for angiotensin II receptors in the in arteriolar smooth muscle.
E. Loss of function mutation for phospholipase C in arteriolar smooth muscle.

Back 23

C. Gain of function mutation for the apical sodium channel in cortical collecting duct cells.

Front 24

28. A gain of function mutation for the apical sodium channel in cortical collecting duct cells causes hypertension by:
A. Increasing the discharge of the sympathetic nervous system to the heart.
B. Increasing the secretion of aldosterone by the adrenal cortex.
C. Increasing the renal reabsorption of salt and water.
D. Increasing the release of renin from the kidney.
E. Increasing the activity of angiotensin converting enzyme.

Back 24

C. Increasing the renal reabsorption of salt and water.

Front 25

29. The following statement about essential (primary) hypertension is CORRECT:
A. Total peripheral resistance but not cardiac output is increased.
B. Cardiac output but not total peripheral resistance is increased.
C. In the early stages, cardiac output is increased.
D. In the late stages, cardiac output is increased.
E. in the early stages, total peripheral resistance is increased.

Back 25

C. In the early stages, cardiac output is increased.

Front 26

30. Studies on the role of genetics in essential hypertension show that:
A. None of the variability in blood pressure is inherited.
B. Hypertension is an inherited disease with little or no effect of the environment.
C. About half of the variability in blood pressure is inherited and the other half is due environmental influences.
D. Hypertension is likely to be caused by a single gene.
E. The effect of particular variants of genes are independent of the
environment.

Back 26

C. About half of the variability in blood pressure is inherited and the other half is due environmental influences.

Front 27

31. The role of the sympathetic nervous system (SNS) in essential hypertension is still under investigation, but some important facts are known. Which of the following statements is CORRECT?
A. Insulin causes decreased SNS activity.
B. Increased SNS causes renal loss of salt and water.
C. Leptin causes increased SNS activity.
D. A chronic increase in SNS activity inhibits cardiac hypertrophy and arterial smooth muscle growth (medial hypertrophy).
E. Increased SNS activity inhibits the renin-angiotensin-aldosterone system.

Back 27

C. Leptin causes increased SNS activity.

Front 28

32. The role of the sympathetic nervous system (SNS) in essential hypertension is still under investigation, but some important facts are known. Which of the following statements is CORRECT?
A. Insulin causes decreased SNS activity.
B. Most individuals with hypertension have increased or normal SNS activity.
C. Leptin causes decreased SNS activity.
D. A chronic increase in SNS activity inhibits cardiac hypertrophy.
E. Increased SNS activity inhibits the renin-angiotensin-aldosterone system

Back 28

B. Most individuals with hypertension have increased or normal SNS activity.

Front 29

33. The role of the renin-aldosterone-aldosterone-system (RAAS) in essential hypertension is still under investigation, but some important facts are known. Which of the following statements concerning a role for the RAAS in essential hypertension is NOT CORRECT?
A. Angiotensin converting enzyme inhibitors lower arterial pressure.
B. Most individuals with hypertension have increased or normal RAAS activity.
C. Angiotensin II receptor blockers lower arterial pressure.
D. Aldosterone antagonists lower arterial pressure.
E. Stimulation of the RAAS leads to urinary loss of salt and water.

Back 29

E. Stimulation of the RAAS leads to urinary loss of salt and water.

Front 30

34. The role of the renin-aldosterone-aldosterone-system (RAAS) in essential hypertension is still under investigation, but some important facts are known. Which of the following statements concerning a role for the RAAS in essential hypertension is NOT CORRECT?
A. Angiotensin II decreases central (brain) SNS activity.
B. Most individuals with hypertension have increased or normal RAAS activity.
C. Angiotensin II increases peripheral NE release.
D. Aldosterone antagonists lower arterial pressure.
E. The RAAS leads to urinary retention of salt and water.

Back 30

A. Angiotensin II decreases central (brain) SNS activity.

Front 31

35. Leptin:
A. Secretion is inhibited by increased fat deposition in adipose tissue.
B. Stimulates food intake.
C. Decreases metabolic rate.
D. Stimulates the SNS.
E. Causes vasodilatation

Back 31

D. Stimulates the SNS.

Front 32

36. Obesity increases arterial pressure by the following mechanism(s):

A. Obesity raises insulin resistance, which is about half of total peripheral resistance. The resulting increase in total peripheral resistance increases arterial pressure.
B. Obesity increases both leptin and insulin. Both of these hormones increase sympathetic nervous system (SNS) activity and insulin causes the kidney to save salt and water. The resulting increase in SNS activity and blood volume increase arterial pressure.
C. Increased fat deposition requires more blood vessels and this raises total peripheral resistance. The resulting increase in total peripheral resistance increases arterial pressure.
D. Increased fat deposition increases leptin secretion. The increased leptin acts directly on the arterioles to decrease total peripheral resistance. This raises arterial pressure.
E. The same gene makes people obese and raises their blood pressure.

Back 32

B. Obesity increases both leptin and insulin. Both of these hormones increase sympathetic nervous system (SNS) activity and insulin causes the kidney to save salt and water. The resulting increase in SNS

Front 33

37. Characteristics of the metabolic syndrome include a LOWER THAN NORMAL:
A. Waist circumference.
B. Blood triglycerides.
C. HDL cholesterol.
D. Blood pressure.
E. Fasting blood glucose.

Back 33

C. HDL cholesterol.

Front 34

38. Metabolic syndrome is common in the United States. The following statement about metabolic syndrome is NOT CORRECT:
A. People with metabolic syndrome are at increased risk for coronary heart disease.
B. People with metabolic syndrome are at increased risk for stroke.
C. People with metabolic syndrome often have low LDL cholesterol.
D. People with metabolic syndrome often have elevated fasting blood glucose.
E. People with metabolic syndrome often have an elevated waist circumference.

Back 34

C. People with metabolic syndrome often have low LDL cholesterol.

Front 35

39. The following agents cause both vasoconstriction and medial hypertrophy:
A. Nitric oxide and angiotensin II
B. Nitric oxide and norepinephrine
C. Angiotensin II and norepinephrine
D. Adenosine and nitric oxide
E. Adenosine and angiotensin II

Back 35

C. Angiotensin II and norepinephrine

Front 36

40. Agents that cause increased cAMP or cGMP cause relaxation of vascular smooth muscle by:
A. Competing with calcium ions for calmodulin.
B. Competing with calcium-calmodulin for binding to myosin light chain kinase.
C. Inhibiting myosin light chain kinase.
D. Phosphorylating myosin.
E. Increasing cross bridge cycling.

Back 36

C. Inhibiting myosin light chain kinase

Front 37

41. Vascular smooth muscle and cardiac muscle DIFFER in that in vascular smooth muscle:
A. Increased cytosolic calcium ion concentration leads to increased cross bridge cycling.
B. No calcium enters the cell from the outside.
C. Striations are readily apparent.
D. Increased cAMP increases force of contraction.
E. Cross bridge cycling is initiated by phosphorylation of myosin.

Back 37

E. Cross bridge cycling is initiated by phosphorylation of myosin.

Front 38

42. Thiazide diuretics lower arterial pressure by:
A. Acting directly on vascular smooth muscle to antagonize calcium ion entry. This lowers total peripheral resistance.
B. Blocking the effect of norepinephrine on the heart. This reduces cardiac contractility and cardiac output.
C. Reducing the activity of the phospholipase C/ IP3/ DAG pathway. This results in relaxation of vascular smooth muscle, lower total peripheral resistance and arterial pressure.
D. Blocking angiotensin converting enzyme activity. This reduces the formation of angiotensin I, and lowers total peripheral resistance.
E. Reducing the renal tubular reabsorption of sodium. This reduces blood volume, ventricular end diastolic volume and cardiac output.

Back 38

E. Reducing the renal tubular reabsorption of sodium. This reduces blood volume, ventricular end diastolic volume and cardiac output.

Front 39

43. Angiotensin II receptor blockers lower arterial pressure by:
A. Acting directly on vascular smooth muscle to increase cGMP. This relaxes vascular smooth muscle and lowers total peripheral resistance.
B. Reducing the activity of the phopholipase C/ IP3/ DAG pathway. This results in relaxation of vascular smooth muscle, and lowers total peripheral resistance and arterial pressure.
C. Reducing the reabsorption of sodium by binding to renal tubular sodium channels. This reduces blood volume, ventricular end diastolic volume and cardiac output.
D. Blocking angiotensin converting enzyme activity. This reduces the formation of angiotensin II, and lowers total peripheral resistance.
E. Reducing the activity of the G protein/ cAMP/ protein kinase pathway. This results in relaxation of vascular smooth muscle, lower total peripheral resistance and arterial pressure.

Back 39

B. Reducing the activity of the phopholipase C/ IP3/ DAG pathway. This results in relaxation of vascular smooth muscle, and lowers total peripheral resistance and arterial pressure.

Front 40

44. Antagonism of beta adrenergic receptors lowers arterial pressure by:
A. Acting directly on vascular smooth muscle to increase cGMP. This relaxes vascular smooth muscle and lowers total peripheral resistance.
B. Increasing the activity of the phopholipase C/ IP3/ DAG pathway. This results in relaxation of vascular smooth muscle, and lowers total peripheral resistance and arterial pressure.
C. Reducing the reabsorption of sodium by binding to renal tubular sodium channels. This reduces blood volume, ventricular end diastolic volume and cardiac output.
D. Blocking angiotensin converting enzyme activity. This reduces the formation of angiotensin II, and lowers total peripheral resistance.
E. Reducing the activity of the G protein/ cAMP/ protein kinase pathway. This results in reduced cardiac contractility, cardiac output and arterial pressure.

Back 40

E. Reducing the activity of the G protein/ cAMP/ protein kinase pathway. This results in reduced cardiac contractility, cardiac output and arterial pressure.

Front 41

45. Aldosterone antagonists lower arterial pressure by:
A. Reducing copies of the cortical collecting duct sodium channels. This increases excretion of sodium channels, lowers blood volume, cardiac output and arterial pressure.
B. Acting directly on vascular smooth muscle to increase cGMP. This relaxes vascular smooth muscle and lowers total peripheral resistance.
C. Increasing the activity of the phopholipase C/ IP3/ DAG pathway. This results in relaxation of vascular smooth muscle, and lowers total peripheral resistance and arterial pressure.
D. Blocking angiotensin converting enzyme activity. This reduces the formation of angiotensin II, and lowers total peripheral resistance.
E. Reducing the activity of the G protein/ cAMP/ protein kinase pathway. This results in reduced cardiac contractility, cardiac output and arterial pressure.

Back 41

A. Reducing copies of the cortical collecting duct sodium channels. This increases excretion of sodium channels, lowers blood volume, cardiac output and arterial pressure.

Front 42

46. Ventricular systole consists of the following components:
A. Isovolumetric relaxation and ventricular ejection.
B. Isovolumetric contraction and ventricular ejection.
C. Isovolumetric contraction and isometric relaxation.
D. Atrial contraction and ventricular ejection.
E. Atrial contraction and isovolumetric contraction.

Back 42

B. Isovolumetric contraction and ventricular ejection.

Front 43

50. Which of the following valve disorders is characterized by a systolic murmur and elevated left ventricular-aortic pressure pressure difference during systole?
A. Aortic stenosis
B. Aortic regurgitation (insufficiency)
C. Mitral stenosis
D. Mitral regurgitation (insufficiency)

Back 43

A. Aortic stenosis

Front 44

51. Which of the following valve disorders is characterized by a diastolic murmur and a low diastolic aortic pressure?
A. Aortic stenosis
B. Aortic regurgitation (insufficiency)
C. Mitral stenosis
D. Mitral regurgitation (insufficiency)

Back 44

B. Aortic regurgitation (insufficiency)

Front 45

52. Which of the following valve disorders is characterized by a systolic murmur and markedly elevated left atrial pressure during ventricular systole?
A. Aortic stenosis
B. Aortic regurgitation (insufficiency)
C. Mitral stenosis
D. Mitral regurgitation (insufficiency)

Back 45

D. Mitral regurgitation (insufficiency)

Front 46

53. Which of the following valve disorders is characterized by a diastolic murmur and an elevated left atrial pressure during ventricular diastole?
A. Aortic stenosis
B. Aortic regurgitation (insufficiency)
C. Mitral stenosis
D. Mitral regurgitation (insufficiency)

Back 46

C. Mitral stenosis

Front 47

54. The sequence of the spread of excitation in the heart is

A. AV node -> atria -> SA node -> Purkinje system -> ventricles

B. SA node -> atria -> AV node -> Purkinje system -> ventricles

C. atria -> SA node -> AV node -> Purkinje system -> ventricles
D. AV node -> atria -> SA node -> ventricles -> Purkinje system
E. AV node -> atria -> Purkinje system -> SA node -> ventricles

Back 47

B. SA node -> atria -> AV node -> Purkinje system -> ventricles

Front 48

59. The following statement about the outputs of the left and right hearts is CORRECT:
A. The two outputs are in parallel.
B. The two outputs are in series.
C. The output of the left heart is usually about twice the output of the right heart.
D. The output of the right heart is usually about twice the output of the left heart.
E. The rate of the left heart is usually about twice the output of the right heart.

Back 48

B. The two outputs are in series.

Front 49

60. The following factors normally increase cardiac output.
A. Decreased heart rate.
B. Decreased plasma epinephrine.
C. Increased parasympathetic discharge.
D. Increased sympathetic nervous system discharge.
E. Decreased end diastolic ventricular volume.

Back 49

D. Increased sympathetic nervous system discharge.

Front 50

61. The following factors normally decrease cardiac output.
A. Increased heart rate.
B. Increased sympathetic nervous system discharge.
C. Decreased parasympathetic discharge.
D. Increased plasma epinephrine.
E. Decreased end diastolic ventricular volume.

Back 50

E. Decreased end diastolic ventricular volume.

Front 51

64. In a particular patient, stroke volume is 100 ml and left ventricular end diastolic volume is 200 ml. Ejection fraction is:
A. 200%
B. 150%
C. 100%
D. 50%
E. 25%

Back 51

D. 50%

Front 52

65. In a particular patient, stroke volume is 50 ml and left ventricular end diastolic volume is 200 ml. Ejection fraction is:
A. 200%
B. 150%
C. 100%
D. 50%
E. 25%

Back 52

E. 25%

Front 53

68. Increased cardiac contractility results from:
A. Phosphorylation of key proteins involved in regulation of cell calcium ion concentration.
B. Phosphorylation of nodal cell “funny” channels.
C. Inhibition of protein kinase A activity.
D. Decreased cellular cAMP.
E. Increased sarcomere length.

Back 53

A. Phosphorylation of key proteins involved in regulation of cell calcium ion concentration.

Front 54

69. Increased cardiac contractility results from:
A. Dephosphorylation of key proteins involved in regulation of cell calcium ion concentration.
B. Phosphorylation of nodal cell “funny” channels.
C. Stimulation of protein kinase A activity.
D. Decreased cellular cAMP.
E. Increased sarcomere length.

Back 54

C. Stimulation of protein kinase A activity.

Front 55

70. A change in cardiac contractility is a change in:
A. Force of contraction resulting from a change in sarcomere length.
B. Force of contraction resulting from a change in end diastolic volume.
C. Force of contraction resulting from a change in resting fiber length.
D. Force of contraction at a given end diastolic volume.
E. Force of contraction resulting from a change in overlap of actin and myosin.

Back 55

D. Force of contraction at a given end diastolic volume.

Front 56

71. Activation of beta adrenergic receptors changes cardiac muscle force of contraction by:
A. Increasing cellular cAMP.
B. Activation of tyrosine kinase.
C. Activation of phospholipase C.
D. Increasing cellular IP3.
E. Increasing cellular DAG.

Back 56

A. Increasing cellular cAMP.

Front 57

72. Increased contractility of cardiac muscle involves the phosphorylation of:
A. Protein kinase A.
B. Phospholamban.
C. Protein kinase C.
D. Inositol tris phosphate.
E. cAMP.

Back 57

B. Phospholamban.

Front 58

77. The best definition of pressure overload of the heart is:
A. A state in which a ventricle is required to develop an elevated systolic pressure in order to sustain an adequate cardiac output.
B. The inability of the heart to provide cardiac output sufficient to meet the metabolic needs of the body, or the ability to do so only at abnormally high left and/or right ventricular end diastolic pressures.
C. A state in which a ventricle is required to pump an elevated volume in order to sustain an adequate cardiac output.
D. The inability of the heart to provide cardiac output sufficient to meet the metabolic needs of the body because of reduced contractility.
E. The inability of the heart to provide cardiac output sufficient to meet the metabolic needs of the body because of reduced diastolic ventricular filling.

Back 58

A. A state in which a ventricle is required to develop an elevated systolic pressure in order to sustain an adequate cardiac output.

Front 59

78. With systolic dysfunction:
A. Ejection fraction is decreased.
B. Ejection fraction is increased.
C. End-diastolic ventricular volume is decreased.
D. Contractility is increased.
E. Cardiac output is increased.

Back 59

A. Ejection fraction is decreased.

Front 60

79. With diastolic dysfunction, at a normal diastolic left ventricular pressure:
A. Ejection fraction is decreased.
B. Contractility is decreased.
C. End diastolic ventricular volume is decreased.
D. Cardiac output is increased.
E. Ventricular diastolic compliance is increased.

Back 60

C. End diastolic ventricular volume is decreased.

Front 61

80. Myocardial ischemia:
A. Is defined as a region of myocardial necrosis.
B. Only causes systolic dysfunction.
C. Only causes diastolic dysfunction.
D. Causes both diastolic and systolic dysfunction.
E. Causes increased diastolic compliance.

Back 61

D. Causes both diastolic and systolic dysfunction.

Front 62

81. Mitral stenosis:
A. Results in a systolic murmur.
B. Only causes systolic dysfunction.
C. Only causes diastolic dysfunction.
D. Causes both diastolic and systolic dysfunction.
E. Causes increased diastolic compliance.

Back 62

C. Only causes diastolic dysfunction.

Front 63

82. Cardiac tamponade:
A. Results from cardiac fibrosis.
B. Only causes systolic dysfunction.
C. Is an accumulation of fluid around the heart limiting the ability of the ventricles to fill.
D. Causes reduced systemic venous pressure.
E. Causes elevated cardiac ouput.

Back 63

C. Is an accumulation of fluid around the heart limiting the ability of the ventricles to fill.

Front 64

83. Ventricular diastolic compliance:
A. Is increased by the accumulation of fibrous connective tissue.
B. Is decreased by incomplete relaxation.
C. Is independent of the supply of ATP to the calcium pumps.
D. Is reduced in physiologic hypertrophy.
E. Does not affect ventricular filling.

Back 64

B. Is decreased by incomplete relaxation.

Front 65

84. In chronic heart failure the hemodynamic defense reaction includes:
A. Increased contractility and heart rate.
B. Urinary loss of salt and water.
C. Reduced secretion of aldosterone.
D. Reduced secretion of vasopressin.
E. Reduced secretion of renin

Back 65

A. Increased contractility and heart rate.

Front 66

85. In chronic heart failure activation of the sympathetic nervous system:
A. Is the result of reduced plasma volume.
B. Results in decreased total peripheral resistance.
C. Results in partial restoration of stroke volume.
D. Is the result of increased firing of the arterial baroreceptors.
E. Results in dilation of peripheral veins.

Back 66

C. Results in partial restoration of stroke volume.

Front 67

96. In chronic heart failure, renal retention of salt and water increases blood volume, but leads to edema formation. A diuretic reduces edema by increasing the urinary loss of salt and water and causing a decrease in ___________ and an increase in __________:
A. Capillary hydrostatic pressure ………. interstitial hydrostatic pressure.
B. Capillary hydrostatic pressure ………. plasma protein concentration.
C. Interstitial hydrostatic pressure ……… interstitial protein concentration.
D. Plasma protein concentration ………. capillary hydrostatic pressure.
E. Interstitial hydrostatic pressure …….. interstitial protein concentration.

Back 67

B. Capillary hydrostatic pressure ………. plasma protein concentration.

Front 68

97. In chronic heart failure, pulmonary edema:
A. Results from right heart failure.
B. Raises the diffusion distance between alveolar air and capillary blood.
C. Raises pulmonary compliance.
D. Raises arterial oxygen saturation.
E. Raises ventilation perfusion equality.

Back 68

B. Raises the diffusion distance between alveolar air and capillary blood.

Front 69

98. With left heart failure, the mechanics of inspiration are changed. Compared to a normal individual, during inspiration:
A. Intrapleural pressure is lower (more negative).
B. Transpulmonary pressure is decreased.
C. Alveolar pressure is lower (more negative).
D. Pulmonary compliance is higher because of reduced surfactant.
E. PO2 at the end of pulmonary capillaries is increased.

Back 69

A. Intrapleural pressure is lower (more negative).

Front 70

100. There are several signaling pathways involved in cardiac hypertrophy. The following one is correct:
A. Norepinephrine -> Gs -> cAMP -> transcription factors
B. Angiotensin II -> Gs -> cAMP -> transcription factors
C. Aldosterone -> Gq -> IP3 -> calcium -> transcription factors
D. Cell stretch -> nuclear receptor -> translocation to
nucleus -> transcription factors
E. Aldosterone -> Gs -> cAMP -> transcription factors

Back 70

A. Norepinephrine -> Gs -> cAMP -> transcription factors

Front 71

101. The downward spiral of heart failure results from all of the following EXCEPT:
A. Abnormalities in proteins responsible for cell signaling.
B. Apoptosis
C. Necrosis
D. Growth of fibrous connective tissue
E. Drugs that block the effect of angiotensin II on the heart.

Back 71

E. Drugs that block the effect of angiotensin II on the heart.

Front 72

102. The downward spiral of heart failure results from all of the following EXCEPT:
A. Energy starvation.
B. Apoptosis
C. Drugs that block the effect of aldosterone on the heart.
D. Growth of fibrous connective tissue
E. Progressive dilatation (remodeling).

Back 72

C. Drugs that block the effect of aldosterone on the heart.

Front 73

103. The decreased effectiveness of the sympathetic nervous system (SNS) in the downward spiral of heart failure results from all of the following EXCEPT:
A. Decreased expression of Gs protein.
B. Decreased expression of Gi protein
C. Decreased numbers of beta-adrenergic receptors.
D. Reduced NE release from SNS nerve endings.
E. Decreased beta-adrenergic affinity for norepinephrine.

Back 73

B. Decreased expression of Gi protein

Front 74

104. With the downward spiral of heart failure, changes in the expression of proteins involved in excitation-contraction coupling include the following change in the sarcoplasmic reticulum:
A. Deceased copies of voltage gated sodium channels.
B. Decreased copies of calcium pumps.
C. Decreased copies of sodium/potassium pumps.
D. Increased copies of ryanodine receptors (release channels).
E. Increased copies of phospholamban.

Back 74

B. Decreased copies of calcium pumps.

Front 75

105. With the downward spiral of heart failure, changes in the expression of proteins involved in excitation-contraction coupling include the following change in the sarcoplasmic reticulum:
A. Decreased copies of voltage gated sodium channels.
B. Increased copies of calcium pumps.
C. Decreased copies of sodium/potassium pumps.
D. Increased copies of ryanodine receptors (release channels).
E. Decreased copies of phospholamban.

Back 75

E. Decreased copies of phospholamban.

Front 76

107. In chronic heart failure, norepinephrine and angiotensin II stimulate proliferation of:
A. Cardiac myocytes.
B. Sympathetic nerve endings.
C. Endothelial cells.
D. Fibroblasts.

Back 76

D. Fibroblasts.

Front 77

108. In chronic heart failure, aldosterone and vasopressin stimulate proliferation of:
A. Cardiac myocytes.
B. Sympathetic nerve endings.
C. Endothelial cells.
D. Fibroblasts.

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D. Fibroblasts.