BMS204 L14 QS Bank PDF

Quiz on Regulation of COP Part One: Simple MCQs (15 questions) 1. Which of the following is NOT a mechanism of intrinsic regulation of Cardiac Output (COP)? a) Starling's Law b) Heterometric Autoregulation c) Sympathetic Stimulation d) Homeometric Autoregulation 2. What is the effect...

Quiz on Regulation of COP Part One: Simple MCQs (15 questions) 1. Which of the following is NOT a mechanism of intrinsic regulation of Cardiac Output (COP)? a) Starling's Law b) Heterometric Autoregulation c) Sympathetic Stimulation d) Homeometric Autoregulation 2. What is the effect of increased sympathetic stimulation on the heart rate? a) Decreases heart rate b) No effect on heart rate c) Increases heart rate d) Stabilizes heart rate 3. Which hormone directly increases heart rate by affecting the metabolism of the Sinoatrial Node (SAN)? a) Glucagon b) Thyroxine c) Corticosteroids d) Catecholamines 4. What is the primary effect of parasympathetic stimulation on the heart? a) Increases heart rate b) Decreases heart rate  c) Increases stroke volume d) Decreases stroke volume 5. Which of the following is an example of a xanthine derivative that can increase the force of cardiac contraction? a) Acetylcholine b) Caffeine c) Digitalis d) Ephedrine 6. What does the term "preload" refer to in the context of cardiac function? a) Afterload b) End-diastolic volume c) Stroke volume d) Cardiac output 7. Which of the following is a cause of physiological hypertrophy of the heart? a) Aortic stenosis b) Hypertension c) Continued strenuous exercise d) Myocardial ischemia 8. What is the maximum heart rate that can significantly increase cardiac output? a) 75 beats/min b) 140 beats/min c) 200 beats/min d) 250 beats/min 9. Which of the following is NOT a cause of pathological hypertrophy of the heart? a) Aortic stenosis b) Systemic hypertension c) Long-distance running d) Aortic regurgitation 10. What is the effect of acetylcholine on cardiac output? a) Increases cardiac output b) Decreases cardiac output c) No effect on cardiac output d) Stabilizes cardiac output 11. Which of the following is NOT a catecholamine that can increase cardiac output? a) Ephedrine b) Amphetamine c) Norepinephrine d) Acetylcholine 12. What is the primary mechanism by which digitalis increases cardiac output in heart failure patients? a) Increasing heart rate b) Decreasing heart rate c) Increasing the force of contraction d) Decreasing the force of contraction 13. Which of the following factors can decrease the force of cardiac contraction and thus decrease cardiac output?  a) Oxygen excess b) Carbon dioxide lack c) Alkalosis d) Myocardial ischemia 14. What is the term for the difference between cardiac work at rest and at maximal exercise? a) Cardiac output b) Stroke volume c) Cardiac reserve d) Ejection fraction 15. Which of the following is NOT a mechanism of cardiac reserve? a) Heart rate reserve b) Stroke volume reserve c) Hypertrophy d) Hypotension Part Two: Complex MCQs (20 questions) 1. How does the homeometric autoregulation of cardiac output primarily differ from heterometric autoregulation? a) Homeometric autoregulation involves changes in end-diastolic volume. b) Homeometric autoregulation is a transient response to increased preload. c) Homeometric autoregulation is a sustained response to increased afterload. d) Homeometric autoregulation is primarily mediated by the autonomic nervous system. 2. Explain the role of the autonomic nervous system in regulating cardiac output. a) The autonomic nervous system only regulates heart rate. b) The autonomic nervous system only regulates stroke volume. c) The autonomic nervous system regulates both heart rate and stroke volume through sympathetic and parasympathetic stimulation. d) The autonomic nervous system plays no role in regulating cardiac output. 3. How does an increase in preload lead to an increase in cardiac output, according to Starling's Law? a) Increased preload directly increases heart rate. b) Increased preload decreases stroke volume. c) Increased preload increases the force of cardiac contraction by stretching the ventricular muscle fibers. d) Increased preload activates the sympathetic nervous system. 4. What is the significance of the observation that end-diastolic volume returns to normal during homeometric autoregulation, while the stroke volume remains elevated? a) It indicates that the heart is not working as efficiently. b) It suggests that the increased cardiac output is solely due to increased heart rate. c) It implies that the contractility of the heart has increased, allowing for more efficient ejection of blood. d) It demonstrates that the autonomic nervous system is not involved in this type of regulation. 5. How does an increase in afterload affect cardiac output?  a) Increased afterload initially decreases cardiac output, followed by a compensatory increase through homeometric autoregulation. b) Increased afterload directly increases cardiac output by increasing stroke volume. c) Increased afterload has no effect on cardiac output. d) Increased afterload only affects heart rate. 6. What is the primary mechanism by which hypertrophy increases cardiac reserve? a) By increasing heart rate. b) By decreasing stroke volume. c) By increasing the force of contraction and allowing for greater ejection of blood with each beat. d) By decreasing the end-diastolic volume. 7. Why does excessive increase in heart rate eventually lead to a decrease in cardiac output? a) It leads to fatigue of the cardiac muscle. b) It shortens the diastolic period, reducing ventricular filling time and thus decreasing stroke volume. c) It decreases the force of contraction. d) It increases the end-systolic volume. 8. What are the limits of cardiac reserve? a) Heart rate limits, excessive vasodilation, and hypertrophy. b) Stroke volume limits, excessive vasoconstriction, and atrophy. c) Heart rate limits, excessive dilatation, and hypertrophy. d) Blood volume limits, excessive vasodilation, and atrophy. 9. What is the difference between physiological and pathological hypertrophy?  a) Physiological hypertrophy is beneficial, while pathological hypertrophy is always harmful. b) Physiological hypertrophy is caused by exercise, while pathological hypertrophy is caused by diseases. c) Physiological hypertrophy increases cardiac output, while pathological hypertrophy decreases cardiac output. d) Physiological hypertrophy is reversible, while pathological hypertrophy is irreversible. 10. How does oxygen lack affect cardiac output? a) Oxygen lack increases cardiac output. b) Oxygen lack decreases cardiac output by reducing the force of contraction. c) Oxygen lack has no effect on cardiac output. d) Oxygen lack only affects heart rate. 11. What is the role of catecholamines in regulating cardiac output? a) Catecholamines decrease heart rate and stroke volume. b) Catecholamines increase heart rate and the force of contraction, thus increasing cardiac output. c) Catecholamines have no effect on cardiac output. d) Catecholamines only affect the venous return. 12. How does the Frank-Starling mechanism contribute to the regulation of cardiac output? a) It ensures that the left and right ventricles pump the same amount of blood. b) It allows the heart to adapt to changes in venous return by adjusting the stroke volume. c) It prevents the heart from overfilling. d) All of the above. 13. What is the effect of increased peripheral resistance on cardiac output? a) Increased peripheral resistance increases cardiac output. b) Increased peripheral resistance decreases cardiac output. c) Increased peripheral resistance has no effect on cardiac output. d) Increased peripheral resistance only affects heart rate. 14. How does the sympathetic nervous system affect venous return? a) It decreases venous return by constricting veins. b) It increases venous return by constricting veins. c) It has no effect on venous return. d) It only affects the heart rate. 15. What is the significance of the rapid relaxation of the ventricles caused by forceful contraction due to sympathetic stimulation? a) It helps in more filling of the ventricles during diastole, increasing end-diastolic volume and thus stroke volume. b) It helps to reduce the workload on the heart. c) It prevents the heart from overfilling. d) It has no significant effect on cardiac function. 16. Why is excessive dilatation of the heart detrimental to cardiac output? a) It increases the heart rate excessively. b) It reduces the force of contraction, thus decreasing stroke volume. c) It decreases the end-diastolic volume. d) It leads to hypertrophy. 17. How does myocardial ischemia affect cardiac output? a) Myocardial ischemia increases cardiac output.  b) Myocardial ischemia decreases cardiac output by reducing the force of contraction. c) Myocardial ischemia has no effect on cardiac output. d) Myocardial ischemia only affects heart rate. 18. What is the role of the heart rate reserve in increasing cardiac output during exercise? a) It allows the heart to increase the stroke volume significantly. b) It enables the heart to pump more blood by increasing the number of beats per minute. c) It has no role in increasing cardiac output during exercise. d) It only affects the venous return. 19. How does the stroke volume reserve contribute to the increase in cardiac output during exercise? a) It allows the heart to increase the heart rate significantly. b) It enables the heart to pump more blood with each beat by increasing the stroke volume. c) It has no role in increasing cardiac output during exercise. d) It only affects the venous return. 20. Why is excessive hypertrophy detrimental to cardiac output in the long term? a) It leads to excessive vasodilation. b) It may outgrow its blood supply, leading to ischemia and decreased contractility. c) It reduces the heart rate excessively. d) It decreases the stroke volume. Answer Guide: Part One:  1. c 2. c 3. b 4. b 5. b 6. b 7. c 8. b 9. c 10. b 11. d 12. c 13. d 14. c 15. d Part Two: 1. c 2. c 3. c 4. c 5. a 6. c 7. b 8. c  9. b 10. b 11. b 12. d 13. b 14. b 15. a 16. b 17. b 18. b 19. b 20. b Done