FINAL EXAMINATION OF PHYSIOLOGY Date:January 14,2004 Time:8:30 a.m.-10:30 a.m. ANSWERS FOR REFERENCE I.MULTIPLE CHOICE QUESTIONS (20%) Select the single best answer 1.C2.B3.C4.E5.A6.A7.C 8.D9. C 10.D 2. II.TERMS (30%) 1.Threshold potential 2.Level of depolarization needed to trigger an action potential (most neurons have a threshold at -50 mV,i.e.10 to 15 mV depolarization). 3. 4.Blood coagulation 5.A process in which liquid blood is changed into a semisolid mass (a blood clot). 6. 7.Intrinsic factor (in stomach) 8.A substance secreted by the parietal cells of the stomach lining for the absorption of vitamin B12. 9. 10.Body temperature 11.Temperature of the body;normally 37 oC in humans;usually measured to obtain a quick evaluation of a person's health. 12. 13.Referred pain 14.Pain that is felt at a place in the body different from the injured or diseased part where the pain would be expected. 15
FINAL EXAMINATION OF PHYSIOLOGY Date: January 14, 2004 Time: 8:30 a.m.-10:30 a.m. ANSWERS FOR REFERENCE I. MULTIPLE CHOICE QUESTIONS (20%) Select the single best answer 1. C 2. B 3. C 4. E 5. A 6. A 7. C 8. D 9. C 10. D 2. II. TERMS (30%) 1. Threshold potential 2. Level of depolarization needed to trigger an action potential (most neurons have a threshold at -50 mV, i.e. 10 to 15 mV depolarization). 3. 4. Blood coagulation 5. A process in which liquid blood is changed into a semisolid mass (a blood clot). 6. 7. Intrinsic factor (in stomach) 8. A substance secreted by the parietal cells of the stomach lining for the absorption of vitamin B12. 9. 10. Body temperature 11. Temperature of the body; normally 37 oC in humans; usually measured to obtain a quick evaluation of a person's health. 12. 13. Referred pain 14. Pain that is felt at a place in the body different from the injured or diseased part where the pain would be expected. 15
16.Menstrual cycle 17.The monthly cycle of hormonal changes from the beginning of one menstrual period to the beginning of the next. 18. III.QUESTIONS (40%) 1.Describe the mechanism of the initiation and termination of action potential in neuron. 2.(1)Depolarization 3.Activation of Na+channel,Regenerative Cycle of Na+influx 4.(2)Repolarization 5.Inactivation of Na+channel 6.Activation of K+channel 7. 8.Describes the effects of arterial PC02,[H+]and P02 on alveolar ventilation and their mechanisms. 9.1)The normal range for arterial PC02 is 38-40 mm Hg.When this increases, even slightly,it results in deeper,more rapid respirations. 10.C02 penetrates blood-brain barrier,combines with H20 to form carbonic acid (H2C03).It is the hydrogen ion concentration [H+]in the cerebrospinal fluid that stimulates chemoreceptors located in the medulla oblongata. 11.2)Lowering the pH mainly stimulates the aortic and carotid bodies,leading to deeper,more rapid respirations,though to a limited extent. 12.3)a.A decrease in arterial blood P02 stimulates the chemoreceptors in the carotid and aortic bodies,causing reflex stimulation to the respiratory center and deeper,more rapid respirations. 13.b.A direct inhibitory effect on the respiratory center. 14. 15.What is glomerular filtration rate?Please list the factors affecting glomerular filtration
16. Menstrual cycle 17. The monthly cycle of hormonal changes from the beginning of one menstrual period to the beginning of the next. 18. III. QUESTIONS (40%) 1. Describe the mechanism of the initiation and termination of action potential in neuron. 2. (1) Depolarization 3. Activation of Na+ channel, Regenerative Cycle of Na+ influx 4. (2) Repolarization 5. Inactivation of Na+ channel 6. Activation of K+ channel 7. 8. Describes the effects of arterial PCO2, [H+] and PO2¯ on alveolar ventilation and their mechanisms. 9. 1) The normal range for arterial PCO2 is 38-40 mm Hg. When this increases, even slightly, it results in deeper, more rapid respirations. 10. CO2 penetrates blood-brain barrier, combines with H2O to form carbonic acid (H2CO3). It is the hydrogen ion concentration [H+] in the cerebrospinal fluid that stimulates chemoreceptors located in the medulla oblongata. 11. 2) Lowering the pH mainly stimulates the aortic and carotid bodies, leading to deeper, more rapid respirations, though to a limited extent. 12. 3) a. A decrease in arterial blood PO2 stimulates the chemoreceptors in the carotid and aortic bodies, causing reflex stimulation to the respiratory center and deeper, more rapid respirations. 13. b. A direct inhibitory effect on the respiratory center. 14. 15. What is glomerular filtration rate? Please list the factors affecting glomerular filtration
16.Definition:The quantity of glomerular filtrate formed per unit time in all nephrons of both kidneys,125 ml/min. 17.Factors:Renal arterial pressure 18.Intrabular pressure 19.Glomerular surface area 20.Total renal plasma flow 21. 22.What are the endocrinologic causes of dwarfism and cretinism,and how does each lead to short stature? 23.Dwarfism:Growth hormone deficiency 24.Cretinism:Lack of thyroid hormone 25.Biological effects of growth hormone and thyroid hormone on physical development 26. 27. IV.CASE (10%) 1.As the K+concentration rises in the interstitial fluid of the ischemic zone, the ratio of the intracellular K+concentration ([K+]i)to the extracellular K+ concentration ([K+]o)would decrease.The myocardial cell membranes at rest (phase 4)are much more permeable to K+than to any other relevant ion.Hence,the resting membran potential is very close to that estimated by the Nernst equation for K+. As the [K+]i/[K+]o ratio diminishes,the resting membrane potential becomes less negative,as predicted by the Nernst equation. 2. 3.The fast Na+channels in the myocardial cell membranes are voltage sensitive. As the resting membrane potential of myocardial cells becomes progressively less negative (i.e.,partially depolarized),more and more of the fast Na+channels in those cells become inactivated because of their voltage dependency.Hence,when the wave of excitation reaches the partially depolarized cells,a diminished number of fast Na+channels are available to be activated.The upstroke of the action potential
16. Definition: The quantity of glomerular filtrate formed per unit time in all nephrons of both kidneys, ~125 ml/min. 17. Factors: Renal arterial pressure 18. Intrabular pressure 19. Glomerular surface area 20. Total renal plasma flow 21. 22. What are the endocrinologic causes of dwarfism and cretinism, and how does each lead to short stature? 23. Dwarfism: Growth hormone deficiency 24. Cretinism: Lack of thyroid hormone 25. Biological effects of growth hormone and thyroid hormone on physical development 26. 27. IV. CASE (10%) 1. As the K+ concentration rises in the interstitial fluid of the ischemic zone, the ratio of the intracellular K+ concentration ([K+]i) to the extracellular K+ concentration ([K+]o) would decrease. The myocardial cell membranes at rest (phase 4) are much more permeable to K+ than to any other relevant ion. Hence, the resting membran potential is very close to that estimated by the Nernst equation for K+. As the [K+]i/[K+]o ratio diminishes, the resting membrane potential becomes less negative, as predicted by the Nernst equation. 2. 3. The fast Na+ channels in the myocardial cell membranes are voltage sensitive. As the resting membrane potential of myocardial cells becomes progressively less negative (i.e., partially depolarized), more and more of the fast Na+ channels in those cells become inactivated because of their voltage dependency. Hence, when the wave of excitation reaches the partially depolarized cells, a diminished number of fast Na+ channels are available to be activated. The upstroke of the action potential
in myocardial cells is mediated by the influx of Na+through the fast Na+channels. In the myocardial cells in the ischemic zone of the heart,fewer Na+channels are available for activation than in the myocardial cells in the normal regions of the heart.Therefore,in the ischemic cells,the upstroke of the action potential is less steep than normal,and the amplitude of the action potential is diminished. The velocity of impulse propagation varies directly with the amplitude and with the slope of the upstroke of the action potential.Hence,propagation is abnormally slow in the ischemic zone. 4. 5.The firing rate of the SA node cells would diminish as a consequence of the increased vagal activity.The acetylcholine (ACh)released from the vagus nerve endings activates the ACh-regulated K+channels and decreases the conductance of the If channels.The increased K+conductance tends to hyperpolarize the automatic cell membranes,and therefore the transmembrane potential at the beginning of slow diastolic depolarization is more negative than it is in the absence of vagal activity. This would tend to increase the cardiac cycle length (i.e.,decrease heart rate). Also,the vagally induced diminution of the conductance of the If channels would reduce the influx of Na+into the cell,and would thereby decrease the slope of slow diastolic depolarization.This also would tend to decrease heart rate. 6. 7.Increased vagal activity tends to retard AV conduction;that is,the time from the beginning of arterial depolarization to the beginning of ventricular depolarization may be prolonged.Intense vagal activity may even prevent the cardiac impulse from being propagated from the atria to the ventricles.The ACh released from the vagus nerve endings in the AV node activates the ACh-regulated K+channels and thereby hyperpolarizes the conducting fibers in the AV node.The neurally released ACh also tends to decrease the Ca2+current through the Ca2+channels in the cell membranes of the conducting fibers (which are slow-response fibers).The effects of the ACh on the K+and Ca2+currents tend to impede Av conduction. 8
in myocardial cells is mediated by the influx of Na+ through the fast Na+ channels. In the myocardial cells in the ischemic zone of the heart, fewer Na+ channels are available for activation than in the myocardial cells in the normal regions of the heart. Therefore, in the ischemic cells, the upstroke of the action potential is less steep than normal, and the amplitude of the action potential is diminished. The velocity of impulse propagation varies directly with the amplitude and with the slope of the upstroke of the action potential. Hence, propagation is abnormally slow in the ischemic zone. 4. 5. The firing rate of the SA node cells would diminish as a consequence of the increased vagal activity. The acetylcholine (ACh) released from the vagus nerve endings activates the ACh-regulated K+ channels and decreases the conductance of the If channels. The increased K+ conductance tends to hyperpolarize the automatic cell membranes, and therefore the transmembrane potential at the beginning of slow diastolic depolarization is more negative than it is in the absence of vagal activity. This would tend to increase the cardiac cycle length (i.e., decrease heart rate). Also, the vagally induced diminution of the conductance of the If channels would reduce the influx of Na+ into the cell, and would thereby decrease the slope of slow diastolic depolarization. This also would tend to decrease heart rate. 6. 7. Increased vagal activity tends to retard AV conduction; that is, the time from the beginning of arterial depolarization to the beginning of ventricular depolarization may be prolonged. Intense vagal activity may even prevent the cardiac impulse from being propagated from the atria to the ventricles. The ACh released from the vagus nerve endings in the AV node activates the ACh-regulated K+ channels and thereby hyperpolarizes the conducting fibers in the AV node. The neurally released ACh also tends to decrease the Ca2+ current through the Ca2+ channels in the cell membranes of the conducting fibers (which are slow-response fibers). The effects of the ACh on the K+ and Ca2+ currents tend to impede AV conduction. 8
9.When conduction in the AV node or bundle of His is blocked,the atrial and ventricular rhythms are "dissociated."The arterial rhythm will be set by the SA node,and the arterial rate will usually be between 60 and 90 beats/min.The ventricular rhythm will be set by specialized conduction (Purkinje)fibers,which would discharge at rates of about 30 to 45 beats/min
9. When conduction in the AV node or bundle of His is blocked, the atria1 and ventricular rhythms are "dissociated." The arterial rhythm will be set by the SA node, and the arterial rate will usually be between 60 and 90 beats/min. The ventricular rhythm will be set by specialized conduction (Purkinje) fibers, which would discharge at rates of about 30 to 45 beats/min