1. What do antiporters in cell membranes do?
A. Move single solutes out of a cell
B. Move two solutes together out of a cell
C. Move one solute in and another solute out of a cell
D. Actively transport single solutes using the energy of adenosine triphosphate (ATP)
E. Move single solutes in whichever direction is against their concentration gradient
2. A patient poisoned with cyanide cannot utilize ATP. Which of the following transport processes would be most directly affected by this loss?
A. Transport of Na+ out of cells
B. Transport of glucose into red blood cells
C. Transport of amino acids into cells
D. Osmosis of water into cells
E. Diffusion of CO2out of cells.
3. A neurotoxin is applied to resting skeletal muscle cells, irreversibly increasing sodium conductance but having no effect on potassium conductance. The transmembrane potential will
C. not change.
D. transiently hyperpolarize, then return to what it was before applying the neurotoxin.
E. transiently depolarize, then return to what it was before applying the neurotoxin.
4. After reaching the peak of the action potential, nerve fibers repolarize rapidly because
A. K+ channels are inactivated.
B. Na+ channels are activated.
C. Na+ channels are inactivated.
D. there are no net ionic fluxes.
E. the Na+−K+ ATPase removes the Na+ that entered during the rising phase.
5. Before open heart surgery, a patient’s heart might be stopped by injecting isotonic potassium chloride (KCl) into the coronary arteries. Which of the following mechanisms produces this effect?
A. The cardiac muscle membrane potentials would fall to near zero.
B. The Na+−K+ ATPase pump is inhibited.
C. K+ flows freely into cardiac myocytes.
D. Cl− equilibrates across cardiac myocyte membranes.
E. Ca2+ leaks out of the cardiac myocytes.
6. Synaptic inhibition may be caused by
A. increase in Cl− conductance at the postsynaptic membrane.
B. increase in Ca2+ conductance at the postsynaptic membrane.
C. decrease in K+ conductance at the postsynaptic membrane.
D. increase in Na+ conductance at the postsynaptic membrane.
E. increase in Ca2+ conductance at the presynaptic membrane.
7. Stretch of muscle fibers
A. is a direct cause of contraction in some smooth muscles.
B. has no effect on contraction in visceral smooth muscle.
C. induces contraction only when mediated by acetylcholine.
D. causes a direct and sustained contraction in skeletal muscle.
E. has no effect on the strength of contraction in skeletal muscle.
8. Before suturing a deep skin wound, the physician infiltrates the surrounding tissue with lidocaine. How does this block transmission in pain fibers?
A. It facilitates Na+ influx into nerve fibers.
B. It promotes K+ efflux from nerve fibers.
C. It blocks Na+ channel activation, which prevents generation of action potentials.
D. It blocks the Na+−K+ ATPase pump.
E. It depolarizes the nerve fibers’ membrane potentials.
9. Why does a patient with myasthenia gravis have muscle weakness?
A. Decreased presynaptic Ca2+-binding sites
B. Decreased postsynaptic acetylcholine receptor sites
C. Decreased release of acetylcholine from motor nerve terminals
D. Decreased myelin on motor nerve fibers
E. Decreased Ca2+ in the muscle fiber sarcoplasmic reticulum
10. When the arm is fully outstretched, which of the following is true about the biceps muscle?
A. The muscle is at its best mechanical advantage for flexing the forearm.
B. The overlap between thick and thin filaments in the muscle fibers is at a maximum.
C. The muscle can develop more force at this position than when the arm is flexed.
D. The muscle cannot be stimulated tetanically.
E. Shortening the muscle will allow more neuromuscular junctions to be activated.
11. Why do muscles undergo rigor mortis immediately after death?
A. Most of the Ca2+ is sequestered into the sarcoplasmic reticulum.
B. The cross-bridges are cycling in a tetanic contraction.
C. Myosin and actin are separated and cannot interact.
D. Myosin heads are unable to detach from actin thin filaments.
E. ATP molecules remain bound to myosin heads
12. What would be the effect on the heart of treating a cardiac patient with a calcium channel–blocking drug?
A. Increased preload
B. Increased Ca2+ stored within the sarcoplasmic reticulum of cardiac myocytes
C. Increased contractility
D. No change in contractility
E. Decreased contractility
Answers and Explanations
1. C Antiporters, also called exchangers, move two solutes in opposite directions (therefore B is incorrect) using the energy from moving one solute with its electrochemical gradient to move the other solute against its electrochemical gradient (p. 5).
A,E Antiporters always move two solute species.
D Although some primary active transporters move solutes in opposite directions (e.g., the Na+−K+ ATPase), they use the energy of ATP rather than the electrochemical gradient of one of the solutes to provide the energy.
2. A Although all of these processes would ultimately be affected, the Na+−K+ pump uses ATP directly and would be affected first (p. 4).
B Glucose is transported into red blood cells by a uniporter.
C Amino acids are transported into cells by secondary active transport.
D Osmosis is passive and depends only on the concentration of particles in the cells.
E CO2 and O2 move across cell membranes by free diffusion.
3. B Any increase in Na+ conductance relative to K+ conductance will depolarize the membrane (p. 13).
A,D An increase of K+ conductance relative to Na+ conductance will hyperpolarize the membrane.
C,E The depolarization continues as long as the high Na+ conductance is maintained by the toxin.
4. C Na+ channel inactivation lowers the inward Na+ current and allows the outward K+ current to repolarize the membrane (p. 13).
A K+ channel inactivation would depolarize, not repolarize.
B Na+ channel activation generates the rising phase of the action potential.
D There is a net outward ionic flux.
E Although the Na+−K+ ATPase contributes a small outward current at all times, it is the transiently high outward K+ current that drives the falling phase of the action potential.
5. A The membrane potential in cardiac myocytes depends primarily on a K+ concentration difference, which would be near zero with isotonic KCl outside the muscle cells (p. 12). With a zero membrane potential, action potentials cannot be generated.
B The pump is not affected.
C K+ concentration is the same inside and outside of the cells because they are bathed in an isotonic solution, and so K+will not flow into the myocytes.
D Cl− passively follows the cations and does not affect membrane potential differences.
E Ca2+ would still remain within depolarized cells.
6. A An increase in chloride conductance hyperpolarizes and/or clamps the membrane potential and inhibits depolarization of the postsynaptic membrane by an excitatory postsynaptic potential (EPSP) (p. 19).
B–D An increase in Ca2+ or Na+ conductance or a decrease in K+ conductance would depolarize the postsynaptic membrane.
E An increase in Ca2+ conductance at the presynaptic membrane would cause the release of a neurotransmitter.
7. A Stretch can cause depolarization and generation of action potentials in some smooth muscle, including visceral muscles (B), due to the opening of stretch-gated channels.
C Stretch acts directly on the cell membrane without a neurotransmitter.
D,E Stretch does not depolarize skeletal muscle fibers, but stretch will change the overlap of thick and thin filaments and alter the strength of contraction.
8. C Lidocaine blocks Na+ channels, which prevents the generation of action potentials and thus blocks transmission of sensory information in pain fibers.
A,B Lidocaine does not increase Na+ influx into or K+ efflux from nerve fibers.
D,E Lidocaine does not affect the pump or the membrane potential.
9. B A reduced number of acetylcholine receptor sites makes the muscle fibers less sensitive to released acetylcholine. When some of the fibers fail to respond to neural stimulation, this produces muscle weakness (p. 19).
A Presynaptic Ca2+ binding is normal.
C The amount of acetylcholine released declines somewhat with normal use but is adequate except when there is a deficit in receptors at the postjunctional membrane.
D Myasthenia gravis does not affect myelination.
E Ca2+ within muscle fibers is unaffected.
10. C As described by the length–force curve, the greatest force can be developed at the maximum physiological length (p. 25).
A Although muscle force is maximized, the fully extended position offers the least mechanical advantage.
B Overlap between thick and thin filaments increases as the muscle shortens. With the arm fully outstretched, the overlap is at a minimum.
D A muscle can be stimulated tetanically at any length.
E Muscle length does not affect neuromuscular junctions.
11. D It requires binding of ATP to detach cross-bridges from actin- binding sites. This cannot occur once ATP becomes depleted (pp. 24–25).
A The depletion of ATP allows Ca2+ to escape from the sarcoplasmic reticulum.
B The cross-bridges are fixed, not cycling.
C Myosin and actin are attached.
E ATP is depleted and is not available to bind.
12. E Calcium channel–blocking drugs reduce the influx of Ca2+. This reduces the stimulating effect of Ca2+ influx, so contractility falls (p. 28).
A Preload is a function of filling pressure, not ionic flux.
B Over time, the decreased Ca2+ entry would lead to lower Ca2+ stored in the sarcoplasmic reticulum.
C,D Contractility is proportional to intracellular Ca2+ concentration during systole, so it is reduced.