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Rush - Advanced Pharmacology -
NSG 531 - Exam 3 Questions and
Correct Answers the Latest Update
what is the difference between cardiac myocyte action potential and that of the
CNS or ANS?
✓ nerve cell action potential is very short
✓ cardiac action potential is much longer
✓ they are longer to have adequate filling time in order to get a good contraction for a
reasonable bolus of blood
✓ the only way this can happen is if the action potential is longer
✓ this will also mean that the refractory period will be longer
What are the 5 phases of the non-pacemaker action potential?
✓ 0 - depolarization
✓ 1 - partial repolarization
✓ 2 - plateau
✓ 3 - repolarization
✓ 4 - resting membrane potential
what happens during phase 0 of the non-pacemaker action potential
✓ depolarization
✓ voltage gated sodium channels are opening up until we get past threshold
what happens during phase 1 of the non-pacemaker action potential
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✓ partial repolarization
what happens during phase 2 of the non-pacemaker action potential
✓ plateau
✓ calcium channels open (L-type because they are long)
✓ potassium is still open
✓ potassium out and calcium in - they are opposing each other in voltage giving the
plateau
✓ this is when the ventricles are filling
what happens during phase 3 of the non-pacemaker action potential
✓ repolarization
✓ calcium channels are closed
✓ potassium channels are the only thing open taking their positive charge with them
making the interior more negative
what happens during phase 4 of the non-pacemaker action potential
✓ resting membrane potential where we are in between action potentials there is no
net change in ovltage inside the cell
When does contraction take place?
✓ begins towards the end of repolarization and ends at some point during
repolarization
refractory period
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✓ during phase 0, 1, 2, and part of phase 3 the cell is refractory to the initiation of new
action potentials
✓ many antiarrhythmic drugs increase the Refractory period which reduces myocyte
excitability
what are the benefits of the refractory period
✓ limits frequency of cardiac contractions
✓ allows for adequate filling time
✓ prevents sustained contractions
how are pacemaker cells different from non-pacemaker cell
✓ no resting membrane potential - no point where it is flat
✓ there are very few sodium channels in pacemaker - sodium channels are not driving
depolarization - calcium is
✓ only 3 phases
✓ comprised of cells within the SA node
✓ generate regular, spontaneous action potentials
what are the phases of pacemaker action potential
✓ 0 - rapid depolarization
✓ 3 - repolarization
✓ 4 - slow depolarization
what happens during phase 0 of the pacemaker action potential
✓ Rapid depolarization
✓ something is coming to open voltage gated calcium channels (L-type) calcium comes
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rushing in
what happens during phase 3 of the pacemaker action potential
✓ repolarization
✓ potassium channels now open up, potassium rushes out, repolarizes
what happens during phase 4 of the pacemaker action potential
✓ slow depolarization
✓ with potassium rushing out we are all the way down at -60
✓ funny sodium channels open up until voltage reaches -50
✓ T-type (transient) calcium channels open up until voltage reaches -40
✓ L-type calcium channels then open back up
Describe how non-pacemaker APs can mimic pacemkaer APs
✓ Hypoxia and ischemia
✓ when the resting membrane potential is not getting enough oxygen it is going to
become more positive because you need oxygen to produce ATP. If we are deficient
in ATP then the NA K ATPase pump wont be functioning
✓
✓ if someone is hypoxic in a focal area - say they have a resting membrane potential at
-45 - the fast sodium channels won't open - they start using calcium to open - so
they would convert into action potentials that use calcium (hence how they mimic
pacemaker APs)
excitation-contraction coupling
✓ sequence of events from motor neuron signaling to a skeletal muscle fiber to
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Rush - Advanced Pharmacology -
NSG 531 - Exam 3 Questions and
Correct Answers the Latest Update
what is the difference between cardiac myocyte action potential and that of the
CNS or ANS?
✓ nerve cell action potential is very short
✓ cardiac action potential is much longer
✓ they are longer to have adequate filling time in order to get a good contraction for a
reasonable bolus of blood
✓ the only way this can happen is if the action potential is longer
✓ this will also mean that the refractory period will be longer
What are the 5 phases of the non-pacemaker action potential?
✓ 0 - depolarization
✓ 1 - partial repolarization
✓ 2 - plateau
✓ 3 - repolarization
✓ 4 - resting membrane potential
what happens during phase 0 of the non-pacemaker action potential
✓ depolarization
✓ voltage gated sodium channels are opening up until we get past threshold
what happens during phase 1 of the non-pacemaker action potential
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✓ partial repolarization
what happens during phase 2 of the non-pacemaker action potential
✓ plateau
✓ calcium channels open (L-type because they are long)
✓ potassium is still open
✓ potassium out and calcium in - they are opposing each other in voltage giving the
plateau
✓ this is when the ventricles are filling
what happens during phase 3 of the non-pacemaker action potential
✓ repolarization
✓ calcium channels are closed
✓ potassium channels are the only thing open taking their positive charge with them
making the interior more negative
what happens during phase 4 of the non-pacemaker action potential
✓ resting membrane potential where we are in between action potentials there is no
net change in ovltage inside the cell
When does contraction take place?
✓ begins towards the end of repolarization and ends at some point during
repolarization
refractory period
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✓ during phase 0, 1, 2, and part of phase 3 the cell is refractory to the initiation of new
action potentials
✓ many antiarrhythmic drugs increase the Refractory period which reduces myocyte
excitability
what are the benefits of the refractory period
✓ limits frequency of cardiac contractions
✓ allows for adequate filling time
✓ prevents sustained contractions
how are pacemaker cells different from non-pacemaker cell
✓ no resting membrane potential - no point where it is flat
✓ there are very few sodium channels in pacemaker - sodium channels are not driving
depolarization - calcium is
✓ only 3 phases
✓ comprised of cells within the SA node
✓ generate regular, spontaneous action potentials
what are the phases of pacemaker action potential
✓ 0 - rapid depolarization
✓ 3 - repolarization
✓ 4 - slow depolarization
what happens during phase 0 of the pacemaker action potential
✓ Rapid depolarization
✓ something is coming to open voltage gated calcium channels (L-type) calcium comes
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rushing in
what happens during phase 3 of the pacemaker action potential
✓ repolarization
✓ potassium channels now open up, potassium rushes out, repolarizes
what happens during phase 4 of the pacemaker action potential
✓ slow depolarization
✓ with potassium rushing out we are all the way down at -60
✓ funny sodium channels open up until voltage reaches -50
✓ T-type (transient) calcium channels open up until voltage reaches -40
✓ L-type calcium channels then open back up
Describe how non-pacemaker APs can mimic pacemkaer APs
✓ Hypoxia and ischemia
✓ when the resting membrane potential is not getting enough oxygen it is going to
become more positive because you need oxygen to produce ATP. If we are deficient
in ATP then the NA K ATPase pump wont be functioning
✓
✓ if someone is hypoxic in a focal area - say they have a resting membrane potential at
-45 - the fast sodium channels won't open - they start using calcium to open - so
they would convert into action potentials that use calcium (hence how they mimic
pacemaker APs)
excitation-contraction coupling
✓ sequence of events from motor neuron signaling to a skeletal muscle fiber to
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