RUSH - ADVANCED PHARMACOLOGY - NSG 531 - EXAM 3
QUESTIONS AND CORRECT ANSWERS
1.what is the difference between cardiac myocyte action potential and that of the CNS or ANS? -
(answer)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? - (answer)0 - depolarization
1 - partial repolarization
2 - plateau
3 - repolarization
4 - resting membrane potential
what happens during phase 0 of the non-pacemaker action potential - (answer)depolarization
voltage gated sodium channels are opening up until we get past threshold
what happens during phase 1 of the non-pacemaker action potential - (answer)partial repolarization
what happens during phase 2 of the non-pacemaker action potential - (answer)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 - (answer)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 - (answer)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? - (answer)begins towards the end of repolarization and ends at some
point during repolarization
refractory period - (answer)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 - (answer)limits frequency of cardiac contractions
allows for adequate filling time
prevents sustained contractions
how are pacemaker cells different from non-pacemaker cell - (answer)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 - (answer)0 - rapid depolarization
3 - repolarization
4 - slow depolarization
what happens during phase 0 of the pacemaker action potential - (answer)Rapid depolarization
something is coming to open voltage gated calcium channels (L-type) calcium comes rushing in
, what happens during phase 3 of the pacemaker action potential - (answer)repolarization
potassium channels now open up, potassium rushes out, repolarizes
what happens during phase 4 of the pacemaker action potential - (answer)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 - (answer)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 - (answer)sequence of events from motor neuron signaling to a skeletal
muscle fiber to contraction of the fiber's sarcomeres
conversion of depolarizing currents into contractile force
L-type calcium channels open up in phase 2 in nonpacemaker - calcium comes flooding into myocytes, so
we now have calcium in the cell and a sarcoplasmic recticulum (a resovior for calcium)
receptors called RYR (ligand gated calcium channels)
calcium then comes out - coming int the cell from the calcium channels and the sarcoplasmic recticulum
describe how calcium binds to cause contraction - (answer)when there is an influx of calcium in the cell
there is a myosin head separated by troponin. little binding sites for the myosin exist on the aktin but it
can't get to it because of the troponin. calcium therefore binds to the tropinin causing a confirmational
change in troponin so it will move and take the tropomyosin with it. the myosin can then bind to the
aktin molecules when it binds it activates ATP
QUESTIONS AND CORRECT ANSWERS
1.what is the difference between cardiac myocyte action potential and that of the CNS or ANS? -
(answer)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? - (answer)0 - depolarization
1 - partial repolarization
2 - plateau
3 - repolarization
4 - resting membrane potential
what happens during phase 0 of the non-pacemaker action potential - (answer)depolarization
voltage gated sodium channels are opening up until we get past threshold
what happens during phase 1 of the non-pacemaker action potential - (answer)partial repolarization
what happens during phase 2 of the non-pacemaker action potential - (answer)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 - (answer)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 - (answer)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? - (answer)begins towards the end of repolarization and ends at some
point during repolarization
refractory period - (answer)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 - (answer)limits frequency of cardiac contractions
allows for adequate filling time
prevents sustained contractions
how are pacemaker cells different from non-pacemaker cell - (answer)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 - (answer)0 - rapid depolarization
3 - repolarization
4 - slow depolarization
what happens during phase 0 of the pacemaker action potential - (answer)Rapid depolarization
something is coming to open voltage gated calcium channels (L-type) calcium comes rushing in
, what happens during phase 3 of the pacemaker action potential - (answer)repolarization
potassium channels now open up, potassium rushes out, repolarizes
what happens during phase 4 of the pacemaker action potential - (answer)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 - (answer)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 - (answer)sequence of events from motor neuron signaling to a skeletal
muscle fiber to contraction of the fiber's sarcomeres
conversion of depolarizing currents into contractile force
L-type calcium channels open up in phase 2 in nonpacemaker - calcium comes flooding into myocytes, so
we now have calcium in the cell and a sarcoplasmic recticulum (a resovior for calcium)
receptors called RYR (ligand gated calcium channels)
calcium then comes out - coming int the cell from the calcium channels and the sarcoplasmic recticulum
describe how calcium binds to cause contraction - (answer)when there is an influx of calcium in the cell
there is a myosin head separated by troponin. little binding sites for the myosin exist on the aktin but it
can't get to it because of the troponin. calcium therefore binds to the tropinin causing a confirmational
change in troponin so it will move and take the tropomyosin with it. the myosin can then bind to the
aktin molecules when it binds it activates ATP
