RUSH - ADVANCED
PHARMACOLOGY - NSG 531 -
EXAM 3 WITH ACTUAL CORRECT
QUESTIONS AND VERIFIED
DETAILED ANSWERS ALREADY
GRADED A+ GUARANTEED PASS
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
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 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 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
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
the ATP will be used to generate the sliding of the aktin and the myosin filaments against each other
shortening the muscle cell causing contraction
Describe how adrenergic stimulation increases the force of contraction through inotropic effects
NE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
leads to phosphorylation of Ca channels and opens them
increases inward movement of Ca
there is also increased release of Ca from the SR
increases actin/myosin interaction
increases force of contraction
Describe how adrenergic stimulation increases the force of contraction through chronotropic effects
NE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
results in phosphorylation of Ca2 channels and opens them
increases inward movement of Ca2
shortens phase 0 by increasing the opening of L-type calcium in pacemaker
heightened sympathetic state
shortens effective refractory period
increases rate of contraction
how do catecholamines effect the NaK ATPase Pump
epi to beta 1 - g coupled protein receptor
increase in cAMP
activate protein kinase
phosphorylate and increase in ATPase proteins available on the cell surface
this is why we give epi during hypoxia - cardiac arrest - so that we can initiate more action potentials
how does cholinergic stimulation work to decrease heart rate
effects on m2 receptors
acetylcholine binds to g coupled, alpha subunit comes off
can bind to t-type calcium channel - opens after funny sodium and before L-type - if it binds it will inhibit
PHARMACOLOGY - NSG 531 -
EXAM 3 WITH ACTUAL CORRECT
QUESTIONS AND VERIFIED
DETAILED ANSWERS ALREADY
GRADED A+ GUARANTEED PASS
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
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 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 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
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
the ATP will be used to generate the sliding of the aktin and the myosin filaments against each other
shortening the muscle cell causing contraction
Describe how adrenergic stimulation increases the force of contraction through inotropic effects
NE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
leads to phosphorylation of Ca channels and opens them
increases inward movement of Ca
there is also increased release of Ca from the SR
increases actin/myosin interaction
increases force of contraction
Describe how adrenergic stimulation increases the force of contraction through chronotropic effects
NE and epi bind to adenylyl cyclase coupled g proteins (beta 1)
results in phosphorylation of Ca2 channels and opens them
increases inward movement of Ca2
shortens phase 0 by increasing the opening of L-type calcium in pacemaker
heightened sympathetic state
shortens effective refractory period
increases rate of contraction
how do catecholamines effect the NaK ATPase Pump
epi to beta 1 - g coupled protein receptor
increase in cAMP
activate protein kinase
phosphorylate and increase in ATPase proteins available on the cell surface
this is why we give epi during hypoxia - cardiac arrest - so that we can initiate more action potentials
how does cholinergic stimulation work to decrease heart rate
effects on m2 receptors
acetylcholine binds to g coupled, alpha subunit comes off
can bind to t-type calcium channel - opens after funny sodium and before L-type - if it binds it will inhibit
