Term
| What are two types of cardiac myocytes and what is the difference in their funcitons |
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Definition
contractile cells do excitation contraction coupling and produce the strength of contraction.
pacemaker cells initiate contraction but they do not contribute to the strength of contraction. |
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Term
| Examples of Pacemaker cells |
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Definition
| SA node, AV node, Purkinje Fibers |
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Term
| These cells initiate depolarization and are autorythmic |
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Definition
pacemaker cells.
SA, AV, purkinje |
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Term
| are cardiac myocytes more similar to skeletal or smooth muscle |
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Definition
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Term
| When looking at a micrograph of a single cardiac myocyte what are the striations that go deep into the center of the myocyte |
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Definition
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Term
| What is the location and purpose of intercalated discs |
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Definition
| They are in between the individual myocytes where the membranes fuse to form permeable communicationg junctions that allow for rapid diffusion of ions. |
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Term
| What do gap junctions allow for |
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Definition
| Spread of the depolarization by the Ca++ ions throughout the cells. Contraction as a unit. |
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Term
| What are each of the phases of the action potential for a contractile cardiac myocyte |
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Definition
0- depolarization due to VG Na+ channels opening.
1- initial repolarization due to closure of VG Na+ channels.
2- Plateau due to the VG Ca++ channels that are slow to open and slow to close. K+ permeability decreases about five-fold preventing early return of a.p. to the resting level.
3- rapid repolarization due to decrease in permeability to Ca++ and increase in permeability to K+. So no more positive charges are coming in(Ca) and a few positive charges are leaving(K).
4-resting membrane potential resets in preparation for the next a.p. |
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Term
| What happens to the permeability of Na during an action potential in a cardiac myocyte |
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Definition
| during phase 0 it shoots up rapidly and in phase 1 it falls just as rapidly. |
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Term
| What happens to the permeability of K during a contractile cardiac myocyte a.p. |
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Definition
| during phase 2 it drops and then begins to rise again during phase 3 and in phase 4 it is high again during the reset. |
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Term
What happens to the permeability of Ca++ during the contractile cardiac myocyte a.p.
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Definition
| During phase 2 it rise significantly and during phase 3 it slowly lowers until it resets during phase 4. |
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Term
| which has a longer refractory period, cardiac muscle fibers or skeletal muscle fibers and why? |
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Definition
| cardiac mm fibers becuase the a.p. is so long so the refractory period must be longer. The functional advantage is that you can't stack a.p.'s in cardiac myocytes meaning you can't get tetany. It allows the ventricles to have a diastole phase and refill before systole. |
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Term
| What will happen if you get a contraction during the relative refractory period? |
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Definition
| It won't be as good as a normal contraction. |
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Term
| What are the two refractory periods? Which one will allow for another contraction. |
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Definition
| absolute and relative. You can have a new a.p. during the relative if it is a very intense stimulation. You can never have an a.p. during the absolute refractory period. |
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Term
| What are the steps of excitation contraction coupling in cardiac myocytes |
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Definition
| AP generated by the fast VG Na+ channels. Ca++ enters the cell through the DHPR(VGCC) and stimulates CICR from the SR. BOTH of these sources of Ca bind to the troponin C to allow for actin/myosin interaction. When the contraction is finished and it is time for relaxation Ca is pumped back into the SR by the SERCA, out of the cell by the ATPase, and out of the cell by the Na/Ca exchanger which pumps 3 Na in for every 1 Ca that is pumped out causing a slight depolarization. |
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Term
| What is the major mechanism for altering the force of cardiac myocyte contraction since we can't stack a.p.'s |
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Definition
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Term
| What are the ways that we can manipulate Ca++ to alter the force of contraction? |
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Definition
| adrenergic receptor stimulation , beta blockers, verapamil, and nifedipine |
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Term
| How do verapamil and nifedipine work? |
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Definition
| They are VG Ca++ channel blockers |
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Term
| How do beta blockers alter Ca++ in the cells? |
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Definition
| they block betal adrenergic receptors which is going to decrease th permeability of VG Ca++ channel opening which will decrease HR which will decrease CO which will decrease BP. |
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Term
| What is digoxin and what does it do. What is its other name? |
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Definition
| It is also called Digitalis(or something like that) and it is used for heart failure to increase cardiac contraction and therefore cardiac output. It does this by inhibiting the Na/K pump meaning that Na is going to build up inside of the cell. When Na levels get high enough the Na/Ca exchanger is slowed and sometimes even reversed so that it bring Ca INTO the cell and takes Na out instead of the other way around. With more Ca in the cell you are going to increase cardiac myocyte contractility(HR) and CO. |
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Term
| What are some structural differences between cardiac myocytes that are contractile and those that are not. |
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Definition
| pacemakcer cells don't have as much actine and myosin, they aren't organized into sarcomeres, they don't have t-tubules, and they have a faster conducting rate. The action potential looks way different. |
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Term
| What is the I-f and what is it due to? |
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Definition
| The funny current is in pacemaker cells and it is due to the spontaneously leaking of Na into the cells causing a slow depolarization until threshold is met and then the ap occurs activating VG Ca++ and eventually VG K+ channels to repolarize. It is activated with hyperpolarization or by cyclic nucleotides (e.g. beta adrenergic- cAMP) |
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Term
What will NEpi do to the automatic depolarization slope?
Ach? |
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Definition
NEpi will make the slope steeper(faster spontaneous depolarization.
Ach will make the slope less steep (slower spontaneous depolarization). |
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Term
| What are the three stages of the automatic rhythmicity and action potential for conductile cardiac myocytes? |
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Definition
I-f(spontaneous leakiness of Na into the cell--> automatic depolarization)
I-Ca (fast Na channels are inactivated and slow Ca channels are activated causing the ap)
I-K (when these open the cell repolarizes and you get a little bit of an overshoot before the K channels close and the I-f channels open once again. |
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Term
| What are the paces of the 3 types of conductile cells. Which one is the pacemaker in a healthy person? |
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Definition
SA nodal cells (60-80/min)
AV nodal fibers (40-55/min)
Purkinje fibers(15-35/min)
The SA node is the pacemaker in the healthy person. |
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Term
What phases do the contractile cells
have the the conductile cells do not have? |
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Definition
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Term
| what is the difference in phase 0 in conductile vs contractile |
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Definition
| in conductile cells phase 0 is due to the VG Ca channels and in contractile cells phase 0 is due to the VG Na channels. |
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Term
| What is the cause of the differences is phase 4 |
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Definition
conductile- VG Na channels leaking causing automatic depolarization.
contractile- phase 4 is the resetting phase after the VG K channels close. |
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